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Clausen, F., Marklund, N. & Hillered, L. (2019). Acute Inflammatory Biomarker Responses to Diffuse Traumatic Brain Injury in the Rat Monitored by a Novel Microdialysis Technique. Journal of Neurotrauma, 36(2), 201-211
Open this publication in new window or tab >>Acute Inflammatory Biomarker Responses to Diffuse Traumatic Brain Injury in the Rat Monitored by a Novel Microdialysis Technique
2019 (English)In: Journal of Neurotrauma, ISSN 0897-7151, E-ISSN 1557-9042, Vol. 36, no 2, p. 201-211Article in journal (Refereed) Published
Abstract [en]

Neuroinflammation is a major contributor to the progressive brain injury process induced by traumatic brain injury (TBI), and may play an important role in the pathophysiology of axonal injury. The immediate neuroinflammatory cascade cannot be characterized in the human setting. Therefore, we used the midline fluid percussion injury model of diffuse TBI in rats and a novel microdialysis (MD) method providing stable diffusion-driven biomarker sampling. Immediately post-injury, bilateral amphiphilic tri-block polymer coated MD probes (100 kDa cut off membrane) were inserted and perfused with Dextran 500 kDa-supplemented artificial cerebrospinal fluid (CSF) to optimize protein capture. Six hourly samples were analyzed for 27 inflammatory biomarkers (9 chemokines, 13 cytokines, and 5 growth factors) using a commercial multiplex biomarker kit. TBI (n = 6) resulted in a significant increase compared with sham-injured controls (n = 6) for five chemokines (eotaxin/CCL11, fractalkine/CX3CL1, LIX/CXCL5, monocyte chemoattractant protein [MCP]1α/CCL2, macrophage inflammatory protein [MIP]1α /CCL3), 10 cytokines (interleukin [IL]-1α, IL-1β, IL-4, IL-6, IL-10, IL-13, IL-17α, IL-18, interferon [IFN]-γ, tumor necrosis factor [TNF]-α), and four growth factors (epidermal growth factor [EGF], granulocyte-macrophage colony-stimulating factor [GM-CSF], leptin, vascular endothelial growth factor [VEGF]). Therefore, diffuse TBI was associated with an increased level of 18 of the 27 inflammatory biomarkers at one through six time points, during the observation period whereas the remaining 9 biomarkers were unaltered. The study shows that diffuse TBI induces an acute increase in a number of inflammatory biomarkers. The novel MD technique provides stable MD sampling suitable for further studies on the early neuroinflammatory cascade in TBI.

Keywords
diffuse axonal injury, inflammatory biomarkers, MD, rat, TBI
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-378744 (URN)10.1089/neu.2018.5636 (DOI)000459444800003 ()29790398 (PubMedID)
Funder
Swedish Research CouncilVINNOVAErik, Karin och Gösta Selanders Foundation
Available from: 2019-03-11 Created: 2019-03-11 Last updated: 2019-03-11Bibliographically approved
Vlachogiannis, P., Hillered, L., Khalil, F., Enblad, P. & Ronne-Engström, E. (2019). Interleukin-6 Levels in Cerebrospinal Fluid and Plasma in Patients with Severe Spontaneous Subarachnoid Hemorrhage. World Neurosurgery, 122, E612-E618
Open this publication in new window or tab >>Interleukin-6 Levels in Cerebrospinal Fluid and Plasma in Patients with Severe Spontaneous Subarachnoid Hemorrhage
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2019 (English)In: World Neurosurgery, ISSN 1878-8750, E-ISSN 1878-8769, Vol. 122, p. E612-E618Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Inflammatory processes play a key role in the pathophysiology of subarachnoid hemorrhage (SAH). This study evaluated whether different temporal patterns of intrathecal and systemic inflammation could be identified in the acute phase after SAH. The intensity of the inflammation was also assessed in clinical subgroups. METHODS: Cerebrospinal fluid (CSF) and blood samples were collected at days 1, 4, and 10 after ictus in 44 patients with severe SAH. Interleukin-6 (IL-6) was analyzed by a routine monoclonal antibody-based method. Median IL-6 values for each day were calculated. Day 4 IL-6 values were compared in dichotomized groups (age, sex, World Federation of Neurosurgical Societies [WFNS] grade, Fisher scale grade, outcome, vasospasm, central nervous system infection and systemic infections). RESULTS: CSF IL-6 levels were significantly elevated from day 1 to days 4 and 10, whereas plasma IL-6 showed a different trend at lower levels. Median CSF IL-6 concentrations for days 1, 4, and 10 were 876.5, 3361, and 1567 ng/L, whereas plasma was 26, 27.5, and 15.9 ng/L, respectively. No significant differences in CSF concentrations were observed between the subgroups, with the most prominent one being in day 4 IL-6 in the WFNS subgroups (grades 1-3 vs. 4-5, 1158.5 vs. 5538 ng/L; P = 0.056). Patients with systemic infection had significantly higher plasma IL-6 concentrations than patients without infection (31 vs. 16.05 ng/L, respectively; P = 0.028). CONCLUSIONS: Distinctly different inflammatory patterns could be seen intrathecally compared with the systemic circulation. In plasma, a significant difference in the intensity of the inflammation was seen in cases with systemic infection. No other subgroup showed statistically significant differences.

Place, publisher, year, edition, pages
ELSEVIER SCIENCE INC, 2019
Keywords
Inflammatory response, Interleukin-6, Neuroinflammation, SAH, Subarachnoid hemorrhage
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-377213 (URN)10.1016/j.wneu.2018.10.113 (DOI)000457328100075 ()
Available from: 2019-02-25 Created: 2019-02-25 Last updated: 2019-02-25Bibliographically approved
Dyhrfort, P., Shen, Q., Clausen, F., Eriksson, M., Enblad, P., Kamali-Moghaddam, M., . . . Hillered, L. (2019). Monitoring of Protein Biomarkers of Inflammation in Human Traumatic Brain Injury Using Microdialysis and Proximity Extension Assay Technology in Neurointensive Care. Journal of Neurotrauma, 36(20), 2872-2885
Open this publication in new window or tab >>Monitoring of Protein Biomarkers of Inflammation in Human Traumatic Brain Injury Using Microdialysis and Proximity Extension Assay Technology in Neurointensive Care
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2019 (English)In: Journal of Neurotrauma, ISSN 0897-7151, E-ISSN 1557-9042, Vol. 36, no 20, p. 2872-2885Article in journal (Refereed) Published
Abstract [en]

Traumatic brain injury (TBI) is followed by secondary injury mechanisms strongly involving neuroinflammation. To monitor the complex inflammatory cascade in human TBI, we used cerebral microdialysis (MD) and multiplex proximity extension assay (PEA) technology and simultaneously measured levels of 92 protein biomarkers of inflammation in MD samples every three hours for five days in 10 patients with severe TBI under neurointensive care. One mu L MD samples were incubated with paired oligonucleotide-conjugated antibodies binding to each protein, allowing quantification by real-time quantitative polymerase chain reaction. Sixty-nine proteins were suitable for statistical analysis. We found five different patterns with either early (<48 h; e.g., CCL20, IL6, LIF, CCL3), mid (48-96 h; e.g., CCL19, CXCL5, CXCL10, MMP1), late (>96 h; e.g., CD40, MCP2, MCP3), biphasic peaks (e.g., CXCL1, CXCL5, IL8) or stable (e.g., CCL4, DNER, VEGFA)/low trends. High protein levels were observed for e.g., CXCL1, CXCL10, MCP1, MCP2, IL8, while e.g., CCL28 and MCP4 were detected at low levels. Several proteins (CCL8, -19, -20, -23, CXCL1, -5, -6, -9, -11, CST5, DNER, Flt3L, and SIRT2) have not been studied previously in human TBI. Cross-correlation analysis revealed that LIF and CXCL5 may play a central role in the inflammatory cascade. This study provides a unique data set with individual temporal trends for potential inflammatory biomarkers in patients with TBI. We conclude that the combination of MD and PEA is a powerful tool to map the complex inflammatory cascade in the injured human brain. The technique offers new possibilities of protein profiling of complex secondary injury pathways.

Place, publisher, year, edition, pages
MARY ANN LIEBERT, INC, 2019
Keywords
biomarkers, inflammation, microdialysis, molecular tools, neurointensive care, proteomics, traumatic brain injury
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-396069 (URN)10.1089/neu.2018.6320 (DOI)000472621900001 ()31017044 (PubMedID)
Funder
Swedish Research CouncilVinnova
Available from: 2019-10-30 Created: 2019-10-30 Last updated: 2019-10-30Bibliographically approved
Lewén, A., Dyhrfort, P., Clausen, F., Enblad, P. & Hillered, L. (2018). A Dedicated 21-Plex Pea Panel For High-Sensitive Protein Biomarker Detection Using Micro-Dialysis In Traumatic Brain Injury. Paper presented at 3rd Joint Symposium of the International-and-National-Neurotrauma-Societies-and-AANS/CNS-Section on Neurotrauma and Critical Care, AUG 11-16, 2018, Toronto, CANADA. Journal of Neurotrauma, 35(16), A130-A130
Open this publication in new window or tab >>A Dedicated 21-Plex Pea Panel For High-Sensitive Protein Biomarker Detection Using Micro-Dialysis In Traumatic Brain Injury
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2018 (English)In: Journal of Neurotrauma, ISSN 0897-7151, E-ISSN 1557-9042, Vol. 35, no 16, p. A130-A130Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
MARY ANN LIEBERT, INC, 2018
Keywords
Biomarker, Inflammation / Immune Function, Monitoring, Neurocritical Care
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-363876 (URN)000441527400353 ()
Conference
3rd Joint Symposium of the International-and-National-Neurotrauma-Societies-and-AANS/CNS-Section on Neurotrauma and Critical Care, AUG 11-16, 2018, Toronto, CANADA
Available from: 2018-11-12 Created: 2018-11-12 Last updated: 2018-11-12Bibliographically approved
Rostami, E., Engquist, H., Howells, T., Johnson, U., Ronne-Engström, E., Nilsson, P., . . . Enblad, P. (2018). Early low cerebral blood flow and high cerebral lactate: prediction of delayed cerebral ischemia in subarachnoid hemorrhage. Journal of Neurosurgery, 128(6), 1762-1770
Open this publication in new window or tab >>Early low cerebral blood flow and high cerebral lactate: prediction of delayed cerebral ischemia in subarachnoid hemorrhage
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2018 (English)In: Journal of Neurosurgery, ISSN 0022-3085, E-ISSN 1933-0693, Vol. 128, no 6, p. 1762-1770Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE Delayed cerebral ischemia (DCI) following subarachnoid hemorrhage (SAH) is one of the major contributors to poor outcome. It is crucial to be able to detect early signs of DCI to prevent its occurrence. The objective of this study was to determine if low cerebral blood flow (CBF) measurements and pathological microdialysis parameters measured at the bedside can be observed early in patients with SAH who later developed DCI. METHODS The authors included 30 patients with severe SAH. The CBF measurements were performed at Day 0-3 after disease onset, using bedside xenon-CT. Interstitial glucose, lactate, pyruvate, glycerol, and glutamate were measured using microdialysis. RESULTS Nine of 30 patients developed DCI. Patients with DCI showed significantly lower global and regional CBF, and lactate was significantly increased in these patients. A high lactate/pyruvate ratio was also detected in patients with DCI. CONCLUSIONS Early low CBF measurements and a high lactate and lactate/pyruvate ratio may be early warning signs of the risk of developing DCI. The clinical value of these findings needs to be confirmed in larger studies.

Keywords
CBF, CBF = cerebral blood flow, CPP = cerebral perfusion pressure, DCI, DCI = delayed cerebral ischemia, GCS, GCS-M = Glasgow Coma Scale, GCS-motor, GOSE = Glasgow Outcome Scale–Extended, ICP = intracranial pressure, L/P = lactate/pyruvate, MD = microdialysis, NIC = neurointensive care, ROI = region of interest, SAH, SAH = subarachnoid hemorrhage, Xe-CT = xenon-CT, cerebral blood flow, delayed cerebral ischemia, lactate, lactate/pyruvate ratio, subarachnoid hemorrhage, vascular disorders, vasospasm, xenon-CT
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-330940 (URN)10.3171/2016.11.JNS161140 (DOI)000440653000023 ()28574309 (PubMedID)
Available from: 2017-10-07 Created: 2017-10-07 Last updated: 2018-10-12Bibliographically approved
Abu Hamdeh, S., Rollman Waara, E., Möller, C., Söderberg, L., Basun, H., Alafuzoff, I., . . . Marklund, N. (2018). Rapid amyloid-β oligomer and protofibril accumulation in traumatic brain injury. Brain Pathology, 28(4), 451-462
Open this publication in new window or tab >>Rapid amyloid-β oligomer and protofibril accumulation in traumatic brain injury
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2018 (English)In: Brain Pathology, ISSN 1015-6305, E-ISSN 1750-3639, Vol. 28, no 4, p. 451-462Article in journal (Refereed) Published
Abstract [en]

Deposition of amyloid-β (Aβ) is central to Alzheimer's disease (AD) pathogenesis and associated with progressive neurodegeneration in traumatic brain injury (TBI). We analyzed predisposing factors for Aβ deposition including monomeric Aβ40, Aβ42 and Aβ oligomers/protofibrils, Aβ species with pronounced neurotoxic properties, following human TBI. Highly selective ELISAs were used to analyze N-terminally intact and truncated Aβ40 and Aβ42, as well as Aβ oligomers/protofibrils, in human brain tissue, surgically resected from severe TBI patients (n = 12; mean age 49.5 ± 19 years) due to life-threatening brain swelling/hemorrhage within one week post-injury. The TBI tissues were compared to post-mortem AD brains (n = 5), to post-mortem tissue of neurologically intact (NI) subjects (n = 4) and to cortical biopsies obtained at surgery for idiopathic normal pressure hydrocephalus patients (iNPH; n = 4). The levels of Aβ40 and Aβ42 were not elevated by TBI. The levels of Aβ oligomers/protofibrils in TBI were similar to those in the significantly older AD patients and increased compared to NI and iNPH controls (P < 0.05). Moreover, TBI patients carrying the AD risk genotype Apolipoprotein E epsilon3/4 (APOE ε3/4; n = 4) had increased levels of Aβ oligomers/protofibrils (P < 0.05) and of both N-terminally intact and truncated Aβ42 (P < 0.05) compared to APOE ε3/4-negative TBI patients (n = 8). Neuropathological analysis showed insoluble Aβ aggregates (commonly referred to as Aβ plaques) in three TBI patients, all of whom were APOE ε3/4 carriers. We conclude that soluble intermediary Aβ aggregates form rapidly after TBI, especially among APOE ε3/4 carriers. Further research is needed to determine whether these aggregates aggravate the clinical short- and long-term outcome in TBI.

Keywords
Alzheimer's disease, amyloid β oligomers, amyloid-β, traumatic brain injury
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-341911 (URN)10.1111/bpa.12532 (DOI)000439749700001 ()28557010 (PubMedID)
Funder
The Swedish Brain FoundationSwedish Research CouncilSwedish Institute
Note

De två första författarna delar förstaförfattarskapet.

Available from: 2018-02-15 Created: 2018-02-15 Last updated: 2019-07-03Bibliographically approved
Wicher, G. K., Wallenquist, U., Lei, Y., Enoksson, M., Li, X., Fuchs, B., . . . Forsberg Nilsson, K. (2017). Interleukin-33 Promotes Recruitment of Microglia/Macrophages in Response to Traumatic Brain Injury. Journal of Neurotrauma, 34(22), 3173-3182
Open this publication in new window or tab >>Interleukin-33 Promotes Recruitment of Microglia/Macrophages in Response to Traumatic Brain Injury
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2017 (English)In: Journal of Neurotrauma, ISSN 0897-7151, E-ISSN 1557-9042, Vol. 34, no 22, p. 3173-3182Article in journal (Refereed) Published
Abstract [en]

Traumatic brain injury (TBI) is a devastating condition, often leading to life-long consequences for patients. Even though modern neurointensive care has improved functional and cognitive outcomes, efficient pharmacological therapies are still lacking. Targeting peripherally derived, or resident inflammatory, cells that are rapid responders to brain injury is promising, but complex, given that the contribution of inflammation to exacerbation versus improved recovery varies with time post-injury. The injury-induced inflammatory response is triggered by release of alarmins, and in the present study we asked whether interleukin-33 (IL-33), an injury-associated nuclear alarmin, is involved in TBI. Here, we used samples from human TBI microdialysate, tissue sections from human TBI, and mouse models of central nervous system injury and found that expression of IL-33 in the brain was elevated from nondetectable levels, reaching a maximum after 72 h in both human samples and mouse models. Astrocytes and oligodendrocytes were the main producers of IL-33. Post-TBI, brains of mice deficient in the IL-33 receptor, ST2, contained fewer microglia/macrophages in the injured region than wild-type mice and had an altered cytokine/chemokine profile in response to injury. These observations indicate that IL-33 plays a role in neuroinflammation with microglia/macrophages being cellular targets for this interleukin post-TBI.

Keywords
alarmin, glia, microglia, traumatic brain injury, neuroinflammation
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-341988 (URN)10.1089/neu.2016.4900 (DOI)000414560000013 ()28490277 (PubMedID)
Funder
Swedish Research Council
Available from: 2018-02-16 Created: 2018-02-16 Last updated: 2018-07-13Bibliographically approved
Vlachogiannis, P., Hillered, L., Khalil, F., Enblad, P. & Ronne, E. (2017). Interleukin-6 levels in cerebrospinal fluid and plasma in patients with severe spontaneous subarachnoid hemorrhage. Paper presented at 28th International Symposium on Cerebral Blood Flow, Metabolism and Function / 13th International Conference on Quantification of Brain Function with PET, APR 01-04, 2017, Int Soc Cerebral Blood Flow & Metab, Berlin, GERMANY. Journal of Cerebral Blood Flow and Metabolism, 37, 496-496
Open this publication in new window or tab >>Interleukin-6 levels in cerebrospinal fluid and plasma in patients with severe spontaneous subarachnoid hemorrhage
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2017 (English)In: Journal of Cerebral Blood Flow and Metabolism, ISSN 0271-678X, E-ISSN 1559-7016, Vol. 37, p. 496-496Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
Sage Publications, 2017
National Category
Endocrinology and Diabetes Hematology Neurology
Identifiers
urn:nbn:se:uu:diva-331037 (URN)000400157400728 ()
Conference
28th International Symposium on Cerebral Blood Flow, Metabolism and Function / 13th International Conference on Quantification of Brain Function with PET, APR 01-04, 2017, Int Soc Cerebral Blood Flow & Metab, Berlin, GERMANY
Note

Supplement: 1, Meeting Abstract: PS06-089

Available from: 2017-10-11 Created: 2017-10-11 Last updated: 2017-10-11
Lindblom, R. P., Tovedal, T., Norlin, B., Hillered, L., Popova, S., Alafuzoff, I. & Thelin, S. (2017). Mechanical reperfusion with leucocyte-filtered blood does not prevent injury following global cerebral ischaemia. European Journal of Cardio-Thoracic Surgery, 51(4), 773-781
Open this publication in new window or tab >>Mechanical reperfusion with leucocyte-filtered blood does not prevent injury following global cerebral ischaemia
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2017 (English)In: European Journal of Cardio-Thoracic Surgery, ISSN 1010-7940, E-ISSN 1873-734X, Vol. 51, no 4, p. 773-781Article in journal (Refereed) Published
Abstract [en]

OBJECTIVES: Prolonged global cerebral ischaemia leads to irreversible injury, often with lethal outcome. Brain injuries are partly caused by the uncontrolled reperfusion that occurs once the circulation is re-established. Recent animal experiments suggest that controlled reperfusion following lengthy ischaemia might prevent severe brain injury. This study aimed at further exploring cerebral alterations and outcome following prolonged global cerebral ischaemia and mechanically manipulated reperfusion.

METHODS: Three groups of pigs were included; one sham operated (n = 3) and two that underwent 30-min global cerebral ischaemia. All vessels that supply the brain were isolated intrathoracically, after which they were occluded for 30 min in the ischaemic groups. In one of the ischaemic groups uncontrolled reperfusion was applied (URep, n = 6), i.e. normal circulation was restored 30 min after arrested cerebral circulation. The second ischaemic group received mechanical reperfusion (MRep, n = 6) with leucocyte-filtered blood at constant flow and pressure for 20 min using extracorporeal circulation following the 30-min ischaemia, after which normal blood flow resumed. All animals were monitored for 3 h after start of uncontrolled reperfusion. Haemodynamic parameters, arterial and sagittal sinus blood gases, cerebral oxygen extraction rates and intraparenchymal biomarkers using microdialysis were measured. Brain histology was performed post-mortem.

RESULTS: Global brain ischaemia led to the same extent of severe morphological changes at the level of light microscopy in the two ischaemic experimental groups, regardless of reperfusion protocol. Furthermore, no significant differences were found between the URep and MRep groups regarding cerebral blood gases or microdialysis biomarkers.

CONCLUSIONS: Mechanical reperfusion following the current protocol does not modify brain alterations caused by 30 min of arrested cerebral circulation.

National Category
Basic Medicine
Identifiers
urn:nbn:se:uu:diva-315862 (URN)10.1093/ejcts/ezw367 (DOI)000398558800026 ()28007877 (PubMedID)
Available from: 2017-02-21 Created: 2017-02-21 Last updated: 2018-01-13Bibliographically approved
von Seth, M., Lipcsey, M., Engström, P., Larsson, A., Hillered, L., Maripuu, E., . . . Sjölin, J. (2017). Rapid Bolus Administration Does Not Increase the Extravasation Rate of Albumin: A Randomized Controlled Trial in the Endotoxemic Pig. Shock, 47(4), 514-519
Open this publication in new window or tab >>Rapid Bolus Administration Does Not Increase the Extravasation Rate of Albumin: A Randomized Controlled Trial in the Endotoxemic Pig
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2017 (English)In: Shock, ISSN 1073-2322, E-ISSN 1540-0514, Vol. 47, no 4, p. 514-519Article in journal (Refereed) Published
Abstract [en]

Some experimental data suggest that rapid bolus administration of albumin causes less plasma-expanding effects than slow, continuous infusion. To determine whether rapid bolus administration, in comparison with slow infusion, results in greater extravasation of albumin in experimental septic shock we performed a randomized controlled trial with 32 endotoxemic pigs. The animals were monitored and ventilated with standard intensive care equipment and given 10 mL x kg 5% albumin labeled with Technetium-99m, either as a rapid 15-minute bolus (Bolus group, n = 16) or as a 2-hour (h) infusion (Infusion group, n = 16). Radioactivity was monitored in plasma, extracellular microdialysate and urine for 6 h. Physiological parameters were monitored hourly. Radioactivity in the liver, spleen, kidney and lung was analyzed post-mortem.The plasma area under the curve (AUC) activity0-6h was 4.4 ± 0.9 x 10 in the Bolus group and 4.4 ± 1.1 x 10 counts x min x mL x h in the Infusion group. Blood hemoglobin levels increased in both groups, suggesting severe capillary leakage. Yet, there were no group differences in albumin radioactivity in plasma, muscle tissue, urine or in the post-mortem analysis of the organs. Following albumin administration, circulatory and respiratory parameters were similar in the two groups.In conclusion, the present results suggest that albumin might be given as a bolus without leading to increased extravasation of albumin, in contrast to previous animal experiments in rodents.

Keywords
Albumin, animal models, capillary leak syndrome, endotoxin, fluid resuscitation, sepsis
National Category
Infectious Medicine Hematology Surgery
Identifiers
urn:nbn:se:uu:diva-305826 (URN)10.1097/SHK.0000000000000761 (DOI)000396226300016 ()27749758 (PubMedID)
Available from: 2016-10-23 Created: 2016-10-22 Last updated: 2017-08-13Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-2808-9292

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