Effect of acidosis and alkalosis on postischemic Ca gain in isolated rat heart.
Effect of acidosis and alkalosis on postischemic Ca gain in isolated rat heart.
复制标题
酸中毒和碱中毒对离体大鼠心脏缺血后钙增加的影响。
DOI：
10.1152/ajpheart.1990.258.3.h821
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Winifred G. Nayler
中科院分区：
文献类型：
--
作者：
Sianna Panagiotopoulos;M. Daly;Winifred G. Nayler
在灌流的SD大鼠心脏上，观察了再灌流缓冲液的pH对缺血后组织钙、钠变化的影响。再灌流开始于37℃下缺血15、25或60min，再灌注60min后，只要维持酸性条件，pH 6.4或6.6的再灌流可减弱再灌流引起的钙增加(再灌流15min后，pH值分别为3.08+/-0.22、1.37+/-0.41和16.96+/-1.18摩尔钙增加/g干重)。相反，缺血60分钟后在碱性条件下(pH 7.9)再灌流则加剧了钙增加(分别为27.45+/-4.75和8.92+/-1.53摩尔钙增加/g干重)。在缺血15分钟或25分钟后的再灌流期间，也有类似的，但不太明显的钙增加。再灌流期间的钠含量，但在有氧灌流期间不是，也被发现是pH敏感的，酸中毒导致减少，碱中毒增加。这些结果不能用pH对高能磷酸盐恢复的影响、再灌流期间“回流”的百分比或再灌流引起的组织水或静息张力的增加来解释。这一结果与酸中毒对缺血后钙超载的“抑制”作用可能与pH对Na(+)-H+交换和细胞内钙储存的影响有关。
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.