Endothelium dependent mechanism of oxygen induced redistribution of blood flow in hemorrhagic shock

We evaluated changes in regional endothelium-NO-dependent control of vascular tone and oxygen induced redistribution of blood flow in shock Shock was induced in rats by withdrawal of 30% of the total blood volume. This was followed by an infusion of acetyl choline (ACh) (1 mcg/kg/min. for 15 min. and 10 mcg/kg/min. for 30 min.). Exposure to hyperbaric oxygen (HBO) (0.3 MPa) was started in the middle of high dose ACh infusion and continued after its cessation. Ultrasonic flow meters were used to monitor blood flow in the distal aorta (DA) and the superior mesenteric artery (SMA). In shocked animals ACh at both doses decreased mean arterial blood pressure and DA vascular resistance and increased DA blood flow significantly (by 12±4 and 25±5% at 1 and 10 mcg/kg/min, respectively, p<0.01). SMA resistance and flow did not change after low dose ACh. During high dose ACh, SMA flow decreased significantly by 27±5% (p<0.01). After cessation of ACh, HBO induced significant increase in mean arterial blood pressure, decrease in distal aortic flow and increase in SMA flow. Neutralization of NO seems to be one of the mechanisms of the hemodynamic effects of HBO. It is suggested that different degrees of NO production and /or vascular endothelial dysfunction in the splanchnic and muscle beds may underlie HBO induced redistribution of blood flow in hemorrhagic shock.