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[用冰泥局部降温对心肌的不适当保存]

[Inappropriate preservation of myocardium by topical cooling with iced slush].

作者信息

Takeuchi K, Takashima K, Munakata M, Ono Y, Fukui K, Suzuki S, del Nido P J

机构信息

First Department of Surgery, Hirosaki University, School of Medicine, Aomori, Japan.

出版信息

Nihon Kyobu Geka Gakkai Zasshi. 1996 Sep;44(9):1691-7.

PMID:8911040
Abstract

Topical cooling with iced slush has been applied as a conventional myocardial preservation in open heart surgery. However, there might be several disadvantages due to topical cooling with iced slush which melted to be liquid, because of membrane integrity decreased during ischemia. To understand more detailed mechanism of deterioration for myocardium by immersion in some liquid during ischemia, we subjected isolated crystalloid perfused rabbit hearts to a 30 minute of ischemia with immersion in Krebs-Henseleit (K-H) solution (I), K-H+hexamethlyamiloride which was Na+/H+ channel blocker (II) and histidine containing cardioplegia (HBS) designed to accelerate anaerobic glycolysis by a proton buffering (III), followed by a 30 minute of reperfusion. These groups were compared to the hearts hanging in air during ischemia (control). Phosphocreatine (PCr), ATP and intracellular pH were measured by 31 PNMR in group I, II, III. Developed pressure (Dev P) and diastolic pressure (EDP) with a intracavitary balloon were also evaluated with monitoring of 2 mmHg diastolic contracture during ischemia. Dev P declined to 46%, 54% of preischemic value in group I and group II, respectively, although % recovery of control heart was 74% after ischemia-reperfusion process. Diastolic function was severely deteriorated in group I and II, as compared to control heart. ATP and intracellular pH showed a similar decline as PCr in group I and II which was not seen in group III during ischemia. HBS prevented the deterioration of PCr, ATP and intracellular pH during ischemia along with excellent recovery of myocardial function. We therefore conclude that 1) significant deterioration of myocardium occurs with ischemia if the heart preserved in Krebs-Heseleit solution and the mechanism of injury by immersion in liquid on the heart appears to be due to proton accumulation caused by intracellular acidification and loss of high energy phosphate.

摘要

在心脏直视手术中,用冰屑进行局部降温一直是一种传统的心肌保护方法。然而,由于冰屑局部降温后会融化成液体,可能存在一些缺点,因为在缺血期间细胞膜完整性会降低。为了更详细地了解缺血期间心肌浸泡在某些液体中导致恶化的机制,我们将离体晶体灌注兔心在缺血30分钟时分别浸泡在 Krebs-Henseleit(K-H)溶液(I组)、作为Na+/H+通道阻滞剂的K-H + 六甲铵(II组)以及旨在通过质子缓冲加速无氧糖酵解的含组氨酸心脏停搏液(HBS,III组)中,随后再灌注30分钟。将这些组与缺血期间悬挂在空气中的心脏(对照组)进行比较。在I组、II组、III组中,通过31P核磁共振测量磷酸肌酸(PCr)、三磷酸腺苷(ATP)和细胞内pH值。还通过监测缺血期间2 mmHg的舒张期挛缩,使用心腔内球囊评估了发展压力(Dev P)和舒张压(EDP)。I组和II组的Dev P分别降至缺血前值的46%和54%,而对照组心脏在缺血 - 再灌注过程后的恢复率为74%。与对照组心脏相比,I组和II组的舒张功能严重恶化。在缺血期间,I组和II组中ATP和细胞内pH值的下降与PCr相似,而III组未出现这种情况。HBS可防止缺血期间PCr、ATP和细胞内pH值的恶化,同时心肌功能恢复良好。因此,我们得出结论:1)如果心脏保存在Krebs-Heseleit溶液中,缺血时心肌会发生显著恶化,心脏浸泡在液体中造成损伤的机制似乎是由于细胞内酸化导致的质子积累和高能磷酸的丧失。

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