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倍他米松对犬供心保存中冷停搏液灌注期间心肌活力的影响。

The effect of betamethasone on myocardial viability during cold cardioplegia in canine donor heart preservation.

作者信息

Miyamoto H, Sunamori M, Yoshida T, Suzuki A

机构信息

Department of Thoracic-Cardiovascular Surgery, Tokyo Medical and Dental University, School of Medicine, Japan.

出版信息

Surg Today. 1994;24(5):449-55. doi: 10.1007/BF01427039.

Abstract

This study examined the effect of betamethasone on myocardial viability of reperfused isolated canine hearts following a 6-h hypothermic cardioplegia. The dogs were divided into two groups: group I (n = 9) received nondepolarizing cardioplegia containing betamethasone 250 mg/l while group II (n = 7) was administered cardioplegia without betamethasone. The myocardial concentrations of calcium, ATP, ADP, total adenine nucleotide, cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) were identical in the two groups throughout the experiment. The coronary sinus plasma concentrations of MB fraction of creatine kinase (MB-CK), cAMP and cGMP after 2h of reperfusion were significantly lower in group I than in group II. The myocardial mitochondrial ultrastructure, as assessed by semiquantitative morphometry, was found to be significantly better preserved in group I than in group II at the end of both preservation and reperfusion. In addition, the left ventricular end-systolic pressure volume relation (ESPVR) showed a higher slope and lower intercept in group I than in group II. These results suggest that the addition of betamethasone to nondepolarizing cold cardioplegia enhances myocardial protection via membrane stabilization without affecting the adenine nucleotide metabolism.

摘要

本研究检测了在6小时低温心脏停搏后,倍他米松对再灌注的离体犬心脏心肌活力的影响。将犬分为两组:第一组(n = 9)接受含250 mg/l倍他米松的非去极化心脏停搏液,而第二组(n = 7)给予不含倍他米松的心脏停搏液。在整个实验过程中,两组心肌中的钙、三磷酸腺苷(ATP)、二磷酸腺苷(ADP)、总腺嘌呤核苷酸、环磷酸腺苷(cAMP)和环磷酸鸟苷(cGMP)浓度相同。再灌注2小时后,第一组冠状窦血浆中肌酸激酶MB同工酶(MB-CK)、cAMP和cGMP的浓度显著低于第二组。通过半定量形态学评估发现,在保存期和再灌注期结束时,第一组心肌线粒体超微结构的保存情况明显优于第二组。此外,第一组左心室收缩末期压力-容积关系(ESPVR)的斜率高于第二组,截距低于第二组。这些结果表明,在非去极化冷心脏停搏液中添加倍他米松可通过膜稳定作用增强心肌保护,而不影响腺嘌呤核苷酸代谢。

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