EFFECTS OF OXYGEN ON REGIONAL HEMODYNAMICS IN HEMORRHAGIC-SHOCK

This study investigated mechanisms of the hemodynamic effects of oxyge n in hemorrhagic shock induced by bleeding 30% of the total blood volu me in anesthetized rats. An ultrasonic flowmeter was used to monitor r egional blood flow. Changes in tissue perfusion were assessed by the l aser-Doppler technique. The inhalation of 100% oxygen induced a signif icant increase in mean arterial blood pressure (MABP) and vascular res istance in the hindquarters, with a concomitant decrease in blood flow in the distal aorta and biceps femoris muscle. In contrast, oxygen di d not change vascular resistance in the superior mesenteric artery (SM A) and renal beds and induced a significant increase in blood flow to the renal artery, SMA, and small bowel in hemorrhaged rats. L-Arginine (100 mg/kg iv) but not D-arginine or the vehicle (0.9% NaCl) complete ly abolished the effects of oxygen on blood pressure and reversed its effects on blood flow and resistance in the hindquarters and biceps fe moris muscle. Administration of the nitric oxide (NO) synthase inhibit or N-G-nitro-L-arginine methyl ester (50 mg/kg iv) significantly incre ased MABP and the resistance in the three vascular beds. Pretreatment of hemorrhaged rats with a superoxide dismutase mimic, the NO-stable r adical 2,2,6,6-tetramethylpiperidine-N-oxyl (5 mg/kg iv), resulted in significantly diminished effects of oxygen on hindquarter hemodynamics . These results demonstrate a differential effect of oxygen, which inc reases vascular resistance in the hindquarters without a significant e ffect in the splanchnic and renal beds, thus favoring an increase in s planchnic and renal perfusion. It is suggested that inactivation of NO by reactive oxygen species may underlie the effects of oxygen on hind quarter vascular tone during shock.