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Articles in PresS, published online ahead of print October 10, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00693.2002
Submitted on August 6, 2002
Accepted on October 3, 2002
1 Institute of Pathophysiology, University of Essen Medical School, Center of Internal Medicine, Essen, Germany
2 Institute of Organic Chemistry, University of Essen, Essen, Germany
* To whom correspondence should be addressed. E-mail: gerd.heusch{at}uni-essen.de.
Free oxyradicals are involved in the signal transduction of ischemic preconditioning in rats and rabbits. Data from larger mammals in which the infarct development is closer to that in man are lacking. We have therefore investigated the impact of the radical scavenger ascorbic acid on ischemic preconditioning in pigs. In 33 anesthetized pigs the LAD coronary artery was perfused from an extracorporeal circuit. Infarct size (% area at risk) was determined by TTC staining. In placebo animals undergoing 90 min severe ischemia and 120 min reperfusion infarct size averaged 26.9±3.9% (mean±SEM;n=9). Ischemic preconditioning by 10 min ischemia and 15 min reperfusion reduced infarct size to 6.4±2.4% (p<0.05 vs. placebo;n=9). Intravenous infusion of ascorbic acid (30 min before ischemic preconditioning or ischemia, respectively; 2g bolus followed by 25mg/min until the end of ischemia) had no effect on infarct size per se (22.6±6.5%;n=6), but largely abolished the infarct size reduction by ischemic preconditioning (19.1±5.4%;n=9). Scavenging free oxyradicals with ascorbic acid largely attenuates the beneficial effect of ischemic preconditioning in pigs.
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