Decreased nitric oxide production following extremity ischemia and reperfusion,

Background Nitric oxide (NO), the endogenous vasodilator, is an important regulator of vascular tone. We investigated NO production following lower extremity ischemia. Methods Rabbits underwent 6 hours of bilateral leg ischemia followed by unrestricted reperfusion. Physiologic parameters were continuously measured and blood was assayed for NO2 and NO3. Results Acute ischemia of the lower extremities produced an immediate increase in mean arterial blood pressure while later reperfusion induced a significant decrease (P< 0.0005). There was a fall in femoral blood flow during reperfusion. NO2/ NO3 concentrations decreased significantly to 89% of baseline values after ischemia and 77% after 1 hour of reperfusion (P< 0.005). A significantly higher mortality was found in association with decreased NO2 /NO3 concentrations. Conclusions Nitric oxide appears to be a regulator of regional blood flow during reperfusion following extremity ischemia. Decreased NO production may contribute to impaired regional blood flow and mortality.