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首页> 外文期刊>American Journal of Physiology >Beta-myosin heavy chain myocytes are more resistant to changes in power output induced by ischemic conditions.
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Beta-myosin heavy chain myocytes are more resistant to changes in power output induced by ischemic conditions.

机译：β-肌球蛋白重链肌细胞对缺血性条件引起的功率输出变化具有更大的抵抗力。

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During ischemia intracellular concentrations of P(i) and H+ increase. Also, changes in myosin heavy chain (MHC) isoform toward beta-MHC have been reported after ischemia and infarction associated with coronary artery disease. The purpose of this study was to investigate the effects of myoplasmic changes of P(i) and H+ on the loaded shortening velocity and power output of cardiac myocytes expressing either alpha- or beta-MHC. Skinned cardiac myocyte preparations were obtained from adult male Sprague-Dawley rats (control or treated with 5-n-propyl-2-thiouracil to induce beta-MHC) and mounted between a force transducer and servomotor system. Myocyte preparations were subjected to a series of isotonic force clamps to determine shortening velocity and power output during Ca2+ activations in each of the following solutions: 1) pCa 4.5 and pH 7.0; 2) pCa 4.5, pH 7.0, and 5 mM P(i); 3) pCa 4.5 and pH 6.6; and 4) pCa 4.5, pH 6.6, and 5 mM P(i). Added P(i) and lowered pH each caused isometric force to decline tothe same extent in alpha-MHC and beta-MHC myocytes; however, beta-MHC myocytes were more resistant to changes in absolute power output. For example, peak absolute power output fell 53% in alpha-MHC myocytes, whereas power fell only 38% in beta-MHC myocytes in response to elevated P(i) and lowered pH (i.e., solution 4). The reduced effect on power output was the result of a greater increase in loaded shortening velocity induced by P(i) in beta-MHC myocytes and an increase in loaded shortening velocity at pH 6.6 that occurred only in beta-MHC myocytes. We conclude that the functional response to elevated P(i) and lowered pH during ischemia is MHC isoform-dependent with beta-MHC myocytes being more resistant to declines in power output.
机译：在缺血期间，细胞内P（i）和H +的浓度会增加。同样，在与冠状动脉疾病相关的局部缺血和梗塞后，肌球蛋白重链（MHC）亚型向β-MHC的变化已有报道。这项研究的目的是调查P（i）和H +的胞质变化对表达α-或β-MHC的心肌细胞的缩短速度和输出功率的影响。从成年雄性Sprague-Dawley大鼠（对照或用5-n-丙基-2-硫尿嘧啶治疗以诱导β-MHC）获得皮肤的心肌细胞制剂，并将其安装在力传感器和伺服电机系统之间。对心肌细胞制剂进行一系列等渗力钳以确定在以下每种溶液中Ca2 +活化过程中的缩短速度和功率输出：1）pCa 4.5和pH 7.0; 2）pCa 4.5，pH 7.0和5 mM P（i）; 3）pCa 4.5和pH 6.6;和4）pCa 4.5，pH 6.6和5 mM P（i）。增加的P（i）和降低的pH值均会导致等距力在α-MHC和β-MHC心肌细胞中下降到相同程度;但是，β-MHC心肌细胞对绝对功率输出的变化更具抵抗力。例如，响应于P（i）升高和pH降低（即溶液4），α-MHC肌细胞的峰值绝对功率输出下降了53％，而β-MHC肌细胞的功率仅下降了38％。对功率输出的减小的影响是β（-）MHC心肌细胞中由P（i）诱导的负载缩短速度的更大增加和仅在β-MHC心肌细胞中在pH 6.6时负载的缩短速度增加的结果。我们得出结论，在缺血期间对升高的P（i）和降低的pH的功能反应是MHC亚型依赖性的，其中β-MHC心肌细胞对功率输出的下降更具抵抗力。

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