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一种生电泵对甲壳类动物心脏静息膜极化的作用。

Contribution of an electrogenic pump to the resting membrane polarization in a crustacean heart.

作者信息

Delaleu J C, Holley A

出版信息

J Exp Biol. 1976 Feb;64(1):59-74. doi: 10.1242/jeb.64.1.59.

Abstract
  1. In the neurogenic heart of the isopod crustacean Porcellio dilatatus, external K+ removal depolarized the membrane (K0 effect) whereas subsequent restoration of K+ resulted in a rapid hyperpolarization (K1 effect). 2. The amplitude of the K1 effect depended on the duration of the prior K+ deprivation and on the subsequent K+ concentration. 3. The membrane resistance slightly increased during the K0 effect; during the K1 effect, it only returned to its control value. 4. Ouabain, cooling and replacement of external Na+ by Li+ also produced depolarization. 5. The K1 effect was suppressed by ouabain and markedly depressed by lowering the temperature to 4-6 degrees C. It was abolished if Li+ replaced Na+ during the prior privation of K+; moreover Li+ was unable to act as a substitute for external K+ in generating the K1 effect if used at equivalent concentration, but enhanced the effect at high concentration. 6. The findings are consistent with the presence of an electrogenic sodium pump in the myocardium of Porcellio contributing to the resting membrane potential. 7. Changes in the spontaneous rhythm observed during K0 and K1 are further suggestive of the presence of an electrogenic Na+ pump in the pacemaker neurons of the cardiac ganglion. Another explanation is also proposed. 8. The magnitude of the spontaneous contractions of the heart was increased during the K0 effect and markedly decreased during the K1 effect. An indirect effect of the changes in internal Na+ concentration on the contractile processes is suggested.
摘要
  1. 在等足类甲壳动物膨腹土甲的神经源性心脏中,去除细胞外钾会使膜去极化(K0效应),而随后恢复钾会导致快速超极化(K1效应)。2. K1效应的幅度取决于先前钾缺乏的持续时间和随后的钾浓度。3. 在K0效应期间膜电阻略有增加;在K1效应期间,它仅恢复到对照值。4. 哇巴因、冷却以及用锂离子替代细胞外钠离子也会产生去极化。5. K1效应被哇巴因抑制,并且在温度降至4 - 6摄氏度时显著降低。如果在先前的钾缺乏期间用锂离子替代钠离子,K1效应就会消失;此外,当以等效浓度使用时,锂离子不能替代细胞外钾来产生K1效应,但在高浓度时会增强该效应。6. 这些发现与膨腹土甲心肌中存在电生性钠泵有助于静息膜电位这一情况相符。7. 在K0和K1期间观察到的自发节律变化进一步表明心脏神经节的起搏神经元中存在电生性钠泵。还提出了另一种解释。8. 在K0效应期间心脏自发收缩的幅度增加,而在K1效应期间显著降低。提示细胞内钠离子浓度变化对收缩过程有间接影响。

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