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缺氧停搏期间的心肌保护。实验模型:心室颤动。

Myocardial preservation during anoxic arrest. Experimental model ventricular fibrillation.

作者信息

Vejlsted H, Andersen K, Husum B, Hansen B F, Palm T, Arnbjerg J

出版信息

Scand J Thorac Cardiovasc Surg. 1982;16(2):175-83. doi: 10.3109/14017438209101807.

DOI:10.3109/14017438209101807
PMID:7156929
Abstract

An experimental model with anaesthetized healthy mongrel dogs on extracorporeal circulation is described. Anaesthesia and cardiopulmonary bypass are the same as used in clinical practice. Various methods of myocardial preservation were investigated and their protective effect was judged by cardiac performance after termination of 60 min of anoxic arrest. In this study, the first part of an experimental series, electrically-induced fibrillation during 60 min of normothermic and local hypothermic anoxic arrest was investigated. In group I, the hearts were fibrillated immediately after cross-clamping. In group II, which served as controls, the hearts were allowed to fibrillate spontaneously after aortic cross-clamping. All the hearts in group I went into an ischaemic contracture, whereas those in group II showed a 50% recovery, but with a strongly reduced cardiac performance after termination of anoxic arrest and cardiopulmonary bypass. Measurements of myocardial surface pH demonstrated a rapidly developed acidosis during the period of anoxic arrest. The most impressive finding by light microscopy was pronounced myocardial oedema. External cooling by 4 degrees C glucose 5.5% continuously flushed into the pericardial sac in combination with electrically-induced fibrillation proved to be ineffective as a protective method. None of the eight dogs in this group survived. External cooling combined with intraventricular injection of 4 degrees C glucose 5.5% seemed to protect the hearts against ischaemic damage, insofar that all six hearts in this group were able to take over the circulation after declamping. The working capacity was, however, impaired and a relatively long period of mechanical support and stimulation with inotropic drugs was necessary.

摘要

本文描述了一个在体外循环下对健康杂种麻醉犬进行的实验模型。麻醉和心肺转流与临床实践中使用的相同。研究了各种心肌保护方法,并通过60分钟缺氧停搏结束后的心脏功能来判断其保护效果。在本研究(实验系列的第一部分)中,研究了在常温及局部低温缺氧停搏60分钟期间电诱导的颤动。在第一组中,心脏在夹闭后立即发生颤动。在作为对照组的第二组中,主动脉夹闭后让心脏自然颤动。第一组中的所有心脏都进入了缺血性挛缩,而第二组中的心脏有50%恢复,但在缺氧停搏和心肺转流结束后心脏功能大幅降低。心肌表面pH值的测量表明,在缺氧停搏期间迅速出现酸中毒。光学显微镜下最显著的发现是明显的心肌水肿。持续向心包腔内注入4℃的5.5%葡萄糖进行外部降温并结合电诱导颤动作为一种保护方法被证明是无效的。该组的八只狗无一存活。外部降温结合心室内注射4℃的5.5%葡萄糖似乎能保护心脏免受缺血性损伤,因为该组的所有六个心脏在松开夹闭后都能够恢复循环。然而,工作能力受损,需要较长时间的机械支持和使用强心药物进行刺激。

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