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Biocompatibility reflected by haemostasis variables during cardiopulmonary bypass using heparin-coated circuits
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Thoraxkirurgi. (Thoracic Surgery)
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Rättsmedicin. (Forensic Medicine)
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper. (Thoracic Surgery)
1997 (engelsk)Inngår i: The thoracic and cardiovascular surgeon, ISSN 0171-6425, E-ISSN 1439-1902, Vol. 45, nr 4, s. 163-167Artikkel, omtale (Annet vitenskapelig) Published
Abstract [en]

Cardiopulmonary bypass (CPB) is associated with haemostatic disturbances and signs of acute inflammatory response, most likely related to poor biocompatibility of the artificial surfaces. Some haemostatic variables are known as markers of acute-phase reaction, blood cell trauma, and endothelial damage. The aim of the study was to evaluate the effect of heparin-coating of artificial surfaces on those variables of hemostasis. 14 patients operated on with elective coronary artery revascularization were randomized into two groups. In group H (n = 7), heparin-coated CPB circuits and in control group C (n = 7), noncoated CPB sets were used. Patients in group C received normal heparinization, e.g. bolus 300 IU/kg and additional doses to maintain activated coagulation time (ACT) over 400 sec during CPB. In group H, a bolus heparin dose was reduced by 25% (to 225 IU/kg) in order to compensate for the amount of heparin immobilized on circuit surfaces and the corresponding ACT limit was 300 sec. There were significant increases of the von Willebrand factor (vWf), plasminogen activator inhibitor-1 (PAI) and tissue-plasminogen activator (tPA) starting at CPB end and rising to about twice the baseline levels postoperatively. This reaction was less evident in group H, as indicated by significantly lower levels of tPA compared to group C at CPB end (135% +/- 9 in group H versus 241% +/- 15 in group C, p < 0.0005) and at two hours postoperatively. The rates of tPA and vWF increase were lower in group H, also indicating reduced endothelial damage in this group. Marginally significant, a higher value of PAI was found in the C group early after CPB onset. Group H showed significantly lower concentrations of circulating complex between elastase and alpha 1-antitrypsin at CPB end and postoperatively, implicating a reduced granulocyte activation (60 min after protaminization 41 micrograms/L +/- 5 in group H versus 256 micrograms/L +/- 55 in group C, p < 0.05). It was concluded that the heparin-coated CPB circuits demonstrated improved biocompatibility which may be related to less disturbed haemostasis.

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1997. Vol. 45, nr 4, s. 163-167
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URN: urn:nbn:se:uu:diva-61692DOI: 10.1055/s-2007-1013716PubMedID: 9323816OAI: oai:DiVA.org:uu-61692DiVA, id: diva2:89603
Tilgjengelig fra: 2008-10-17 Laget: 2008-10-17 Sist oppdatert: 2017-11-30bibliografisk kontrollert

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