Effect of Ischemic Preconditioning on Catecholamine Release from the Isolated, Ischemic Reperfused Hearts of Rats.
10.4070/kcj.1995.25.6.1217
- Author:
Jong Wan PARK
;
Young Hoon KIM
;
Myung Suk KIM
- Publication Type:Original Article
- Keywords:
Ischemia-reperfusion injury;
Preconditioning;
Catecholamine
- MeSH:
Animals;
Arrhythmias, Cardiac;
Contracture;
Heart*;
Ischemia;
Ischemic Preconditioning*;
L-Lactate Dehydrogenase;
Rats*;
Reperfusion;
Reperfusion Injury;
Reserpine
- From:Korean Circulation Journal
1995;25(6):1217-1224
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Ischemic preconditioning reduces the infarct size and the severity of arrhythmia in a post-ischemic reperfused heart although the detailed mechanism is unknown. In the ischemic heart, a large amount of catecholamine is released from the adrenergic nerve terminal and this aggravates cell destruction and arrhythmia. In this study, the possibility for ischemic preconditioning to inhibit the release of endogenous catecholamine from the ischemic heart was tested to investigate the probable cardioprotective mechanism of ischemic preconditioning. METHODS: In the isolated, Langendorff perfused rat hearts, we observed the protective effect of ischemic preconditioning against post-ischemic reperfusion injury, and measured the amount of catecholamine released into coronary effuent. In addition, we observed the effect of catecholamine depletion on reperfusion injury in non-preconditioned and preconditioned hearts. RESULTS: During the reperfusion(20min) after ischemia(30min), the cardiac function was markedly depressed with the development of severe contracture. In the heart preconditioned by three sequential episodes of 5min ischemia and 5min reperfusion, the reperfusion contracture decreased significantly and the cardiac function was almost recovered to normal after 20min reperfusion. The release of lactate dehydrogenase was also decreased in the preconditioned heart. The release of endogenous catecholamine was abruptly increased immediately after the reperfusion and the release was exponentially decreased throughout the reperfusion period. THe pattern of catecholamine release was much different from that of lactate dehydrogenase release. In the preconditioned heart, the release was significantly decreased to about half of that in non-preconditioned t\heart. Endogenous catecholamine depletion by reserpine treatment did not affect the post-ischemic functional recovery in both non-preconditioned and preconditioned hearts. CONCLUSION: It is suggested from these results that ischemic preconditioning inhibis the release of endogenous catecholamine during ischemic period, which may be partly related to cardioporotective effect of preconditioning in ischemic and reperfused heart.
