碘乙酸盐和缺氧对离体灌注大鼠心脏磷酸代谢的影响。

Effects of iodoacetate and anoxia on phosphate metabolism in isolated perfused rat hearts.

作者信息

Takenaka F, Watanabe A

出版信息

Arch Int Pharmacodyn Ther. 1976 Jul;222(1):55-61.

Abstract

When perfused with a solution equilibrated with 95% N2 and 5% CO2, the isolated rat heart was gradually depressed but continued to beat for longer than 30 min. Creatine phosphate content strikingly decreased, but lactate content was markedly elevated. When perfused with a fully oxygenated solution containing 0.5 mM of sodium iodoacetate (IAA) of the myocardial contractile force was almost unaltered and the heart rate decreased slightly within 10 min. Thereafter, the heart rate rapidly decreased, and soon cardiac arrest followed. Myocardial content of high-energy phosphates still remained at a considerably high level. The heart arrested by IAA responded to electrical stimulation, contracted and high-energy phosphates were well utilized. Addition of lactate to an oxygenated perfusate containing IAA improved myocardial performance. Citrate and palmitate did not restore the IAA-treated cardiac impairment. The results show that IAA disturbed cardiac conduction more markedly than contractility by blocking cytoplasmic glycolysis and that lactate, unlike citrate and palmitate, produced enough energy to recover cardiac activities in IAA-treated hearts.

摘要

当用与95%氮气和5%二氧化碳平衡的溶液灌注时，离体大鼠心脏逐渐受到抑制，但仍能持续跳动超过30分钟。磷酸肌酸含量显著下降，但乳酸含量明显升高。当用含有0.5 mM碘乙酸钠（IAA）的完全氧合溶液灌注时，心肌收缩力几乎未改变，心率在10分钟内略有下降。此后，心率迅速下降，随后很快发生心脏骤停。高能磷酸盐的心肌含量仍保持在相当高的水平。IAA导致的心脏骤停对电刺激有反应，能收缩且高能磷酸盐得到良好利用。向含有IAA的氧合灌注液中添加乳酸可改善心肌性能。柠檬酸盐和棕榈酸盐不能恢复IAA处理导致的心脏损伤。结果表明，IAA通过阻断细胞质糖酵解对心脏传导的干扰比收缩性更明显，并且与柠檬酸盐和棕榈酸盐不同，乳酸能产生足够的能量来恢复IAA处理心脏的心脏活动。