Whalen D A, Hamilton D G, Ganote C E, Jennings R B
Am J Pathol. 1974 Mar;74(3):381-97.
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.
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。