Abstract
Although reactive oxygen metabolites may play a pivotal role in mediating microvascular reperfusion injury, the source of these radicals is still a matter of controversy. With the use of spectrophotometry and intravital microscopy we studied the role of xanthine oxidase and superoxide radicals in portal triad crossclamping-induced microvascular injury in rats. After 20 min of global hepatic ischemia and splanchnic vascular congestion, followed by 40 min of reperfusion ( n = 8), xanthine oxidase activities in hepatic venous (26.9 ± 4.7 nmol/ml × min) and systemic arterial blood (16.3 ± 2.5 nmol/ml × min) were found significantly ( p < .01) increased when compared with sham-operated controls (6.8 ± 0.9 and 6.0 ± 0.8 nmol/ml × min, n = 8). The increase of xanthine oxidase activity was accompanied by oxygen radical-mediated intravascular hemolysis. Intravital microscopy ( n = 6) revealed accumulation of leukocytes within the postischemic hepatic microvasculature with stasis in sinusoids (75.9 ± 8.9 per liver lobule) and adherence to the endothelial lining of postsinusoidal venules (534.7 ± 125.3 per mm 2endothelial surface). Concomitantly, compromised microvascular reperfusion was characterized by perfusion deficits of individual sinusoids (25.6 ± 4.0% nonperfused sinusoids). The xanthine oxidase inhibitor allopurinol (50 mg/kg b.wt., orally, n = 6) and the radical scavenger superoxide dismutase (60000 IU/kg b.wt., IV, n = 6) effectively ( p < .01) inhibited both sinusoidal leukostasis (16.1 ± 2.6 and 32.1 ± 3.1 cells/lobule) and venular leukocyte adherence (247.6 ± 7.9 and 205.0 ± 38.0 cells/mm 2), and, hence, reduced microcirculatory deteriorations, indicated by the attenuation of sinusoidal perfusion failure (2.8 ± 0.8 and 9.0 ± 3.1%). Our results support the hypothesis that portal triad crossclamping-induced microvascular reperfusion injury is triggered by superoxide radicals derived from the xanthine oxidase system.
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