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搏动性再灌注对全心缺血后心肌高能磷酸化合物的影响。

Effect of pulsatile reperfusion on myocardial high energy phosphates following global ischemia.

作者信息

Chiang B Y, Ye C X, Gau X D, Zhou Y, Hong J P, Wang Y S

机构信息

Department of Cardiothoracic Surgery, Renji Hospital, Shanghai, China.

出版信息

ASAIO Trans. 1991 Jul-Sep;37(3):M485-7.

PMID:1751246
Abstract

To evaluate the effects of pulsatile reperfusion (PR) on the postischemic myocardial phosphometabolites, 17 sheep were put on cardiopulmonary bypass (CPB) and randomly divided into a pulsatile group (P group) and nonpulsatile group (NP group). The heart was arrested by global ischemia for 45 minutes, then defibrillated and reperfused for 2 hours while the circulation was supported by CPB. Myocardial needle biopsies were obtained, and ATP, ADP, and AMP were measured with high performance liquid chromatography. There were no significant differences between the two groups in myocardial ADP and AMP. However, after 120 minutes of reperfusion, the myocardial ATP was restored in the P group, but continued to decrease further in the NP group. Experimental results imply that PR might reduce reperfusion injury and promote recovery of the ischemic myocardium.

摘要

为评估搏动性再灌注(PR)对缺血后心肌磷酸代谢物的影响,将17只绵羊置于体外循环(CPB)下,并随机分为搏动组(P组)和非搏动组(NP组)。心脏通过全心缺血停搏45分钟,然后除颤并再灌注2小时,同时由CPB维持循环。获取心肌穿刺活检组织,并用高效液相色谱法测量三磷酸腺苷(ATP)、二磷酸腺苷(ADP)和一磷酸腺苷(AMP)。两组之间心肌ADP和AMP无显著差异。然而,再灌注120分钟后,P组心肌ATP恢复,而NP组心肌ATP继续进一步下降。实验结果表明,PR可能减轻再灌注损伤并促进缺血心肌的恢复。

相似文献

1
Effect of pulsatile reperfusion on myocardial high energy phosphates following global ischemia.搏动性再灌注对全心缺血后心肌高能磷酸化合物的影响。
ASAIO Trans. 1991 Jul-Sep;37(3):M485-7.
2
Effects of pulsatile reperfusion on globally ischemic myocardium.搏动性再灌注对全脑缺血心肌的影响。 (注:原文中“globally ischemic myocardium”字面意思是“全脑缺血心肌”,但从医学常理推断这里应该是“全心缺血心肌”,可能原文有误,这里按照字面翻译。)
ASAIO J. 1993 Jul-Sep;39(3):M438-43.
3
Is adenosine 5'-triphosphate derangement or free-radical-mediated injury the major cause of ventricular dysfunction during reperfusion? Role of adenine nucleoside transport in myocardial reperfusion injury.腺苷5'-三磷酸紊乱或自由基介导的损伤是再灌注期间心室功能障碍的主要原因吗?腺嘌呤核苷转运在心肌再灌注损伤中的作用。
Circulation. 1990 Nov;82(5 Suppl):IV341-50.
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Intermittent aortic crossclamping prevents cumulative adenosine triphosphate depletion, ventricular fibrillation, and dysfunction (stunning): is it preconditioning?间歇性主动脉交叉钳夹可防止三磷酸腺苷的累积消耗、心室颤动和功能障碍(心肌顿抑):这是一种预处理吗?
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The functional recovery of post-ischemic myocardium requires glycolysis during early reperfusion.缺血后心肌的功能恢复在早期再灌注期间需要糖酵解。
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