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氰化物对雪貂和大鼠心室肌细胞内离子交换的影响。

The effects of cyanide on intracellular ionic exchange in ferret and rat ventricular myocardium.

作者信息

Fry C H, Harding D P, Mounsey J P

出版信息

Proc R Soc Lond B Biol Sci. 1987 Feb 23;230(1258):53-75. doi: 10.1098/rspb.1987.0009.

DOI:10.1098/rspb.1987.0009
PMID:2884664
Abstract

The effects of cyanide on Ca2+ exchange in isolated ventricular myocytes and on the intracellular concentrations of Ca2+, Na+ and H+ have been investigated to assess the contribution that mitochondria might play in cellular Ca2+ metabolism. Ionic levels were measured with ion-selective electrodes. KCN (2.5 mM) inhibited a component of Ca2+ exchange in myocytes that could be attributed to mitochondrial exchange, but was without effect on non-mitochondrial Ca2+ exchange. NaCN (2.5 mM) caused a transient reduction of [H+]i, [Na+]i and [Ca2+]i when applied to the superfusate bathing ventricular trabeculae or papillary muscles. The transient changes of [Na+]i were accentuated when the preparation was exposed to a solution which would be expected to increase the cellular calcium content. The reduction of [Na+]i which accompanies a reduction of the extracellular sodium concentration, [Na]o, was attenuated in the presence of NaCN, but the intracellular acidosis resulting from a reduction of [Na]o was unaffected by NaCN. A small, but significant, rise of [Ca2+]i accompanied a reduction of [Na]o but only when NaCN was present in the superfusate. It is concluded that cyanide ions have a reasonably specific action on cardiac cellular ionic metabolism. Its primary action is to prevent mitochondrial Ca2+ sequestration. It is postulated that a Na+/H+ exchange, possibly at the sarcolemma, could account for some of the changes to sarcoplasmic ionic levels observed. In a solution of low [Na]o, it is concluded that mitochondria could sequester at least 30% of the calcium accumulated by the cell even though the sarcoplasmic [Ca2+] does not exceed 0.3 microM.

摘要

已研究了氰化物对分离的心室肌细胞中Ca2+交换以及细胞内Ca2+、Na+和H+浓度的影响,以评估线粒体在细胞Ca2+代谢中可能发挥的作用。用离子选择性电极测量离子水平。KCN(2.5 mM)抑制了心肌细胞中可归因于线粒体交换的Ca2+交换成分,但对非线粒体Ca2+交换无影响。当将NaCN(2.5 mM)应用于灌注心室小梁或乳头肌的超滤液时,会导致[H+]i、[Na+]i和[Ca2+]i短暂降低。当制剂暴露于预期会增加细胞钙含量的溶液中时,[Na+]i的短暂变化会加剧。在存在NaCN的情况下,伴随细胞外钠浓度[Na]o降低的[Na+]i降低会减弱,但[Na]o降低导致的细胞内酸中毒不受NaCN影响。只有当超滤液中存在NaCN时,[Na]o降低才会伴随[Ca2+]i小幅但显著升高。结论是,氰离子对心脏细胞离子代谢具有相当特异性的作用。其主要作用是阻止线粒体Ca2+的摄取。据推测,可能在肌膜处的Na+/H+交换可以解释观察到的肌浆离子水平的一些变化。在低[Na]o溶液中,得出的结论是,即使肌浆[Ca2+]不超过0.3 microM,线粒体也可以摄取细胞积累的至少30%的钙。

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