MECHANISMS OF MYOCARDIAL HYPERCARBIC ACIDOSIS DURING CARDIAC-ARREST
MECHANISMS OF MYOCARDIAL HYPERCARBIC ACIDOSIS DURING CARDIAC-ARREST
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DOI：
10.1152/jappl.1995.78.4.1579
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发表时间：
1995-04-01
影响因子：
3.3
通讯作者：
MCCANDLESS, D
中科院分区：
文献类型：
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作者：
JOHNSON, BA;WEIL, MH;MCCANDLESS, D
在心脏骤停引起的全球性心肌缺血期间以及由于冠状动脉血流局部受损导致的局部心肌缺血期间，缺血心肌的心肌内二氧化碳分压（Pm - CO₂）会升高到超过400托的水平。这种心肌高碳酸性酸中毒的机制尚未完全清楚，特别是Pm - CO₂的升高是由于氧化代谢增加、二氧化碳清除减少，还是代谢性酸的缓冲作用所致。因此，我们测量了大鼠心脏在心脏骤停复苏前、复苏期间和复苏后的Pm - CO₂以及总二氧化碳含量。在未经治疗的心室颤动4分钟期间，Pm - CO₂从平均63托显著升高到209托。与此同时，细胞内pH从平均7.03单位下降到6.02单位。心肌的总二氧化碳含量同时从17.0毫摩尔/千克下降到16.5毫摩尔/千克。因此，在总二氧化碳含量没有增加，也就是计算得出的心肌碳酸氢盐没有增加的情况下，观察到Pm - CO₂和[H⁺]升高。在大鼠模型中的这些观察结果表明，碳酸氢盐对代谢性酸的缓冲作用，而非二氧化碳产生增加或二氧化碳清除减少，是导致心肌高碳酸血症的主要机制。
During the global myocardial ischemia of cardiac arrest and during regional myocardial ischemia due to local impairment of coronary blood flow, intramyocardial carbon dioxide tensions (Pm-CO2) of ischemic myocardium increase to levels exceeding 400 Torr. The mechanism of such myocardial hypercarbic acidosis is as yet incompletely understood, specifically whether these increases in Pm-CO2 are due to increased oxidative metabolism, decreased CO2 removal, or buffering of metabolic acids. We therefore measured Pm-CO2 and the total CO2 content of rat hearts harvested before, during, and after resuscitation from cardiac arrest. Pm-CO2 significantly increased from an average of 63 to 209 Torr during a 4-min interval of untreated ventricular fibrillation. This was associated with concurrent decreases in intracellular pH from an average of 7.03 to 6.02 units. The total CO2 content of the myocardium simultaneously decreased from 17.0 to 16.5 mmol/kg. Accordingly, increases in Pm-CO2 and [H+] were observed in the absence of increases in the total CO2 content and therefore the calculated myocardial bicarbonate. These observations in the rat model implicate buffering of metabolic acids by bicarbonate rather than increases in CO2 production or decreases in CO2 removal as the predominant mechanism accounting for myocardial hypercarbia.