© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
Involvement of endogenous prostaglandins in ischemic preconditioning in pigs
Abteilung für Pathophysiologie, Zentrum für Innere Medizin, Universitätsklinikum Essen, Hufelandstrasse 55, 45122 Essen, Germany
gerd.heusch{at}uni-essen.de
* Corresponding author. Tel.: +49-201-723-4480; fax: +49-201-723-4521
Objective: In pigs, the infarct size (IS) reduction achieved by a strong preconditioning stimulus (IPs) of 10 min ischemia and 15 min reperfusion is greater than that by a weaker preconditioning stimulus (IPw) of 3 min ischemia and 15 min reperfusion. The cardioprotection achieved by IPw is completely abolished by blockade of bradykinin-B2-receptors. Since activation of bradykinin-B2-receptors subsequently activates cyclooxygenase, we now tested whether or not inhibition of cyclooxygenase with indomethacin interferes with IS reduction by IP. Methods and results: In 42 enflurane-anesthetized pigs, the LAD coronary artery was cannulated, and subendocardial blood flow (ENDO, microspheres, ml/min/g) and IS (%, TTC-staining) were determined. Following 90 min ischemia and 120 min reperfusion, IS averaged 25.5±3.8 (S.E.M.) (ENDO: 0.05±0.01). IS was reduced by IPw to 6.3±2.1 (ENDO: 0.07±0.01) and further reduced by IPs to 2.4±1.0 (ENDO: 0.06±0.01). Indomethacin (10 mg/kg i.v.) did not alter IS per se (20.9±5.4, ENDO: 0.06±0.02), but completely abolished the IS reduction by IPw (23.2±5.9, ENDO: 0.06±0.01). In contrast, indomethacin abolished the IS reduction by IPs in only two of seven pigs (16.1±7.4, ENDO: 0.05±0.01). Conclusion: Prostaglandins are involved in IP. However, with stronger IP stimuli other triggers/mediators can compensate for the lack of prostaglandins.
KEYWORDS Ischemia; Preconditioning; Prostaglandins; Reperfusion
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