Clinical and experimental studies on the role of platelet-activating factor (PAF) in the pathogenesis of septic DIC

Various toxic factors induced by endotoxin (Et) are thought to be deeply involved in the pathogenesis of severe infections. In this study, particular attention was paid to the role of the platelet-activating factor (PAF) in these conditions, and clinical and experimental studies were conducted on th...

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Veröffentlicht in:Surgery today (Tokyo, Japan) Japan), 1993-03, Vol.23 (3), p.228-233
Hauptverfasser: Ono, S, Tamakuma, S, Mochizuki, H, Kinoshita, M, Ohkusa, Y, Aosasa, S, Oda, Y, Ohe, H
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Sprache:eng
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Zusammenfassung:Various toxic factors induced by endotoxin (Et) are thought to be deeply involved in the pathogenesis of severe infections. In this study, particular attention was paid to the role of the platelet-activating factor (PAF) in these conditions, and clinical and experimental studies were conducted on the relationship between PAF and the changes observed in the general parameters after surgical infections. In the clinical study, changes in the PAF concentration in the blood of seven patients with disseminated intravascular coagulation (DIC), five of whom were septic and two non-septic, were monitored by gas/mas spectrometry. The mean PAF level in the septic DIC group tended to be higher than that in the non-septic DIC group. Moreover, in the septic DIC group, the relationship between the increase in the PAF level and platelet count was analyzed with the lapse of time and we surmised a negative correlation between these parameters. Experimentally, we also investigated the role of PAF in Et shock and the effect of an anti-PAF agent and protease inhibitor. The Et-induced fall in blood pressure was similarly prevented by both the anti-PAF agent and protease inhibitor. However, the decrease in the platelet count was more significantly inhibited by the anti-PAF agent than by the protease inhibitor, whereas the parameters of the blood coagulation/fibrinolysis system were more affected by the protease inhibitor than by the anti-PAF agent.
ISSN:0941-1291
1436-2813
DOI:10.1007/bf00309232