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犬心肌缺血诱导的pH值降低是呼吸性酸中毒还是代谢性酸中毒?

Is ischemia-induced pH decrease of dog myocardium respiratory or metabolic acidosis?

作者信息

Ichihara K, Haga N, Abiko Y

出版信息

Am J Physiol. 1984 May;246(5 Pt 2):H652-7. doi: 10.1152/ajpheart.1984.246.5.H652.

Abstract

Ischemia causes myocardial acidosis and elevation of myocardial CO2 tension (PCO2). We performed the present study to examine whether accumulation of hydrogen ion is a cause or result of accumulation of CO2. The myocardial pH and PCO2 were measured simultaneously in the dog heart, and the concentration of HCO-3 [( HCO-3]) was calculated according to the Henderson-Hasselbalch equation. Ischemia was induced by either partial or complete occlusion of the left anterior descending coronary artery (LAD). After LAD occlusion, the myocardial pH decreased with a marked decrease in [HCO-3], indicating that metabolic acidosis occurred. We ascertained in experiments with blood sample in vitro that an addition of lactic acid into blood decreased both [HCO-3] and pH (metabolic acidosis), whereas an addition of CO2 gas into blood increased [HCO-3] and decreased pH (respiratory acidosis). These findings suggest that ischemic acidosis is not respiratory in nature, but metabolic. The myocardial pH decrease due to ischemia, however, cannot be explained by the tissue lactate accumulation alone, because the decrease of [HCO-3] is far greater than the increase of lactic acid during ischemia.

摘要

缺血会导致心肌酸中毒以及心肌二氧化碳张力(PCO2)升高。我们开展本研究以检验氢离子的蓄积是二氧化碳蓄积的原因还是结果。在犬心脏中同时测量心肌pH值和PCO2,并根据亨德森 - 哈塞尔巴尔赫方程计算碳酸氢根离子([HCO-3])浓度。通过部分或完全闭塞左冠状动脉前降支(LAD)诱导缺血。LAD闭塞后,心肌pH值下降,同时[HCO-3]显著降低,表明发生了代谢性酸中毒。我们在体外血液样本实验中确定,向血液中添加乳酸会降低[HCO-3]和pH值(代谢性酸中毒),而向血液中添加二氧化碳气体会增加[HCO-3]并降低pH值(呼吸性酸中毒)。这些发现表明,缺血性酸中毒本质上不是呼吸性的,而是代谢性的。然而,缺血导致的心肌pH值下降不能仅用组织乳酸蓄积来解释,因为缺血期间[HCO-3]的下降远大于乳酸的增加。

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