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本文引用的文献

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ELECTROLYTE ALTERATIONS IN ACUTE MYOCARDIAL ISCHEMIC INJURY.急性心肌缺血性损伤中的电解质改变
Circ Res. 1964 Mar;14:260-9. doi: 10.1161/01.res.14.3.260.
2
Rate of change in myocardial glycogen and lactic acid following arrest of coronary circulation.冠状动脉循环停止后心肌糖原和乳酸的变化率
Circ Res. 1959 Sep;7:721-7. doi: 10.1161/01.res.7.5.721.
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Water and electrolyte metabolism.水和电解质代谢
Physiol Rev. 1954 Apr;34(2):334-417. doi: 10.1152/physrev.1954.34.2.334.
4
Water, nitrogen, and electrolyte content of right and left ventricular walls and interventricular septum of normal canine hearts.正常犬心脏左右心室壁及室间隔的水、氮和电解质含量。
Circ Res. 1966 Sep;19(3):662-7. doi: 10.1161/01.res.19.3.662.
5
Early changes in energy metabolism in the myocardium following acute coronary artery occlusion in anesthetized dogs.麻醉犬急性冠状动脉闭塞后心肌能量代谢的早期变化。
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6
Electrolytes of damaged myocardial mitochondria.
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Regulation of intracellular fluid volume and disease.细胞内液容量的调节与疾病
Am J Med. 1970 Sep;49(3):291-5. doi: 10.1016/s0002-9343(70)80019-5.
8
Fine structural and biochemical changes in dog myocardium during autolysis.犬心肌自溶过程中的超微结构和生化变化
Am J Pathol. 1969 Dec;57(3):539-57.
9
Magnesium exchange in rat ventricle.大鼠心室中的镁交换
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10
Kinetics of calcium accumulation in acute myocardial ischemic injury.急性心肌缺血损伤中钙蓄积的动力学
Am J Pathol. 1972 Jun;67(3):441-52.

短暂缺血期对心肌细胞的影响。I. 对细胞体积调节的影响。

Effect of a transient period of ischemia on myocardial cells. I. Effects on cell volume regulation.

作者信息

Whalen D A, Hamilton D G, Ganote C E, Jennings R B

出版信息

Am J Pathol. 1974 Mar;74(3):381-97.

PMID:4814894
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1910794/
Abstract

The effect of temporary periods of ischemia on the electrolytes and water of myocardial cells were studied in groups of mongrel dogs. Myocardial tissue exposed to 40 minutes of ischemia induced by occlusion of the circumflex branch of the left coronary artery developed no changes in water or electrolytes when compared to nonischemic left ventricle of the same or sham-operated animals, even though this period of ischemia is known to produce irreversible injury to many of the damaged cells. However, reperfusion of the affected myocardium with arterial blood for only 2 minutes resulted in striking increases in tissue H(2)O, Na(-), Cl(-) and Ca(2-). These changes in electrolytes increased in severity with longer periods of reflow, and tissue K(+) was decreased significantly after 10 minutes of reflow had passed. Analysis of the results suggested that the tissue edema was primarily the result of cellular swelling. Myocardium exposed to 15 minutes of ischemia followed by 2 minutes of reflow showed no significant changes aside from a slight increase in Na(+). These studies demonstrate that defects in cell volume regulation occur early in severe ischemic injury.

摘要

在杂种犬组中研究了短暂缺血期对心肌细胞电解质和水的影响。与相同或假手术动物的非缺血左心室相比,暴露于由左冠状动脉回旋支闭塞诱导的40分钟缺血的心肌组织在水或电解质方面没有变化,尽管已知这段缺血期会对许多受损细胞产生不可逆损伤。然而,仅用动脉血对受影响的心肌进行2分钟的再灌注就导致组织H(2)O、Na(-)、Cl(-)和Ca(2 -)显著增加。随着再灌注时间延长,这些电解质变化的严重程度增加,再灌注10分钟后组织K(+)显著降低。结果分析表明,组织水肿主要是细胞肿胀的结果。暴露于15分钟缺血后再灌注2分钟的心肌除Na(+)略有增加外无显著变化。这些研究表明,在严重缺血性损伤早期就会出现细胞体积调节缺陷。