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能量限制后小鼠心肌耐寒性增加的电生理证据。

Electrophysiological evidence of an increase in cold tolerance of cardiac muscles in mice after energy restriction.

作者信息

Wada Y, Shinbo A, Tsukada M, Iijima T, Koizumi A

机构信息

Department of Hygiene, Akita University School of Medicine, Japan.

出版信息

Mech Ageing Dev. 1997 Jul;97(1):35-43. doi: 10.1016/s0047-6374(97)01898-8.

Abstract

Life-prolonging energy restriction (ER) has been known to extend longevity. The heart was selected as the target organ of ER and the electrophysiological properties of ER on the heart were investigated. Action potential parameters were measured on ventricular papillary muscles of C57BL/6 mice (2-6 months of age). Resting membrane potential (Rm) did not change even when the temperature was lowered to 20 degrees C in ER mice (-67.5 +/- 0.8 mV), however, the membrane was depolarized in the control (-61.1 +/- 1.1 mV). Action potential duration measured at 30 and 50% repolarization was significantly prolonged in ER mice at 20-35 degrees C. Ouabain (10 microM) decreased Rm in ER mice at 20 degrees C (-68.6 +/- 1.0 to -63.6 +/- 0.8 mV), but failed to decrease Rm in the control (-60.6 +/- 1.8 to -62.1 +/- 1.2 mV). There were no significant differences in extracted Na, K-ATPase activity or affinity and binding capacity of ouabain between ER and control hearts. These results indicate that in ER mice the lack of effect of temperature on Rm was not due to a change in the physicochemical properties of Na, K-ATPase. The present study collectively suggests that ER increases cold tolerance in the heart of mice.

摘要

延长寿命的能量限制(ER)已知可延长寿命。心脏被选为ER的靶器官,并研究了ER对心脏的电生理特性。在C57BL/6小鼠(2至6个月大)的心室乳头肌上测量动作电位参数。在ER小鼠中,即使温度降至20摄氏度,静息膜电位(Rm)也没有变化(-67.5±0.8 mV),然而,在对照组中膜发生了去极化(-61.1±1.1 mV)。在20至35摄氏度下,ER小鼠在复极化30%和50%时测量的动作电位持续时间显著延长。哇巴因(10 microM)在20摄氏度时降低了ER小鼠的Rm(从-68.6±1.0 mV降至-63.6±0.8 mV),但在对照组中未能降低Rm(从-60.6±1.8 mV降至-62.1±1.2 mV)。ER心脏和对照心脏之间提取的钠钾ATP酶活性、哇巴因的亲和力和结合能力没有显著差异。这些结果表明,在ER小鼠中,温度对Rm缺乏影响不是由于钠钾ATP酶的物理化学性质发生变化。本研究共同表明,ER增加了小鼠心脏的耐寒性。

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