Abstract
Carvedilol, a selective alpha-1 and nonselective beta-adrenoceptor antagonist and potent antioxidant, has been shown to provide a significant decrease in neutrophil-mediated tissue injury. Epigastric skin flaps were elevated in rats, rendered ischemic for 10 h, and subsequently reperfused for 12 h. Forty rats were divided into four equal experimental groups: 1—nonischemic group, 2—ischemic saline control group, 3—ischemic control group without any vehicle treatment, and 4—drug-administered ischemic group. The effects of carvedilol on flap necrosis, neutrophil infiltration, and levels of malondialdehyde and nitric oxide in the flap tissue and serum were examined. The authors found that neutrophil numbers were significantly higher in the saline and nontreated groups. Additionally, serum and tissue levels of malondialdehyde were lower in the carvedilol-treated group, and serum nitric oxide was highest in the carvedilol-treated group. Carvedilol-treated animals had significantly lower areas of necrosis compared with controls. We conclude that administration of carvedilol before ischemia and reperfusion can significantly reduce the extent of flap necrosis and flap neutrophil counts because of ischemia–reperfusion injury.
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