Bond J M, Herman B, Lemasters J J
Department of Cell Biology & Anatomy, University of North Carolina, Chapel Hill 27599.
Biochem Biophys Res Commun. 1991 Sep 16;179(2):798-803. doi: 10.1016/0006-291x(91)91887-i.
We assessed the effect of acidosis on cell killing during anoxia and reoxygenation in cultured rat neonatal cardiac myocytes. After 4.5 hours of anoxia and glycolytic inhibition with 2-deoxyglucose, loss of viability was greater than 90% at pH 7.4. In contrast, at pH 6.2-7.0, viability was virtually unchanged. To model changes of pH and oxygenation during ischemia and reperfusion, myocytes were made anoxic at pH 6.2 for 4 hours, followed by reoxygenation at pH 7.4. Under these conditions, reoxygenation precipitated loss of viability to about half the cells. When pH was increased to 7.4 without reoxygenation, similar lethal injury occurred. No cell killing occurred after reoxygenation at pH 6.2. We conclude that acidosis protects against lethal anoxic injury, and that a rapid return from acidotic to physiologic pH contributes significantly to reperfusion injury to cardiac myocytes - a 'pH paradox'.
我们评估了酸中毒对培养的新生大鼠心肌细胞在缺氧和复氧过程中细胞杀伤的影响。在用2-脱氧葡萄糖进行4.5小时缺氧和糖酵解抑制后,在pH 7.4时,细胞活力丧失超过90%。相比之下,在pH 6.2 - 7.0时,细胞活力几乎没有变化。为了模拟缺血和再灌注过程中pH值和氧合的变化,使心肌细胞在pH 6.2下缺氧4小时,然后在pH 7.4下复氧。在这些条件下,复氧导致约一半细胞的活力丧失。当在不复氧的情况下将pH值提高到7.4时,也会发生类似的致命损伤。在pH 6.2下复氧后未发生细胞杀伤。我们得出结论,酸中毒可防止致命的缺氧损伤,并且从酸中毒快速恢复到生理pH值会显著导致心肌细胞的再灌注损伤——一种“pH值矛盾现象”。