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目的 研究低血钾是如何损害心肌细胞。方法 将 2 4只大白鼠离体心脏随机分成四组 ,即无钾正常钙灌注组 ,无钾低钙灌注组 ,低钾正常钙灌注组和低钾高钙灌注组 ,另 6例作为对照组。先正常灌注液灌注 30分钟 ,使心脏功能维持正常 ;以后实验灌注 30分钟 ,最后恢复正常灌注 30分钟。整个过程用磁共振电子分光镜技术连续监测心肌细胞的三磷酸腺苷 (ATP)、磷酸肌酸 (PCr)、无机磷酸 (Pi)及心肌细胞内Ph (Phi)的浓度变化 ;同时用心电图和多道心脏电生理仪监测心电图、心律及其血液动力学变化。实验完成后立即将离体心脏液氮冷冻 ,用化学方法提取线粒体 ,最后用原子吸收分光镜检查心肌细胞内的线粒体及其钙含量。结果 低钾导致心肌细胞内ATP ,PCr合成明显减少 ,同时伴有心肌细胞内酸中毒 ,而Pi明显增加 ,其程度与低钾程度呈正比。当恢复正常灌注之后 ,其能量代谢紊乱。心律失常及心功能不能恢复 ,当用低钾高钙灌注液灌注时 ,此种变化更为明显。结论 低钾导致心肌细胞线粒体呼吸功能不全 ,引起心肌细胞线粒体能量产生障碍 ,出现ATP ,PCr下降 ,Pi升高和细胞内酸中毒 ,从而导致心律紊乱 ,心功能下降 ,心室纤颤和心脏停搏。这似可说明洋地黄过量伴潜在低钾及低钙时 ,如不补足钾就补钙所造成的危害及其机理 ,为临?
Objective To investigate how hypokalemia damages cardiomyocytes. Methods Twenty-four hearts were randomly divided into four groups: normal calcium-free potassium group, potassium-free low-calcium infusion group, low-potassium normal calcium infusion group and low-potassium high calcium infusion group, and the other 6 as control group . Normal perfusion fluid perfusion for 30 minutes to maintain normal heart function; after experimental perfusion for 30 minutes, and finally returned to normal perfusion for 30 minutes. The whole process of continuous monitoring of myocardial cells using magnetic resonance spectroscopy technology of phosphorylated creatine (PCr), inorganic phosphate (Pi) and cardiomyocytes Ph (Phi) concentration changes; while ECG and multi-channel heart Electrophysiology monitors ECG, heart rate and hemodynamic changes. Immediately after the completion of the experiment, the isolated heart liquid nitrogen was frozen and the mitochondria were extracted by chemical methods. Finally, the mitochondria and calcium content in the myocardial cells were examined by atomic absorption spectroscopy. Results Hypokalemia induced a marked decrease of ATP and PCr synthesis in cardiomyocytes accompanied by intracellular acidosis but Pi increased significantly, which was in direct proportion to the degree of hypokalemia. After resuming normal perfusion, its energy metabolism is disturbed. Arrhythmia and cardiac function can not be restored, when the infusion of low-potassium high-calcium perfusion, this change even more pronounced. CONCLUSION: Hypokalemia leads to mitochondrial respiratory insufficiency of cardiomyocytes, which leads to the disturbance of mitochondrial energy in cardiomyocytes, the decrease of ATP, PCr, the increase of Pi and the intracellular acidosis, leading to heart rhythm disturbance, cardiac function decline, ventricular fibrillation and cardiac arrest . This may seem to illustrate digitalis overdose with potential hypokalemia and low calcium, if not make up for potassium on the harm caused by calcium and its mechanism, Pro?