在振动介导的缺氧模型中,阻断兔心肌细胞钙通道恢复呼吸链酶-底物复合物的活性

V. V. Vorobieva, O. S. Levchenkova, P. Shabanov
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引用次数: 1

摘要

采用振动介导的细胞缺氧模型(振动56次,频率44 Hz,振幅0.5 mm),研究了7.5 mg/kg剂量硝苯地平对兔心肌细胞能量代谢的影响。采用极谱法评估天然心脏线粒体在30%组织匀浆中的能量代谢,方法是在37°C下,在1ml生理盐水培养液中记录线粒体的摄氧量,并与大气氧气平衡。在CCB背景下振动暴露的动物,内源性呼吸速率(Ve)保持在正常动物水平,戊醛敏感性提高39% (p<0.05),丙二酸敏感性降低40% (p<0.05)。与无药物保护的振动组相比,静息时苹果酸氧化酶活性增加,内源性琥珀酸氧化系统的超激活降低。结果表明硝苯地平对心肌细胞坏死具有明显的保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Blockade of Rabbit Cardiomyocyte Calcium Channels Restores the Activity of Enzyme-Substrate Complexes of the Respiratory Chain in a Model of Vibration-Mediated Hypoxia
The effect of nifedipine, a calcium channel blocker (CCB), at a dose of 7.5 mg/kg on the energy metabolism of rabbit cardiomyocytes was evaluated in a vibration-mediated model of cellular hypoxia (56 sessions of vibration 44 Hz, amplitude 0.5 mm). The energy metabolism of native heart mitochondria in a 30% tissue homogenate was assessed using a polarographic method, by recording the rate of oxygen uptake by mitochondria at 37°C in 1 ml of a saline incubation medium, equilibrated with atmospheric oxygen. In the animals exposed to vibration against the background of CCB, the rate of endogenous respiration (Ve) remained at the level of intact animals, with the amytal sensitivity increasing by 39% (p<0.05) and the malonate sensitivity decreasing by 40% (p<0.05). The malate oxidase activity at rest increased, and hyperactivation of the endogenous succinic acid oxidation system decreased as compared to the indices of the animals exposed to vibration without pharmacological protection. The observed results indicate the cardioprotective effect of nifedipine, which prevented the development of cardiomyocyte necrosis.
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