Amrinone relaxes potassium-induced contracture of failing right ventricular muscle of cats.
Amrinone relaxes potassium-induced contracture of failing right ventricular muscle of cats.
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氨力农可缓解钾引起的猫右心室肌衰竭的挛缩。
DOI：
10.1097/00005344-198303000-00028
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发表时间：
1983
影响因子：
3
通讯作者：
Bassett,AL
中科院分区：
文献类型：
--
作者：
Gaide,MS;Fitterman,WS;Wiggins,JR;Myerburg,RJ;Cameron,JS;Bassett,AL
本文观察了氨力农（5.3 × 10 ~（-1）M）对正常猫（n= 6）和右心室衰竭（RVF，n= 6）猫肺动脉部分结扎后3-14天右心室肌等长收缩和K [middle dot]诱发的收缩力的影响。RVF肌肉的峰值等长收缩力（Po）和最大力发展速率（dP/dt）（分别为1.38+/-0.21 g/mm 2 x+/-SEM和11+/-1 g/s/mm 2）显著低于正常肌肉（分别为2.46+/-0.41 g/mm 2，p< 0.025和24+/-3 g/s/mm 2，p<0.005）。RVF肌肉的收缩持续时间（DC）（442+/-32 ms）明显长于正常肌肉（361+/-11 ms，p< 0.025）。RVF和正常肌肉的收缩力峰值（TTP）和K [中点]诱导的收缩力峰值（Po）的时间没有差异。氨力农在正常肌肉中显著增加Po和dP/dt（分别为+ 78+/-24%x +/-SEM; p< 0.01和+ 53+/-17%，p < 0.025），但在RVF肌肉中没有增加（分别为+ 11+/-16%和+ 8+/-19%）。正常肌肉的TTP和DC未被氨力农改变，而RVF肌肉的TTP未改变而DC缩短（-12+/-3%，p < 0.025）。氨力农在正常（-28+/-7%，p< 0.005）和RVF（-26+/-4%，p< 0.025）肌肉中的松弛（Po）相似且显著。这些结果表明，氨力农对衰竭心脏的部分有益作用是通过改变心肌舒张而发生的。
The effects of amrinone (5.3 x 10-1 M) on isometric contraction and K [middle dot]-induced contracture force of right ventricular muscle isolated from normal cats (n= 6) and cats in right ventricular failure (RVF, n= 6), 3-14 days after partial pulmonary artery ligation, were studied. Peak isometric contractile force (Po) and maximal rate of force development (dP/dt) of RVF muscles (1.38+/-0.21 g/mm2 x+/-SEM, and 11+/-1 g/s/mm2, respectively) were significantly lower than normal muscles (2.46+/-0.41 g/mm2, p< 0.025, and 24+/-3 g/s/mm2, p< 0,005, respectively). Duration of contraction (DC) was significantly longer in RVF muscles (442+/-32 ms) than in normal muscles (361+/-11 ms, p< 0.025). Times to peak twitch force (TTP) and peak K [middle dot]-induced contracture force (Po) of RVF and normal muscles were not different. Amrinone increased Po and dP/dt significantly in normal muscles (+ 78+/-24% x+/-SEM; p< 0.01, and+ 53+/-17%, p< 0.025, respectively), but not in RVF muscles (+ 11+/-16% and+ 8+/-19%, respectively). TTP and DC of normal muscle were unchanged by amrinone, whereas TTP was unchanged while DC was shortened (-12+/-3%, p< 0.025) in RVF muscle. Amrinone relaxed, Po, similarly and significantly in normal (-28+/-7%, p< 0.005) and RVF (-26+/-4%, p< 0.025) muscles. These results suggest that part of amrinone's salutary action in the failing heart occurs through modification of myocardial relaxation.