Abstract

One of the most devastating complications of vascular procedures is unclamping hypotension. In this study, we aimed to investigate the roles of Ischemia-reperfusion injury and nitric oxide in the pathophysiology of the unclamping hypotension of the superior mesenteric artery. Arterial blood pressure and plasma nitrite concentration, a stable product of nitric oxide, were recorded during clamping and unclamping of the SMA. Wet-to-dry weight ratio, a marker of microvascular permeability, and malonaldehyde concentration, an indicator of lipid peroxidation, were measured in the intestinal tissue samples. The study consisted of control (Group I, n: 11), occlusion of SMA (Group 2, n:9), L-NAME, an anhibitor of nitric oxide synthase (Group 3, n:7) and catalase (Group 4, n:6) groups. After declamping of SMA, a prominent arterial hypotension was recorded. Neither L-NAME nor catalase did not change the magnitude of unclamping hypotension. In addition, there was no change in plasma nitrite concentration during the experiment. In conclusion, the intensity of reperfusion injury of ischemic intestines and nitric oxide are not responsible for the hypotension seen after unclamping of the SMA.