Effects of lazaroids on intestinal ischemia and reperfusion injury in experimental models.

Abstract

Mesenteric ischemia occurs in a number of clinically relevant pathophysiologic processes, including sepsis, hemorrhage, intestinal transplantation, severe burns, and mesenteric thrombosis. The readmission of molecular oxygen into an ischemic tissue promotes the oxidation of resuscitated tissue with certain pathophysiologic mechanisms. Depending on the duration and the intensity of ischemia, reoxygenation of the intestine that has been reperfused may further induce tissue injury. Intestinal ischemia and reperfusion injury can accelerate complex processes between the endothelium and different cell types leading to microvascular injury, cellular necrosis, and apoptosis. The injury due to reperfusion is found predominantly in the intestinal mucosa and submucosa, causing endothelial detachment. The 21-aminosteroids (lazaroids) are a family of compounds that inhibit lipid membrane peroxidation. Many of the performed studies show conflicting results, which reflect differences in experimental design, evolving time that (I/R) is induced, total or partial vascular occlusion, dosage of the lazaroid, and the exact period of time that the lazaroid is administered.