Effects of nitric oxide on hemodynamic change by adminstration of hypertonic saline dextran in canine hemorrhagic shock *
It has been widely known that a small bolus injection (4ml/kg) of hypertonic saline dextran (HSD) increases cardiac output (CO). Some mechanisms such as an increase in intravascular volume expansion, dilatation of blood vessels, and an increase in cardiac contractility have been reported. However, the mechanisms of the remarkable decrease in systemic vascular resistance (SVR) and the temporary decrease in mean blood pressure (mBP) immediately after injection, remain unclear. We hypothesized that nitric oxide(NO) , an endothelium-derived relaxing factor (EDRF) , may contribute to the decrease in SVR just after the bolus injection of HSD, and clarified whether L-NMMA, a NO synthase inhibitor, reversed the hemodynamic change in a canine model of hemorrhagic shock. Twelve dogs were divided into two groups : an L-NMMA group(n = 6 )and a control group (n = 6 ). In both groups, hemorrhagic shock was achieved by drawing blood from the femoral artery and mBP was maintained at 50 mmHg for 30 min. The animals in the L-NMMA group were administered 5 mg/kg of L-NMMA. Then, all the animals in both groups received HSD (4 ml/kg) for 30 seconds. Hemodynamic data were obtained periodically, and were statistically analyzed using the repeated measure ANOVA. After administration of HSD, mBP immediately decreased, and then CO remarkably increased in both groups. There was a significant difference in SVR between the two groups. In the control group, SVR decreased to 20% of pre-injection, and a steady recovery was achieved after 90 seconds. In the L-NMMA group, SVR decreased more slowly between 40~120 seconds than that in the control group, then it rose to 60% of pre-injection. Since the decrease in SVR was not completely reversed by L-NMMA, we concluded that NO may play partial role in the hemodynamic change induced by HSD. (Accepted on October 29, 2002)
