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  • 451.
    Zetterström, Henrik
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Jonsson, Lars O
    Pressure characteristics of the Ambu CPAP system and  the Servo ventilator 900C  in CPAP mode1987Ingår i: Acta Anaesthesiologica Scandinavica, Vol. 31, s. 104-110Artikel i tidskrift (Refereegranskat)
  • 452.
    Zetterström, Henrik
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Wiklund, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    A new nomogram facilitating adequate haemodilution1986Ingår i: Acta Anaesthesiologica Scandinavica, Vol. 30, s. 300-304Artikel i tidskrift (Refereegranskat)
  • 453.
    Zoerner, Frank
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Department of Operative- and Intensive Care Medicine, Hallands Hospital Halmstad, Halmstad, Sweden.
    Novel Interventions in Cardiac Arrest: Targeted Temperature Management, Methylene Blue, S-PBN, Amiodarone, Milrinone and Esmolol,  Endothelin and Nitric Oxide In Porcine Resuscitation Models2015Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    It is a major clinical problem that survival rates after out-of-hospital cardiac arrest have not markedly improved during the last decades, despite extensive research and the introduction of new interventions. However, recent studies have demonstrated promising treatments such as targeted temperature management (TTM) and methylene blue (MB).

    In our first study, we investigated the effect of MB administered during experi-mental cardiopulmonary resuscitation (CPR) in the setting of postponed hypother-mia in piglets. We set out to study if MB could compensate for a delay to establish targeted TTM. The study demonstrated that MB more than compensated for 30 min delay in induction of TTM. The effect of MB added to that of TTM.

    The second study examined the effects of TTM and S-PBN on the endothelin system and nitric oxide synthases (NOS) after prolonged CA in a porcine CPR mod-el. The study was designed to understand the cardioprotective mechanism of S-PBN and TTM by their influence on the endothelin system and NOS regulation. We veri-fied for the first time, that these two cardioprotective postresuscitative interventions activate endothelin-1 and its receptors concomitantly with eNOS and nNOS in the myocardium. We concluded that nitric oxide and endothelin pathways are implicated in the postresuscitative cardioprotective effects of TTM.

    The third study compared survival and hemodynamic effects of low-dose amio-darone and vasopressin to vasopressin in a porcine hypovolemic CA model. The study was designed to evaluate whether resuscitation with amiodarone and vasopressin compared to vasopressin alone would have an impact on resuscitation success, survival, and hemodynamic parameters after hemorrhagic CA. We found that combined resuscitation with amiodarone and vasopressin after hemorrhagic circulatory arrest resulted in greater 3-hour survival, better preserved hemodynamic parameters and smaller myocardial injury compared to resuscitation with vasopressin only.

    In our fourth study we planned to compare hemodynamic parameters between the treatment group (milrinone, esmolol and vasopressin; MEV) and control group (vasopressin only) during resuscitation from prolonged cardiac arrest in piglets. The study was designed to demonstrate if MEV treatment improved hemodynamics or cardiac damage compared to controls. We demonstrated that MEV treatment reduced cardiac injury compared with vasopressin alone.

    Delarbeten
    1. Improved neuroprotective effect of methylene blue with hypothermia after porcine cardiac arrest
    Öppna denna publikation i ny flik eller fönster >>Improved neuroprotective effect of methylene blue with hypothermia after porcine cardiac arrest
    Visa övriga...
    2013 (Engelska)Ingår i: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 57, nr 8, s. 1073-1082Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Background

    Induced mild hypothermia and administration of methylene blue (MB) have proved to have neuroprotective effects in cardiopulmonary resuscitation (CPR); however, induction of hypothermia takes time. We set out to determine if MB administered during CPR could add to the histologic neuroprotective effect of hypothermia.

    Methods

    A piglet model of extended cardiac arrest (12 min of untreated cardiac arrest and 8 min of CPR) was used to assess possible additional neuroprotective effects of MB when administered during CPR before mild therapeutic hypothermia induced 30 min after restoration of spontaneous circulation (ROSC). Three groups were compared: C group (n = 8) received standard CPR; PH group (n = 8) received standard CPR but 30 min after ROSC these piglets were cooled to 34°C; the PH+MB group (n = 8) received an MB infusion 1 min after commencement of CPR and the same cooling protocol as the PH group. Three hours later, the animals were killed. Immediately after death, the brains were harvested pending histological and immunohistological analysis.

    Results

    Circulatory variables were similar in the groups except that cardiac output was greater in the PH+MB group 2–3 h after ROSC. Cerebral cortical neuronal injury and blood–brain barrier disruption was greatest in the C group and least in the MB group. The neuroprotective effect of MB and hypothermia was significantly greater than that of delayed hypothermia alone.

    Conclusion

    Administration of MB during CPR added to the short term neuroprotective effects of induced mild hypothermia induced 30 min after ROSC.

    Nationell ämneskategori
    Medicin och hälsovetenskap
    Identifikatorer
    urn:nbn:se:uu:diva-199854 (URN)10.1111/aas.12106 (DOI)000323075000017 ()23577658 (PubMedID)
    Tillgänglig från: 2013-05-17 Skapad: 2013-05-17 Senast uppdaterad: 2017-12-06Bibliografiskt granskad
    2. Therapeutic hypothermia activates the endothelin and nitric oxide systems after cardiac arrest in a pig model of cardiopulmonary resuscitation
    Öppna denna publikation i ny flik eller fönster >>Therapeutic hypothermia activates the endothelin and nitric oxide systems after cardiac arrest in a pig model of cardiopulmonary resuscitation
    2013 (Engelska)Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 8, nr 5, s. e64792-Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Post-cardiac arrest myocardial dysfunction is a major cause of mortality in patients receiving successful cardiopulmonary resuscitation (CPR). Mild therapeutic hypothermia (MTH) is the recommended treatment after resuscitation from cardiac arrest (CA) and is known to exert neuroprotective effects and improve short-term survival. Yet its cytoprotective mechanisms are not fully understood. In this study, our aim was to determine the possible effect of MTH on vasoactive mediators belonging to the endothelin/nitric oxide axis in our porcine model of CA and CPR. Pigs underwent either untreated CA or CA with subsequent CPR. After state-of-the-art resuscitation, the animals were either left untreated, cooled between 32-34°C after ROSC or treated with a bolus injection of S-PBN (sodium 4-[(tert-butylimino) methyl]benzene-3-sulfonate N-oxide) until 180 min after ROSC, respectively. The expression of endothelin 1 (ET-1), endothelin converting enzyme 1 (ECE-1), and endothelin A and B receptors (ETAR and ETBR) transcripts were measured using quantitative real-time PCR while protein levels for the ETAR, ETBR and nitric oxide synthases (NOS) were assessed using immunohistochemistry and Western Blot. Our results indicated that the endothelin system was not upregulated at 30, 60 and 180 min after ROSC in untreated postcardiac arrest syndrome. Post-resuscitative 3 hour-long treatments either with MTH or S-PBN stimulated ET-1, ECE-1, ETAR and ETBR as well as neuronal NOS and endothelial NOS in left ventricular cardiomyocytes. Our data suggests that the endothelin and nitric oxide pathways are activated by MTH in the heart.

    Nationell ämneskategori
    Anestesi och intensivvård
    Identifikatorer
    urn:nbn:se:uu:diva-200585 (URN)10.1371/journal.pone.0064792 (DOI)000319435600076 ()23717659 (PubMedID)
    Tillgänglig från: 2013-05-31 Skapad: 2013-05-31 Senast uppdaterad: 2017-12-06Bibliografiskt granskad
    3. Resuscitation with amiodarone increases survival after hemorrhage and ventricular fibrillation in pigs
    Öppna denna publikation i ny flik eller fönster >>Resuscitation with amiodarone increases survival after hemorrhage and ventricular fibrillation in pigs
    2014 (Engelska)Ingår i: Journal of Trauma and Acute Care Surgery, ISSN 2163-0755, Vol. 76, nr 6, s. 1402-1408Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    BACKGROUND: The aim of this experimental study was to compare survival and hemodynamic effects of a low-dose amiodarone and vasopressin compared with vasopressin in hypovolemic cardiac arrest model in piglets. METHODS: Eighteen anesthetized male piglets (with a weight of 25.3 [1.8] kg) were bled approximately 30% of the total blood volume via the femoral artery to a mean arterial blood pressure of 35 mm Hg in a 15-minute period. Afterward, the piglets were subjected to 4 minutes of untreated ventricular fibrillation followed by 11 minutes of open-chest cardiopulmonary resuscitation. At 5 minutes, circulatory arrest amiodarone 1 mg/kg was intravenously administered in the amiodarone group (n = 9), while the control group received the same amount of saline (n = 9). At the same time, all piglets received vasopressin 0.4 U/kg intravenously administered and hypertonic-hyperoncotic solution 3-mL/kg infusion for 20 minutes. Internal defibrillation was attempted from 7 minutes of cardiac arrest to achieve restoration of spontaneous circulation. The experiment was terminated 3 hours after resuscitation. RESULTS: Three-hour survival was greater in the amiodarone group (p = 0.02). After the successful resuscitation, the amiodarone group piglets had significantly lower heart rate as well as greater systolic, diastolic, and mean arterial pressure. Troponin I plasma concentrations were lower and urine output was greater in the amiodarone group. CONCLUSION: Combined resuscitation with amiodarone and vasopressin after hemorrhagic circulatory arrest resulted in greater 3-hour survival, better preserved hemodynamic parameters, and smaller myocardial injury compared with resuscitation with vasopressin only.

    Nyckelord
    Amiodarone, cardiac arrest, ventricular fibrillation, hemorrhage, pigs
    Nationell ämneskategori
    Kirurgi
    Identifikatorer
    urn:nbn:se:uu:diva-228547 (URN)10.1097/TA.0000000000000243 (DOI)000337145500011 ()
    Tillgänglig från: 2014-07-17 Skapad: 2014-07-16 Senast uppdaterad: 2015-02-03Bibliografiskt granskad
    4. Milrinone and esmolol decrease cardiac damage after resuscitation from prolonged cardiac arrest
    Öppna denna publikation i ny flik eller fönster >>Milrinone and esmolol decrease cardiac damage after resuscitation from prolonged cardiac arrest
    Visa övriga...
    (Engelska)Manuskript (preprint) (Övrigt vetenskapligt)
    Abstract [en]

    Background: Long-term survival after cardiac arrest (CA) due to shock-refractory ventricular fibrillation (VF) is low. Clearly, there is a need for new pharmacological interventions in the setting of cardiopulmonary resuscitation (CPR) to improve outcome. Here, hemodynamic parameters and cardiac damage are compared between the treatment group (milrinone, esmolol and vasopressin) and controls (vasopressin only) during resuscitation from prolonged CA in piglets.

    Methods: Twenty-six immature male piglets were subjected to 12 min VF followed by 8 min CPR. The treatment group (n=13) received i.v. boluses vasopressin 0.4 U∙kg−1, esmolol 250 μg∙kg−1 and milrinone 25 μg∙kg−1 after 13 min, followed by i.v. boluses esmolol 375 μg∙kg−1 and milrinone 25 μg∙kg−1 after 18 min and continuous esmolol 15 μg∙kg−1∙h−1 infusion during 180 min reperfusion, while controls (n=13) received equal amounts of vasopressin and saline. A 200J monophasic counter-shock was delivered to achieve resumption of spontaneous circulation (ROSC) after 8 min CPR. If ROSC was not achieved, another 200J defibrillation and bolus vasopressin 0.4 U∙kg−1 were administered in both groups. DC shocks at 360J were applied as one shot min−1 over maximally 5 min. Hemodynamic variables and troponin I as a marker of cardiac injury were recorded.

    Results: Troponin I levels after 180 min reperfusion were lower in the treatment group than in controls (p<0.05). The treatment group received less norepinephrine (p<0.01) and had greater diuresis (p<0.01). There was no difference in survival between groups.

    Conclusions: The combination of milrinone, esmolol and vasopressin decreased cardiac injury compared with vasopressin alone. 

    Nyckelord
    Cardiac arrest, resumption of spontaneous circulation, ROSC, milrinone, vasopressin, esmolol, I/R injury, reperfusion injury, cardioprotection, myocardial ischemia, epinephrine, resuscitation
    Nationell ämneskategori
    Anestesi och intensivvård Medicin och hälsovetenskap
    Forskningsämne
    Anestesiologi och intensivvård
    Identifikatorer
    urn:nbn:se:uu:diva-237869 (URN)
    Tillgänglig från: 2014-12-06 Skapad: 2014-12-06 Senast uppdaterad: 2015-06-11
  • 454.
    Zoerner, Frank
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper.
    Lennmyr, Fredrik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Wiklund, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Martijn, Cécile
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - BMC.
    Semenas, Egidijus
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Milrinone and esmolol decrease cardiac damage after resuscitation from prolonged cardiac arrestManuskript (preprint) (Övrigt vetenskapligt)
    Abstract [en]

    Background: Long-term survival after cardiac arrest (CA) due to shock-refractory ventricular fibrillation (VF) is low. Clearly, there is a need for new pharmacological interventions in the setting of cardiopulmonary resuscitation (CPR) to improve outcome. Here, hemodynamic parameters and cardiac damage are compared between the treatment group (milrinone, esmolol and vasopressin) and controls (vasopressin only) during resuscitation from prolonged CA in piglets.

    Methods: Twenty-six immature male piglets were subjected to 12 min VF followed by 8 min CPR. The treatment group (n=13) received i.v. boluses vasopressin 0.4 U∙kg−1, esmolol 250 μg∙kg−1 and milrinone 25 μg∙kg−1 after 13 min, followed by i.v. boluses esmolol 375 μg∙kg−1 and milrinone 25 μg∙kg−1 after 18 min and continuous esmolol 15 μg∙kg−1∙h−1 infusion during 180 min reperfusion, while controls (n=13) received equal amounts of vasopressin and saline. A 200J monophasic counter-shock was delivered to achieve resumption of spontaneous circulation (ROSC) after 8 min CPR. If ROSC was not achieved, another 200J defibrillation and bolus vasopressin 0.4 U∙kg−1 were administered in both groups. DC shocks at 360J were applied as one shot min−1 over maximally 5 min. Hemodynamic variables and troponin I as a marker of cardiac injury were recorded.

    Results: Troponin I levels after 180 min reperfusion were lower in the treatment group than in controls (p<0.05). The treatment group received less norepinephrine (p<0.01) and had greater diuresis (p<0.01). There was no difference in survival between groups.

    Conclusions: The combination of milrinone, esmolol and vasopressin decreased cardiac injury compared with vasopressin alone. 

  • 455.
    Zoerner, Frank
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Lennmyr, Fredrik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Wiklund, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Martijn, Cécile
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - BMC.
    Semenas, Egidijus
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Milrinone and esmolol decrease cardiac damage after resuscitation from prolonged cardiac arrest2015Ingår i: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 59, nr 4, s. 465-474Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Long-term survival after cardiac arrest (CA) due to shock-refractory ventricular fibrillation (VF) is low. Clearly, there is a need for new pharmacological interventions in the setting of cardiopulmonary resuscitation (CPR) to improve outcome. Here, hemodynamic parameters and cardiac damage are compared between the treatment group (milrinone, esmolol and vasopressin) and controls (vasopressin only) during resuscitation from prolonged CA in piglets.

    METHODS: A total of 26 immature male piglets were subjected to 12-min VF followed by 8-min CPR. The treatment group (n = 13) received i.v. (intravenous) boluses vasopressin 0.4 U/kg, esmolol 250 μg/kg and milrinone 25 μg/kg after 13 min, followed by i.v. boluses esmolol 375 μg/kg and milrinone 25 μg/kg after 18 min and continuous esmolol 15 μg/kg/h infusion during 180 min reperfusion, whereas controls (n = 13) received equal amounts of vasopressin and saline. A 200 J monophasic counter-shock was delivered to achieve resumption of spontaneous circulation (ROSC) after 8 min CPR. If ROSC was not achieved, another 200 J defibrillation and bolus vasopressin 0.4 U/kg would be administered in both groups. Direct current shocks at 360 J were applied as one shot per minute over maximally 5 min. Hemodynamic variables and troponin I as a marker of cardiac injury were recorded.

    RESULTS: Troponin I levels after 180 min reperfusion were lower in the treatment group than in controls (P < 0.05). The treatment group received less norepinephrine (P < 0.01) and had greater diuresis (P < 0.01). There was no difference in survival between groups.

    CONCLUSION: The combination of milrinone, esmolol and vasopressin decreased cardiac injury compared with vasopressin alone.

  • 456.
    Zoerner, Frank
    et al.
    Department of Operative and Intensive Care Medicine, Hallands Hospital Halmstad, Halmstad, Sweden.
    Semenas, Egidijus
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Resuscitation with amiodarone increases survival after hemorrhage and ventricular fibrillation in pigs2014Ingår i: Journal of Trauma and Acute Care Surgery, ISSN 2163-0755, E-ISSN 2163-0763, Vol. 76, nr 6, s. 1402-1408Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND:

    The aim of this experimental study was to compare survival and hemodynamic effects of a low-dose amiodarone and vasopressin compared with vasopressin in hypovolemic cardiac arrest model in piglets.

    METHODS:

    Eighteen anesthetized male piglets (with a weight of 25.3 [1.8] kg) were bled approximately 30% of the total blood volume via the femoral artery to a mean arterial blood pressure of 35 mm Hg in a 15-minute period. Afterward, the piglets were subjected to 4 minutes of untreated ventricular fibrillation followed by 11 minutes of open-chest cardiopulmonary resuscitation. At 5 minutes, circulatory arrest amiodarone 1 mg/kg was intravenously administered in the amiodarone group (n = 9), while the control group received the same amount of saline (n = 9). At the same time, all piglets received vasopressin 0.4 U/kg intravenously administered and hypertonic-hyperoncotic solution 3-mL/kg infusion for 20 minutes. Internal defibrillation was attempted from 7 minutes of cardiac arrest to achieve restoration of spontaneous circulation. The experiment was terminated 3 hours after resuscitation.

    RESULTS:

    Three-hour survival was greater in the amiodarone group (p = 0.02). After the successful resuscitation, the amiodarone group piglets had significantly lower heart rate as well as greater systolic, diastolic, and mean arterial pressure. Troponin I plasma concentrations were lower and urine output was greater in the amiodarone group.

    CONCLUSION:

    Combined resuscitation with amiodarone and vasopressin after hemorrhagic circulatory arrest resulted in greater 3-hour survival, better preserved hemodynamic parameters, and smaller myocardial injury compared with resuscitation with vasopressin only.

  • 457.
    Zoerner, Frank
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Wiklund, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Miclescu, Adriana
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Martijn, Cecile
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - BMC. Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Therapeutic hypothermia activates the endothelin and nitric oxide systems after cardiac arrest in a pig model of cardiopulmonary resuscitation2013Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 8, nr 5, s. e64792-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Post-cardiac arrest myocardial dysfunction is a major cause of mortality in patients receiving successful cardiopulmonary resuscitation (CPR). Mild therapeutic hypothermia (MTH) is the recommended treatment after resuscitation from cardiac arrest (CA) and is known to exert neuroprotective effects and improve short-term survival. Yet its cytoprotective mechanisms are not fully understood. In this study, our aim was to determine the possible effect of MTH on vasoactive mediators belonging to the endothelin/nitric oxide axis in our porcine model of CA and CPR. Pigs underwent either untreated CA or CA with subsequent CPR. After state-of-the-art resuscitation, the animals were either left untreated, cooled between 32-34°C after ROSC or treated with a bolus injection of S-PBN (sodium 4-[(tert-butylimino) methyl]benzene-3-sulfonate N-oxide) until 180 min after ROSC, respectively. The expression of endothelin 1 (ET-1), endothelin converting enzyme 1 (ECE-1), and endothelin A and B receptors (ETAR and ETBR) transcripts were measured using quantitative real-time PCR while protein levels for the ETAR, ETBR and nitric oxide synthases (NOS) were assessed using immunohistochemistry and Western Blot. Our results indicated that the endothelin system was not upregulated at 30, 60 and 180 min after ROSC in untreated postcardiac arrest syndrome. Post-resuscitative 3 hour-long treatments either with MTH or S-PBN stimulated ET-1, ECE-1, ETAR and ETBR as well as neuronal NOS and endothelial NOS in left ventricular cardiomyocytes. Our data suggests that the endothelin and nitric oxide pathways are activated by MTH in the heart.

  • 458.
    Östberg, Erland
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centrum för klinisk forskning, Västerås.
    Pulmonary Atelectasis in General Anaesthesia: Clinical Studies on the Counteracting Effects of Positive End-Expiratory Pressure2019Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    Partial lung collapse, i.e., pulmonary atelectasis, is common during general anaesthesia. The main causal mechanism is reduced lung volume with airway closure and subsequent gas absorption from preoxygenated alveoli. Atelectasis impairs oxygenation and forms the pathophysiological basis for postoperative pulmonary complications. Positive end-expiratory pressure (PEEP) counteracts the loss in lung volume, but its role in preventing atelectasis during anaesthesia is not clear.

    All studies included in this thesis were prospective randomized clinical trials. In the first study, oxygenation was used as a surrogate measure of atelectasis in obese patients undergoing laparoscopic gastric bypass. The subsequent studies used single-slice computed tomography (CT) to evaluate atelectasis in healthy patients undergoing non-abdominal surgery.

    Paper I: We studied the use of continuous positive airway pressure (CPAP) and PEEP during induction of anaesthesia and a reduced inspired oxygen fraction (FiO2) during emergence. Oxygenation was maintained in the group that received CPAP during induction, followed by a PEEP of 10 cmH2O. Postoperative oxygenation was impaired in the group that received a high FiO2 during emergence.

    Paper II: An early oxygen washout manoeuvre to quickly restore nitrogen levels and thus stabilize the alveoli, had no effect on atelectasis at the end of surgery. Both study groups exhibited small atelectasis after being ventilated with a moderate PEEP of 6-8 cmH2O during anaesthesia.

    Paper III: The effect of PEEP versus zero PEEP on atelectasis formation and oxygenation at the end of surgery was compared. The PEEP group maintained oxygenation better and exhibited less atelectasis than the zero-PEEP group, with atelectasis involving a median 1.8% of total lung area compared with 4.6% in the zero-PEEP group (P = 0.002).

    Paper IV: Postoperative atelectasis was compared between a group in which PEEP was maintained during emergence preoxygenation with FiO2 1.0 and a group in which PEEP was withdrawn just before the start of emergence preoxygenation with FiO2 1.0. The two groups had small atelectasis when fully awake at 30 min after extubation, with no statistically significant difference between them.  

    In conclusion, preserved end-expiratory lung volume is the key to avoiding atelectasis, in particular when an increased oxygen reserve is required during airway manipulation. PEEP is both necessary and sufficient to minimize atelectasis in healthy patients undergoing non-abdominal surgery.

    Delarbeten
    1. Preserved oxygenation in obese patients receiving protective ventilation during laparoscopic surgery: a randomized controlled study
    Öppna denna publikation i ny flik eller fönster >>Preserved oxygenation in obese patients receiving protective ventilation during laparoscopic surgery: a randomized controlled study
    Visa övriga...
    2016 (Engelska)Ingår i: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 60, nr 1, s. 26-35Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    BACKGROUND: Venous admixture from atelectasis and airway closure impedes oxygenation during general anaesthesia. We tested the hypothesis that continuous positive airway pressure (CPAP) during pre-oxygenation and reduced fraction of inspiratory oxygen (FIO2 ) during emergence from anaesthesia can improve oxygenation in patients with obesity undergoing laparoscopic surgery.

    METHODS: In the intervention group (n = 20, median BMI 41.9), a CPAP of 10 cmH2 O was used during pre-oxygenation and induction of anaesthesia, but no CPAP was used in the control group (n = 20, median BMI 38.1). During anaesthesia, all patients were ventilated in volume-controlled mode with an FIO2 of 0.4 and a positive end-expiratory pressure (PEEP) of 10 cmH2 O. During emergence, before extubation, the control group was given an FIO2 of 1.0 and the intervention group was divided into two subgroups, which were given an FIO2 of 1.0 or 0.31. Oxygenation was assessed perioperatively by the estimated venous admixture (EVA).

    RESULTS: The median EVA before pre-oxygenation was about 8% in both groups. During anaesthesia after intubation, the median EVA was 8.2% in the intervention vs. 13.2% in the control group (P = 0.048). After CO2 pneumoperitoneum, the median EVA was 8.4% in the intervention vs. 9.9% in the control group (P > 0.05). One hour post-operatively, oxygenation had deteriorated in patients given an FIO2 of 1.0 during emergence but not in patients given an FIO2 of 0.31.

    CONCLUSIONS: A CPAP of 10 cmH2 O during pre-oxygenation and induction, followed by PEEP after intubation, seemed to preserve oxygenation during anaesthesia. Post-operative oxygenation depended on the FIO2 used during emergence.

    Nationell ämneskategori
    Anestesi och intensivvård
    Forskningsämne
    Fysiologi; Anestesiologi och intensivvård
    Identifikatorer
    urn:nbn:se:uu:diva-264212 (URN)10.1111/aas.12588 (DOI)000368139400005 ()26235391 (PubMedID)
    Tillgänglig från: 2015-10-07 Skapad: 2015-10-07 Senast uppdaterad: 2019-04-08
    2. Minimizing atelectasis formation during general anaesthesia-oxygen washout is a non-essential supplement to PEEP
    Öppna denna publikation i ny flik eller fönster >>Minimizing atelectasis formation during general anaesthesia-oxygen washout is a non-essential supplement to PEEP
    Visa övriga...
    2017 (Engelska)Ingår i: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967, Vol. 122, nr 2, s. 92-98Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Background: Following preoxygenation and induction of anaesthesia, most patients develop atelectasis. We hypothesized that an immediate restoration to a low oxygen level in the alveoli would prevent atelectasis formation and improve oxygenation during the ensuing anaesthesia. Methods: We randomly assigned 24 patients to either a control group (n=12) or an intervention group (n=12) receiving an oxygen washout procedure directly after intubation. Both groups were, depending on body mass index, ventilated with a positive end-expiratory pressure (PEEP) of 6-8 cmH(2)O during surgery. The atelectasis area was studied by computed tomography before emergence. Oxygenation levels were evaluated by measuring blood gases and calculating estimated venous admixture (EVA). Results: The atelectasis areas expressed as percentages of the total lung area were 2.0 (1.5-2.7) (median [interquartile range]) and 1.8 (1.4-3.3) in the intervention and control groups, respectively. The difference was non-significant, and also oxygenation was similar between the two groups. Compared to oxygenation before the start of anaesthesia, oxygenation at the end of surgery was improved in the intervention group, mean (SD) EVA from 7.6% (6.6%) to 3.9% (2.9%) (P=.019) and preserved in the control group, mean (SD) EVA from 5.0% (5.3%) to 5.6% (7.1%) (P=.59). .Conclusion: Although the oxygen washout restored a low pulmonary oxygen level within minutes, it did not further reduce atelectasis size. Both study groups had small atelectasis and good oxygenation. These results suggest that a moderate PEEP alone is sufficient to minimize atelectasis and maintain oxygenation in healthy patients.

    Ort, förlag, år, upplaga, sidor
    TAYLOR & FRANCIS LTD, 2017
    Nyckelord
    Atelectasis, computed tomography, general anaesthesia, oxygenation, PEEP, protective ventilation, ventilator settings
    Nationell ämneskategori
    Anestesi och intensivvård
    Identifikatorer
    urn:nbn:se:uu:diva-323496 (URN)10.1080/03009734.2017.1294635 (DOI)000401756500004 ()28434271 (PubMedID)
    Tillgänglig från: 2017-06-22 Skapad: 2017-06-22 Senast uppdaterad: 2019-04-08Bibliografiskt granskad
    3. Positive End-expiratory Pressure Alone Minimizes Atelectasis Formation in Nonabdominal Surgery: A Randomized Controlled Trial
    Öppna denna publikation i ny flik eller fönster >>Positive End-expiratory Pressure Alone Minimizes Atelectasis Formation in Nonabdominal Surgery: A Randomized Controlled Trial
    Visa övriga...
    2018 (Engelska)Ingår i: Anesthesiology, ISSN 0003-3022, E-ISSN 1528-1175, Vol. 128, nr 6, s. 1117-1124Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Background: Various methods for protective ventilation are increasingly being recommended for patients undergoing general anesthesia. However, the importance of each individual component is still unclear. In particular, the perioperative use of positive end-expiratory pressure (PEEP) remains controversial. The authors tested the hypothesis that PEEP alone would be sufficient to limit atelectasis formation during nonabdominal surgery. Methods: This was a randomized controlled evaluator-blinded study. Twenty-four healthy patients undergoing general anesthesia were randomized to receive either mechanical ventilation with PEEP 7 or 9 cm H2O depending on body mass index (n = 12) or zero PEEP (n =12). No recruitment maneuvers were used. Hie primary outcome was atelectasis area as studied by computed tomography in a transverse scan near the diaphragm, at the end of surgery, before emergence. Oxygenation was evaluated by measuring blood gases and calculating the ratio of arterial oxygen partial pressure to inspired oxygen fraction (Pao(2)/Fio(2) ratio). Results: At the end of surgery, the median (range) atelectasis area, expressed as percentage of the total lung area, was 1.8 (0.3 to 9.9) in the PEEP group and 4.6 (1.0 to 10.2) in the zero PEEP group. Tire difference in medians was 2.8% (95% CI, 1.7 to 5.7%; A = 0.002). Oxygenation and carbon dioxide elimination were maintained in the PEEP group, but both deteriorated in the zero PEEP group. Conclusions: During nonabdominal surgery, adequate PEEP is sufficient to minimize atelectasis in healthy lungs and thereby maintain oxygenation. Titus, routine recruitment maneuvers seem unnecessary, and the authors suggest that they should only be utilized when clearly indicated.

    Ort, förlag, år, upplaga, sidor
    LIPPINCOTT WILLIAMS & WILKINS, 2018
    Nationell ämneskategori
    Anestesi och intensivvård
    Identifikatorer
    urn:nbn:se:uu:diva-363070 (URN)10.1097/ALN.0000000000002134 (DOI)000441172900012 ()29462011 (PubMedID)
    Tillgänglig från: 2018-10-12 Skapad: 2018-10-12 Senast uppdaterad: 2019-04-08Bibliografiskt granskad
    4. Positive end-expiratory pressure and postoperative atelectasis: A randomized controlled trial
    Öppna denna publikation i ny flik eller fönster >>Positive end-expiratory pressure and postoperative atelectasis: A randomized controlled trial
    Visa övriga...
    2019 (Engelska)Ingår i: Anesthesiology, ISSN 0003-3022, E-ISSN 1528-1175Artikel i tidskrift (Refereegranskat) In press
    Abstract [en]

    Background

    Positive end-expiratory pressure (PEEP) increases lung volume and protects against alveolar collapse during anesthesia. During emergence, safety preoxygenation preparatory to extubation makes the lung susceptible to gas absorption and alveolar collapse, especially in dependent regions being kept open by PEEP. We hypothesized that withdrawing PEEP before starting emergence preoxygenation would limit postoperative atelectasis formation.

    Methods

    This was a randomized controlled evaluator-blinded trial in 30 healthy patients undergoing non-abdominal surgery under general anesthesia and mechanical ventilation with PEEP 7 or 9 cm H2O depending on body mass index. A computed tomography scan at the end of surgery assessed baseline atelectasis. The study subjects were thereafter allocated to either maintained PEEP (n = 16) or zero PEEP (n = 14) during emergence preoxygenation. The primary outcome was change in atelectasis area as evaluated by a second computed tomography scan 30 min after extubation. Oxygenation was assessed by arterial blood gases.

    Results

    Baseline atelectasis was small and increased modestly during awakening, with no statistically significant difference between groups. With PEEP applied during awakening, the increase in atelectasis area was median (range) 1.6 (-1.1 to 12.3) cm2 and without PEEP 2.3 (-1.6 to 7.8) cm2. The difference was 0.7 cm2 (95% CI, -0.8 to 2.9 cm2; P = 0.400). Postoperative atelectasis for all patients was median 5.2 cm2 (95% CI, 4.3 to 5.7 cm2), corresponding to median 2.5% of the total lung area (95% CI, 2.0 to 3.0%). Postoperative oxygenation was unchanged in both groups when compared to oxygenation in the preoperative awake state.

    Conclusion

    Withdrawing PEEP before emergence preoxygenation does not reduce atelectasis formation after non-abdominal surgery. Despite using 100% O2 during awakening, postoperative atelectasis is small and does not affect oxygenation, possibly conditional on an open lung during anesthesia, as achieved by intraoperative PEEP.

    Nationell ämneskategori
    Anestesi och intensivvård
    Forskningsämne
    Anestesiologi och intensivvård
    Identifikatorer
    urn:nbn:se:uu:diva-381346 (URN)
    Tillgänglig från: 2019-04-08 Skapad: 2019-04-08 Senast uppdaterad: 2019-04-08
  • 459.
    Östberg, Erland
    et al.
    Västerås & Koping Hosp, Dept Anaesthesia & Intens Care, Västerås, Sweden..
    Auner, Udo
    Vasteras Hosp, Dept Radiol, Västerås, Sweden..
    Enlund, Mats
    Clin Res Ctr, Västerås, Sweden..
    Zetterström, Henrik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Edmark, Lennart
    Västeras & Koping Hosp, Dept Anaesthesia & Intens Care, Västerås, Sweden..
    Minimizing atelectasis formation during general anaesthesia-oxygen washout is a non-essential supplement to PEEP2017Ingår i: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967, Vol. 122, nr 2, s. 92-98Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Following preoxygenation and induction of anaesthesia, most patients develop atelectasis. We hypothesized that an immediate restoration to a low oxygen level in the alveoli would prevent atelectasis formation and improve oxygenation during the ensuing anaesthesia. Methods: We randomly assigned 24 patients to either a control group (n=12) or an intervention group (n=12) receiving an oxygen washout procedure directly after intubation. Both groups were, depending on body mass index, ventilated with a positive end-expiratory pressure (PEEP) of 6-8 cmH(2)O during surgery. The atelectasis area was studied by computed tomography before emergence. Oxygenation levels were evaluated by measuring blood gases and calculating estimated venous admixture (EVA). Results: The atelectasis areas expressed as percentages of the total lung area were 2.0 (1.5-2.7) (median [interquartile range]) and 1.8 (1.4-3.3) in the intervention and control groups, respectively. The difference was non-significant, and also oxygenation was similar between the two groups. Compared to oxygenation before the start of anaesthesia, oxygenation at the end of surgery was improved in the intervention group, mean (SD) EVA from 7.6% (6.6%) to 3.9% (2.9%) (P=.019) and preserved in the control group, mean (SD) EVA from 5.0% (5.3%) to 5.6% (7.1%) (P=.59). .Conclusion: Although the oxygen washout restored a low pulmonary oxygen level within minutes, it did not further reduce atelectasis size. Both study groups had small atelectasis and good oxygenation. These results suggest that a moderate PEEP alone is sufficient to minimize atelectasis and maintain oxygenation in healthy patients.

  • 460.
    Östberg, Erland
    et al.
    Västerås & Köping Hosp, Dept Anesthesia & Intens Care, Västerås, Sweden.
    Thorisson, Arnar
    Västerås & Köping Hosp, Dept Radiol, Västerås, Sweden.
    Enlund, Mats
    Clin Res Ctr, Västerås, Sweden.
    Zetterström, Henrik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Hedenstierna, Göran
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk fysiologi.
    Edmark, Lennart
    Västerås & Köping Hosp, Dept Anesthesia & Intens Care, Västerås, Sweden.
    Positive End-expiratory Pressure Alone Minimizes Atelectasis Formation in Nonabdominal Surgery: A Randomized Controlled Trial2018Ingår i: Anesthesiology, ISSN 0003-3022, E-ISSN 1528-1175, Vol. 128, nr 6, s. 1117-1124Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Various methods for protective ventilation are increasingly being recommended for patients undergoing general anesthesia. However, the importance of each individual component is still unclear. In particular, the perioperative use of positive end-expiratory pressure (PEEP) remains controversial. The authors tested the hypothesis that PEEP alone would be sufficient to limit atelectasis formation during nonabdominal surgery. Methods: This was a randomized controlled evaluator-blinded study. Twenty-four healthy patients undergoing general anesthesia were randomized to receive either mechanical ventilation with PEEP 7 or 9 cm H2O depending on body mass index (n = 12) or zero PEEP (n =12). No recruitment maneuvers were used. Hie primary outcome was atelectasis area as studied by computed tomography in a transverse scan near the diaphragm, at the end of surgery, before emergence. Oxygenation was evaluated by measuring blood gases and calculating the ratio of arterial oxygen partial pressure to inspired oxygen fraction (Pao(2)/Fio(2) ratio). Results: At the end of surgery, the median (range) atelectasis area, expressed as percentage of the total lung area, was 1.8 (0.3 to 9.9) in the PEEP group and 4.6 (1.0 to 10.2) in the zero PEEP group. Tire difference in medians was 2.8% (95% CI, 1.7 to 5.7%; A = 0.002). Oxygenation and carbon dioxide elimination were maintained in the PEEP group, but both deteriorated in the zero PEEP group. Conclusions: During nonabdominal surgery, adequate PEEP is sufficient to minimize atelectasis in healthy lungs and thereby maintain oxygenation. Titus, routine recruitment maneuvers seem unnecessary, and the authors suggest that they should only be utilized when clearly indicated.

  • 461.
    Östberg, Erland
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper.
    Thorisson, Arnar
    Enlund, Mats
    Zetterström, Henrik
    Hedenstierna, Göran
    Edmark, Lennart
    Positive end-expiratory pressure and postoperative atelectasis: A randomized controlled trial2019Ingår i: Anesthesiology, ISSN 0003-3022, E-ISSN 1528-1175Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background

    Positive end-expiratory pressure (PEEP) increases lung volume and protects against alveolar collapse during anesthesia. During emergence, safety preoxygenation preparatory to extubation makes the lung susceptible to gas absorption and alveolar collapse, especially in dependent regions being kept open by PEEP. We hypothesized that withdrawing PEEP before starting emergence preoxygenation would limit postoperative atelectasis formation.

    Methods

    This was a randomized controlled evaluator-blinded trial in 30 healthy patients undergoing non-abdominal surgery under general anesthesia and mechanical ventilation with PEEP 7 or 9 cm H2O depending on body mass index. A computed tomography scan at the end of surgery assessed baseline atelectasis. The study subjects were thereafter allocated to either maintained PEEP (n = 16) or zero PEEP (n = 14) during emergence preoxygenation. The primary outcome was change in atelectasis area as evaluated by a second computed tomography scan 30 min after extubation. Oxygenation was assessed by arterial blood gases.

    Results

    Baseline atelectasis was small and increased modestly during awakening, with no statistically significant difference between groups. With PEEP applied during awakening, the increase in atelectasis area was median (range) 1.6 (-1.1 to 12.3) cm2 and without PEEP 2.3 (-1.6 to 7.8) cm2. The difference was 0.7 cm2 (95% CI, -0.8 to 2.9 cm2; P = 0.400). Postoperative atelectasis for all patients was median 5.2 cm2 (95% CI, 4.3 to 5.7 cm2), corresponding to median 2.5% of the total lung area (95% CI, 2.0 to 3.0%). Postoperative oxygenation was unchanged in both groups when compared to oxygenation in the preoperative awake state.

    Conclusion

    Withdrawing PEEP before emergence preoxygenation does not reduce atelectasis formation after non-abdominal surgery. Despite using 100% O2 during awakening, postoperative atelectasis is small and does not affect oxygenation, possibly conditional on an open lung during anesthesia, as achieved by intraoperative PEEP.

78910 451 - 461 av 461
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