Episodes Of Reperfusion Research Articles

Oxygen free radical induced damage in kidneys subjected to warm ischemia and reperfusion. Protective effect of superoxide dismutase.

Superoxide anion free radical (O2-.) has been implicated in the pathogenesis of tissue injury consequent to ischemia/reperfusion in several different organs, including heart and bowel. Superoxide dismutase (SOD), an enzyme free radical scavenger specific for O2-., has been used successfully to protect these organs from structural damage during reoxygenation of ischemic tissue. It has been suggested that the catalytic action of xanthine oxidase in injured tissue is an important source of O2-. during reoxygenation. In order to evaluate the potential of SOD to protect against kidney damage resulting from transient ischemia followed by reperfusion with oxygenated blood, a model of warm renal ischemia was studied. LBNF1 rats underwent right nephrectomy and occlusion of the left renal artery for 45 minutes. Survival in the group of ischemic untreated rats (N = 30) was 56% at 7 days and serum creatinine was greatly elevated (p less than 0.01) in rats remaining alive over the full 7-day period. In strong contrast to these results, all of the animals treated with SOD before reperfusion (N = 18) were alive after 7 days similar to sham operated control rats (N = 8). Serum creatinine in the SOD treated rats was significantly elevated only to postoperative day 3 and thereafter returned to normal. Rats treated with inactive SOD (N = 4) or SOD before ischemia (N = 4) had decreased survival rates compared to ischemic untreated animals and prolonged elevation of serum creatinine. When the ischemia time was extended to 60 minutes, only 19% of the untreated animals (N = 16) survived at 7 days whereas nearly 60% of the SOD-treated animals survived (N = 19). Serum creatinine was greatly elevated during the full 7-day observation period in all surviving rats in the untreated ischemic group, whereas serum creatinine returned to normal (p less than 0.05) after 4 days in the surviving rats treated with SOD. To test whether the action of xanthine oxidase contributed to the kidney damage after reoxygenation, 45 min. ischemic rat kidneys were treated with allopurinol. All of the animals treated with allopurinol (N = 12) were alive at 7 days. Serum creatinine values returned to normal after the episode of ischemia and reperfusion but more slowly than after SOD treatment. Histologic evaluation of kidney tissue taken from animals after ischemia alone showed extensive renal tubular damage, which was essentially absent in kidneys from SOD-treated animals.(ABSTRACT TRUNCATED AT 400 WORDS)

Wall motion and metabolic changes after coronary occlusion and reperfusion

Experiments were conducted in open-chest pigs in which experimental myocardial ischemia was produced. Two groups of animals were evaluated: (1) those with short episodes of coronary occlusion and reperfusion, and (2) those with an initially longer period of occlusion (equal to the sum of the short multiple occlusions) and reperfusion. Indices of myocardial wall motion as determined by echocardiogram, of energy production as measured by mitochondrial oxidative phosphorylation, and of cellular membrane integrity as measured by calcium uptake by sarcoplasmic reticulum vesicles and calcium content of tissue and mitochondria were obtained. Our observation revealed better myocardial preservation in the group with brief periods of occlusion and reperfusion than those with a sustained period of ischemia followed by reperfusion. The concept that myocardium is less well preserved due to reperfusion damage by intermittent aortic cross-clamping or intermittent coronary perfusion during open heart surgery compared to uninterrupted cardiac arrest needs to be reexamined in light of the data presented and investigated in the hypothermic, cardioplegia model.