| Autor: |
Matjovi, Martin, Radermacher, Peter, Tugtekin, Ilyas, Stehr, Alexander, Theisen, Marc, Vogt, Josef, Wachter, Ulrich, Ploner, Franz, Georgieff, Michael, Träger, Karl |
| Zdroj: |
Shock; September 2001, Vol. 16 Issue: 3 p203-210, 8p |
| Abstrakt: |
We have previously demonstrated that nonselective nitric oxide synthase NOS inhibition did not reverse the LPSinduced deterioration of hepatosplanchnic energy status in porcine endotoxic shock. Therefore, this study investigated the effect of selective inducible NOS iNOS inhibition using 1400W on intestinal and liver perfusion, O2kinetics, and energy metabolism during hyperdynamic porcine endotoxemia. Intravenous E. ColiLPS was continuously infused over 24 h concomitant with fluid resuscitation. After 12 h of endotoxemia, continuous intravenous infusion of 1400W was started until the end of the experiment and was titrated to maintain mean blood pressure MAP at baseline levels. Twelve, 18, and 24 h after starting LPS, we measured hepatic arterial and portal venous blood flow, ileal mucosalarterial PCO2gap, portal as well as hepatic venous lactatepyruvate ratios, and endogenous glucose production rate. Expired NO and plasma nitrate levels were assessed as a measure of NO production. 1400W decreased LPSinduced increase in expired NO and allowed for the maintenance of MAP without modification of cardiac output. Despite unchanged regional macrocirculation, 1400W prevented the progressive rise of ileal mucosalarterial PCO2gap, significantly improved the LPSinduced impairment of hepatosplanchnic redox state, and blunted the decline in liver lactate clearance. Increased glucose production rate was not influenced. Thus, the selective iNOS inhibition with 1400W prevented circulatory failure and largely attenuated otherwise progressive LPSinduced deterioration of intestinal and hepatocellular energy metabolism. |
| Databáze: |
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