Myocardial protection of warm cardioplegic induction on the isolated perfused rat heart model.
Myocardial protection through different cardioplegia approaches is an important issue for successful cardiovascular surgery. The objective of this prospective randomized study was to evaluate the effect of myocardial protection of warm (37 degrees C) and cold (6 degrees C) cardioplegic induction, respectively, using a Langendorff isolated rat heart perfusion model. Twenty-eight isolated rat hearts on the Langendorff perfusion model were randomly divided into two groups: group T (n = 14) received warm (37 degrees C) cardioplegic induction, followed by cold (6 degrees C) cardioplegia after ECG showed straight line; alternatively, group C (n = 14) received only cold cardioplegic induction. After undergoing ischemia for 80 min, both group T and group C received reperfusion with Krebs-Henseleit Buffer (KHB) for 40 min. An additional group A (n = 7) received KHB continuously for 120 min and served as the control group for the assessment of Na(+)/K(+)-ATPase activity. The coronary flow, concentration of creatine kinase (CK) in coronary effluent, and cardiac function were evaluated at different time periods. Na(+)/K(+)-ATPase activity was assessed at the end of reperfusion. The coronary flow, content of CK in coronary effluent, heart rate, dp/dtmax, and left ventricular peak pressure (LVPP) were significantly greater (p < .05) in group T than group C during the reperfusion period. The negative value of -dp/dtmax and left ventricular end-diastolic pressure (LVEDP) was significantly lower (p < .05) in group T than group C, during the reperfusion period. The Na(+)/K(+)-ATPase activity assessed at the end of reperfusion period was significantly higher (p < .05) in group A and group T than group C, while no significant difference (p = .13) was found between group T and group A. Compared with cold cardioplegic induction, warm cardioplegic induction provides superior myocardial protection by enhancing coronary flow, reducing myocardial injury, improving cardiac function, and preserving Na(+)/K(+)-ATPase activity.
Li
Shu
S
Department of Extra-Corporeal Circulation at Fu Wai Cardiovascular Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. lishu@public.bta.net.cn
Lin
Jing
J
Lenehan
Eric
E
Liu
Jinping
J
Long
Cun
C
Liu
Jin
J
Geng
Yong J
YJ
D000818:Animals; D002315:Cardiopulmonary Bypass; D003080:Cold Temperature; D003402:Creatine Kinase / Q000032:analysis / Q000378:metabolism; D004195:Disease Models, Animal; D006324:Heart Arrest, Induced; D006358:Hot Temperature; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D011446:Prospective Studies; D051381:Rats; D017208:Rats, Wistar; D015424:Reperfusion / Q000379:methods
D003402:Creatine Kinase