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机构地区:[1]广州中山医科大学生理学教研室,承德医学院低温生理研究室
出 处:《中国应用生理学杂志》1995年第2期102-105,共4页Chinese Journal of Applied Physiology
摘 要:本实验用fura-2荧光技术研究离体鼠心缺氧期间心肌细胞内游离钙浓度([Ca ̄(2+)]_i)增加的机制。实验结果为:(1)Krebs-Henseleit(K-H)液缺氧灌流离体鼠心脏引起[Ca ̄(2+)]_i先慢后快地增加。(2)无钙液缺氧灌流,仍能引起[Ca ̄(2+)]_i增加。(3)含异搏定(1.1×10 ̄(-5)mol/L)的K-H液缺氧灌流[Ca ̄(2+)]_i的变化类似无钙液缺氧灌流,而且两者引起的[Ca ̄(2+)]_i增加,明显低于K-H液缺氧灌流。(4)Licl取代K-H液中NaCl缺氧灌流时引起[Ca ̄(2+)]_i增加速率显著快于K-H液缺氧灌流。上述结果表明:心肌缺氧时[Ca ̄(2+)]_i增加与胞内钙释放、胞外钙通过钙通道内流及Na ̄+-Ca ̄(2+)交换有关。The mechanism of increase in rat cardiac cytosolic free calcium concentration([ Ca ̄(2+))_i)during hypoxia was investigated using fura-2 fluorescence technique. The main results were asfollows:(1)Perfusion of isolated rat hearts with hypoxic and substrate-free K-H solutioncaused an increase in(Ca ̄ (2+))_i at increasing speed.(2) Perfusion with the calcium-free hypoxicand substrate-free K-H solution still led to an increase in(Ca  ̄(2+))_i.(3)The increase in[Ca ̄(2+))_ i induced by perfusion with the K-H solution containing verapamil (1.1 × 10(-5)mol / 1)was similar to that with the calcium-free K-H solution, and the increase in (Ca ̄(2+))_ i in bothcases was significantly less than that during hypoxic K-H solution perfusion. (4)The rate of in-crease in ( Ca ̄ (2+))_ i during hypoxic perfusion with low-sodium K-H solution was significantlyhigher than that with k-H solution. These results suggest that the increase in(Ca ̄(2+))_i is relat-ed to the release of Ca ̄(2+) from intracellular pool, Ca ̄(2+) influx via calcium channel andNa ̄+-Ca ̄(2+) exchange during myocardial hypoxia.
分 类 号:R331.31[医药卫生—人体生理学]
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