Cardiac interstitial bradykinin release during ischemia is enhanced by ischemic preconditioning

Cardiac interstitial bradykinin release during ischemia is enhanced by ischemic preconditioning. Am J Physiol Heart Circ Physiol 279: H116-H121, 2000.--Ischemic preconditioning is known to protect the myocardium from ischemia-reperfusion injury. We examined the transmural release of bradykinin during myocardial ischemia and the influence of ischemic preconditioning on bradykinin release during subsequent myocardial ischemia. Myocardial ischemia was induced by occlusion of the left anterior descending coronary artery in anesthetized cats. Cardiac microdialysis was performed by implantation and perfusion of dialysis probes in the epicardium and endocardium. In eight animals, bradykinin release was greater in the endocardium than in the epicardium (14.4 [+ or -] 2.8 vs. 7.3 [+ or -] 1.7 ng/ml, P [is less than] 0.05) during 30 min of ischemia. In seven animals subjected to preconditioning, myocardial bradykinin release was potentiated significantly from 2.4 [+ or -] 0.6 ng/ml during the control period to 23.1 [+ or -] 2.5 ng/ml during 30 min of myocardial ischemia compared with the non-preconditioning group (from 2.7 [+ or -] 0.6 to 13.4 [+ or -] 1.9 ng/ml, P [is less than] 0.05, n = 6). Thus this study provides further evidence that transmural gradients of bradykinin are produced during ischemia. The results also suggest that ischemic preconditioning enhances bradykinin release in the myocardial interstitial fluid during subsequent ischemia, which is likely one of the mechanisms of cardioprotection of ischemic preconditioning. cardiac microdialysis; angiotensin-converting enzyme inhibitors; captopril; kinin receptors; myocardium