Acidemia and hypernatremia enhance postischemic recovery of excitation-contraction coupling.
Acidemia and hypernatremia enhance postischemic recovery of excitation-contraction coupling.
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酸血症和高钠血症增强兴奋-收缩耦合的缺血后恢复。
DOI：
10.1161/01.res.74.6.1197
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发表时间：
1994
影响因子：
20.1
通讯作者：
Morgan,JP
中科院分区：
文献类型：
--
作者：
Harada,K;Franklin,A;Johnson,RG;Grossman,W;Morgan,JP
本研究的目的是确定Na（+）-H+和Na（+）-Ca 2+交换是否调节缺血后兴奋-收缩偶联的恢复。实验在43只离体等容犬心脏中进行，用血液灌注（pH 7.40，141 mmol/L Na+，34 ℃，以2 Hz起搏）。在左心室（LV）心尖处的3 x 3 mm区域加载水母发光蛋白，用于监测[Ca 2 +]i和LV压力。无血流缺血2至3分钟，随后用（1）未修饰的对照血液进行20分钟的有氧再灌注（141 mmol/L Na+，pH 7.40），（2）酸性血（141 mmol/L Na+，pH 6.60，再灌注0 - 3分钟），（3）高钠血症血（149或157 mmol/L Na+，pH 7.40，再灌注0 - 20分钟）或（4）高渗血（141 mmol/L Na+ + 30 mmol/L甘露醇，pH 7.40，再灌注0 - 20分钟）。用未修饰的对照血液再灌注后，[Ca 2 +]i和LV收缩压和舒张压立即增加，持续2至3分钟，然后恢复至基线或低于基线。室性心律失常发生在此期间（> 80%）。这种短暂的[Ca ~（2+）]i增加被酸血或高钠血灌流液减弱。在酸血或高钠血再灌注时，20分钟时左室发展压力的恢复比未改变的对照再灌注更完全：酸血（n = 7），93 +/- 3%高钠血症（P < .01）（149 mmol/L Na+，n = 7），89 +/- 2%（P <0.02）;高钠血症血液（157 mmol/L Na+，n = 4），91 +/- 2%（P <0.01）;和未修饰的对照血液（n = 17），80 +/-2%。在高渗再灌注时，20分钟时左心室发展压力的恢复没有改善（82 +/- 3%）。从这些结果中我们得出结论：（1）无血流缺血后细胞内Ca ~（2+）短暂增加，可能导致心律失常和收缩元件Ca ~（2+）反应性降低;（2）酸血和高钠血再灌注通过阻止细胞内Ca ~（2+）增加而改善缺血后功能障碍;提示（3）Na（+）-H+和Na（+）-Ca ~（2+）交换在再灌注过程中起重要的调节作用。
The purpose of the present study was to determine whether Na(+)-H+ and Na(+)-Ca2+ exchanges modulate postischemic recovery of excitation-contraction coupling. Experiments were performed in 43 isolated isovolumic dog hearts perfused with blood (pH 7.40, 141 mmol/L Na+, 34 degrees C, paced at 2 Hz). A 3 x 3-mm region at the left ventricular (LV) apex was loaded with aequorin for monitoring [Ca2+]i simultaneously with LV pressure. No-flow ischemia for 2 to 3 minutes was followed by 20 minutes of aerobic reperfusion with (1) unmodified control blood (141 mmol/L Na+, pH 7.40), (2) acidemic blood (141 mmol/L Na+, pH 6.60, at 0 to 3 minutes of reperfusion), (3) hypernatremic blood (149 or 157 mmol/L Na+, pH 7.40, at 0 to 20 minutes of reperfusion), or (4) hyperosmotic blood (141 mmol/L Na+ + 30 mmol/L mannitol, pH 7.40, at 0 to 20 minutes of reperfusion). Reperfusion with unmodified control blood was immediately followed by an increase in [Ca2+]i and LV systolic and diastolic pressure that persisted for 2 to 3 minutes before returning to or below baseline. Ventricular arrhythmia occurred during this period (> 80%). This transient increase of [Ca2+]i was attenuated by acidemic or hypernatremic perfusate. With acidemic or hypernatremic reperfusion, recovery of LV developed pressure at 20 minutes was more complete than with unmodified control reperfusion: acidemic blood (n = 7), 93 +/- 3% (P < .01); hypernatremic blood (149 mmol/L Na+, n = 7), 89 +/- 2% (P < .02); hypernatremic blood (157 mmol/L Na+, n = 4), 91 +/- 2% (P < .01); and unmodified control blood (n = 17), 80 +/- 2%. With hyperosmotic reperfusion, recovery of LV developed pressure at 20 minutes was not improved (82 +/- 3%). From these results we conclude that (1) an increase in intracellular Ca2+ occurs transiently after no-flow ischemia and may cause arrhythmia and decreased Ca2+ responsiveness of the contractile elements, (2) acidemic and hypernatremic reperfusion ameliorates postischemic dysfunction by preventing the increase in intracellular Ca2+, suggesting that (3) Na(+)-H+ and Na(+)-Ca2+ exchange may play important modulatory roles during reperfusion.
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DOI：
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