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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Role of the Na+-H+ exchanger (NHE1) in heart muscle function during transient acidosis. A study in papillary muscles from rat and guinea pig hearts.
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Role of the Na+-H+ exchanger (NHE1) in heart muscle function during transient acidosis. A study in papillary muscles from rat and guinea pig hearts.

机译:Na + -H +交换子(NHE1)在短暂酸中毒期间在心肌功能中的作用。对大鼠和豚鼠心脏的乳头肌的研究。

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摘要

The sodium-hydrogen exchanger (NHE) helps the cell to recover from intracellular acidosis. In this study, we have investigated the effect of HOE 642 (a specific NHE1 blocker) on papillary muscles from rats and guinea pigs during transient acidosis and PKC activation by recording developed force (DF), action potential characteristics, and electrical conductance (stimulus-response interval). Two protocols were used, with or without HOE 642 (10-5 mol/L): papillary muscle was exposed (i) for 15 min to a glucose-free, nonoxygenated HEPES buffer containing lactate (20 mmol/L) (pH 6.8) followed by 15 min recovery or (ii) to a PKC activator (phorbolmyristate acetate (PMA) (10-9 mol/L)) for 30 min. The DF after acidification remained significantly decreased in the NHE-blocked papillary muscles. During recovery from acidosis, papillary muscles exposed to HOE 642 remained at a higher electrical resistance. The present study shows that post-acidotic continued depression of DF and change in tissue electrophysiological properties might occur as a result of blocking the NHE. During infarct development, the tissue-protecting effect of NHE blockade has been well documented. When acidosis or reduced contractile function is present, however, blocking NHE by HOE 642 might not improve the situation.
机译:钠氢交换剂(NHE)帮助细胞从细胞内酸中毒中恢复过来。在这项研究中,我们通过记录发育力(DF),动作电位特性和电导率(刺激-刺激),研究了HOE 642(一种特定的NHE1阻滞剂)对短暂酸中毒和PKC激活过程中大鼠和豚鼠的乳头肌的影响。响应间隔)。使用两种方案,有或没有HOE 642(10-5 mol / L):乳头肌(i)暴露于含乳酸(20 mmol / L)(pH 6.8)的无葡萄糖,无氧HEPES缓冲液中15分钟。然后恢复15分钟,或(ii)加入PKC活化剂(醋酸佛波肉豆蔻酸酯(PMA)(10-9 mol / L))30分钟。在NHE阻滞的乳头肌中,酸化后的DF仍显着降低。从酸中毒恢复期间,暴露于HOE 642的乳头肌保持较高的电阻。本研究表明,由于NHE的阻断,酸中毒后DF的持续降低和组织电生理特性的改变可能会发生。在梗塞发展过程中,NHE阻断的组织保护作用已得到充分证明。但是,当出现酸中毒或收缩功能降低时,通过HOE 642阻止NHE可能不会改善这种情况。

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