Kohyama A, Inoue M, Doi T, Iseki A, Kaji S, Kitahata H, Saitoh T
Department of Anesthesiology, Tokushima University School of Medicine.
Masui. 1993 Jul;42(7):1025-33.
We investigated the effects of intramyocardial acidosis on cardiac function during hypoxia in mongrel dogs (n = 50). Intramyocardial pH in subendocardium of left ventricle was measured continuously using a pH electrode. During hypoxia (PaO2 = 20 mmHg) caused by inhalation of low oxygen fraction, intramyocardial pH decreased significantly following initial enhancement. Intramyocardial pH correlated significantly with arterial pH, base excess, lactic acid (LA) levels, coronary venous PcO2, and coronary venous-arterial PcO2 difference. There were significant correlations between intramyocardial pH with maximum rate of rise of left ventricular pressure (LV dp/dt max), left ventricular end-diastolic pressure (LVEDP), LVEDP/LVP and the time constant of exponential isovolumic left ventricular pressure fall. High arterial LA levels tended to cease myocardial LA uptake and production, turning LA balance into zero. LV dp/dt max was low in such a condition. Myocardial LA production decreased intramyocardial pH, but LV dp/dt max was maintained at high levels of LA production. These observations suggest that myocardial LA production maintains left ventricular function with the increase of ATP by acceleration of anaerobic glycolysis. In conclusion, during hypoxia, intramyocardial acidosis was caused by the increase of arterial LA level, myocardial anaerobic glycolysis and ATP breakdown, and it worsened left ventricular contractile function and relaxation. Arterial LA levels can play a major part in intramyocardial acidosis, but the increase in myocardial LA production might be beneficial to left ventricular contractile function.
我们研究了杂种犬（n = 50）缺氧期间心肌内酸中毒对心脏功能的影响。使用pH电极连续测量左心室心内膜下的心肌内pH值。在吸入低氧分数导致的缺氧（PaO2 = 20 mmHg）期间，心肌内pH值在最初升高后显著下降。心肌内pH值与动脉pH值、碱剩余、乳酸（LA）水平、冠状静脉PcO2以及冠状静脉 - 动脉PcO2差值显著相关。心肌内pH值与左心室压力最大上升速率（LV dp/dt max）、左心室舒张末期压力（LVEDP）、LVEDP/LVP以及左心室等容压力下降的时间常数之间存在显著相关性。高动脉LA水平倾向于停止心肌对LA的摄取和产生，使LA平衡变为零。在这种情况下LV dp/dt max较低。心肌LA产生降低了心肌内pH值，但在LA产生高水平时LV dp/dt max维持在较高水平。这些观察结果表明，心肌LA产生通过加速无氧糖酵解增加ATP来维持左心室功能。总之，在缺氧期间，心肌内酸中毒是由动脉LA水平升高、心肌无氧糖酵解和ATP分解引起的，并且它恶化了左心室的收缩功能和舒张功能。动脉LA水平在心肌内酸中毒中可能起主要作用，但心肌LA产生的增加可能对左心室收缩功能有益。
