Panagiotopoulos S, Daly M J, Nayler W G
Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australia.
Am J Physiol. 1990 Mar;258(3 Pt 2):H821-8. doi: 10.1152/ajpheart.1990.258.3.H821.
The effect of pH of the reperfusion buffer on postischemic changes in tissue Ca and Na was examined in isolated Langendorff-perfused Sprague-Dawley rat hearts. Reperfusion began after 15-, 25-, or 60-min ischemia at 37 degrees C. After 60-min ischemia, reperfusion at pH 6.4 or 6.6 attenuated the reperfusion-induced Ca gain so long as the acidotic conditions were maintained (3.08 +/- 0.22, 1.37 +/- 0.41, and 16.96 +/- 1.18 mumol Ca gain/g dry wt for pH 6.4, 6.6, and 7.4, respectively after 15-min reperfusion). Conversely, reperfusion under alkalotic conditions (pH 7.9) after 60-min ischemia exacerbated the gain (27.45 +/- 4.75 and 8.92 +/- 1.53 mumol Ca gain/g dry wt during 5-min reperfusion at pH 7.9 and 7.4, respectively). Similar, but less pronounced Ca gains occurred during reperfusion after 15- or 25-min ischemia. Sodium content during reperfusion, but not during aerobic perfusion, was also found to be pH sensitive with acidosis causing a reduction and alkalosis an increase. These results could not be explained in terms of an effect of pH on recovery of high-energy phosphates, percentage "reflow" during reperfusion, or reperfusion-induced increases in tissue water or resting tension. The results are in agreement with the hypothesis that the "inhibitory" effect of acidosis on postischemic Ca overload could involve an effect of pH on the Na(+)-H+ exchanger and intracellular Ca storage.
在离体Langendorff灌注的Sprague-Dawley大鼠心脏中,研究了再灌注缓冲液的pH值对缺血后组织钙和钠变化的影响。在37℃下,分别进行15分钟、25分钟或60分钟缺血缺血后开始再灌注。缺血60分钟后,只要维持酸中毒状态(再灌注15分钟后,pH 6.4、6.6和7.4时,每克干重的钙增加量分别为3.08±0.22、1.37±0.41和16.96±1.18μmol),pH 6.4或6.6的再灌注可减轻再灌注诱导的钙增加。相反,缺血60分钟后在碱中毒条件下(pH 7.9)的再灌注会加剧钙增加(pH 7.9和7.4时,在5分钟再灌注期间,每克干重的钙增加量分别为27.45±4.75和8.92±1.53μmol)。在15分钟或25分钟缺血后的再灌注过程中,也出现了类似但不太明显的钙增加。还发现,再灌注期间(而非有氧灌注期间)的钠含量对pH敏感,酸中毒导致降低,碱中毒导致增加。这些结果无法用pH对高能磷酸盐恢复、再灌注期间的“再灌注”百分比、再灌注诱导的组织水分增加或静息张力的影响来解释。这些结果与以下假设一致,即酸中毒对缺血后钙超载的“抑制”作用可能涉及pH对Na(+)-H+交换体和细胞内钙储存的影响。