O'Neill M, Sears C E, Paterson D J
University Laboratory of Physiology, Oxford, United Kingdom.
J Appl Physiol (1985). 1997 Apr;82(4):1046-52. doi: 10.1152/jappl.1997.82.4.1046.
We tested the hypothesis that cardiac ischemia uncouples the beneficial interaction among hyperkalemia, acidosis, and raised plasma catecholamines when these chemicals are changed to mimic their exercise levels. Potassium chloride, lactic acid, and norepinephrine (NE) were infused intravenously for 2 min into anesthetized, artificially ventilated, thoracotomized rabbits during either occlusion of the left circumflex artery (3 min; n = 10) or after a period of prolonged ischemia (20 min; n = 7) that led to a small infarction. NE (1 microg x kg(-1) x min(-1) iv) offset the negative cardiac effects of hyperkalemia (up to 8.7 +/- 0.7 mM) and acidosis (arterial pH 7.09 +/- 0.03) in normal hearts. Cardiac performance was not significantly depressed by either acute or chronic ischemia before any infusions. However, the protective effect of NE during acute ischemia or after prolonged ischemia with hyperkalemia and acidosis was substantially reduced. These results show that cardiac ischemia attenuates the protective action of NE and increases the depressive effects of hyperkalemia and acidosis. Whether myocardial ischemia amplifies the cardiotoxic effects of hyperkalemia and acidosis during vigorous exercise by attenuating the beneficial effect of catecholamines remains to be determined.
当改变氯化钾、乳酸和去甲肾上腺素（NE）的水平以模拟运动时的水平时，心脏缺血会破坏高钾血症、酸中毒和血浆儿茶酚胺升高之间的有益相互作用。在左旋支动脉闭塞期间（3分钟；n = 10）或在导致小面积梗死的长时间缺血（20分钟；n = 7）后，将氯化钾、乳酸和去甲肾上腺素静脉输注2分钟至麻醉、人工通气、开胸的兔子体内。在正常心脏中，NE（1微克·千克⁻¹·分钟⁻¹静脉注射）抵消了高钾血症（高达8.7±0.7毫摩尔/升）和酸中毒（动脉pH 7.09±0.03）对心脏的负面影响。在任何输注之前，急性或慢性缺血均未显著降低心脏功能。然而，在急性缺血期间或长时间缺血伴高钾血症和酸中毒后，NE的保护作用显著降低。这些结果表明，心脏缺血减弱了NE的保护作用，并增强了高钾血症和酸中毒的抑制作用。心肌缺血是否通过减弱儿茶酚胺的有益作用而在剧烈运动期间放大高钾血症和酸中毒的心脏毒性作用仍有待确定。
