Initial contractile response of isolated rat heart cells to halothane, enflurane, and isoflurane.

Initial contractile response of isolated rat heart cells to halothane, enflurane, and isoflurane.
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离体大鼠心脏细胞对氟烷、安氟烷和异氟烷的初始收缩反应。

DOI:
10.1097/00000542-199701000-00018
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发表时间:
1997
期刊:
影响因子:
8.8
通讯作者:
Spurgeon,HA
Spurgeon,HA
中科院分区:
医学1区
文献类型:
--
作者:
Wheeler,DM;Rice,RT;duBell,WH;Spurgeon,HA

文献摘要

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在几种搏动心肌标本中,当它们突然暴露于含有氟烷或安氟醚的溶液中时,观察到抽搐张力或振幅的短暂增加。随着持续暴露于麻醉剂,预期的负性肌力作用在短暂的抽搐增加后变得明显。在异氟烷暴露期间,未报告抽搐增加。据推测,这种短暂的增加抽搐是由肌浆网钙释放的增强引起的,但其他机制尚未被排除。方法新鲜分离的单个大鼠心室细胞在室温下刺激搏动,并突然暴露于含有氟烷的溶液中25 -0.64 mM)、恩氟烷(0.69-1 mM)或异氟烷(0.31-0.54 mM)。在这些曝光过程中,抽搐幅度进行了测量,并使用钙敏感染料indo-1细胞内钙浓度。在一些实验中,全细胞膜片钳技术被用来测量膜电流。此外,在几个细胞中,通过对咖啡因短暂脉冲的反应来评估肌浆网钙含量。结果突然暴露于氟烷或安氟醚的细胞中,抽搐幅度和细胞内钙瞬变均暂时增加。使用异氟烷时未发现此类行为。在继续暴露于所有三种药物后,抽搐幅度和钙瞬变均小于对照组。在搏动表现出增加抽搐,细胞长度(抽搐幅度)和细胞内钙瞬变之间的关系没有改变,发现与对照条件相比。此外,暂时增加抽搐幅度发生在电压钳控制下的细胞收缩时,氟烷被引入,它是不相关的钙电流的任何增加。肌浆网钙含量在氟烷诱导的增加抽搐的时间也没有increased.ConclusionsThe短暂的增加抽搐突然暴露于氟烷或安氟醚是相关的增加细胞内钙在跳动过程中,而不是肌丝对钙的敏感性的任何变化。由于这些结果排除了对这种现象的大多数替代解释,作者得出结论,氟烷,可能还有恩氟烷,增加了每次心跳时肌浆网释放的钙的比例。异氟烷似乎缺乏这种作用。
BackgroundIn several beating cardiac muscle preparations, a short-lived increase in twitch tension or amplitude has been observed when they were exposed abruptly to solutions containing halothane or enflurane. As exposure to the anesthetics was continued, the expected negative inotropic effect became evident after the short-lived increase in twitch. No such increase in twitch has been reported during exposure to isoflurane. It has been hypothesized that this short-lived increase in twitch is caused by an enhancement of calcium release from the sarcoplasmic reticulum, but other mechanisms have not been excluded.MethodsFreshly isolated, single rat ventricular cells were stimulated to beat at room temperature and abruptly exposed to solutions containing halothane (0.25-0.64 mM), enflurane (0.69-1 mM), or isoflurane (0.31-0.54 mM). During these exposures, twitch amplitude was measured and intracellular calcium concentration was followed using the calcium-sensitive dye indo-1. In some experiments, the whole-cell patch-clamp technique was used to measure membrane current. In addition, in several cells the sarcoplasmic reticulum calcium content was assessed through the response to brief pulses of caffeine.ResultsBoth the twitch amplitude and the intracellular calcium transient were increased temporarily in cells abruptly exposed to halothane or enflurane. No such behavior was found with isoflurane. After continued exposure to all three agents, both the twitch amplitude and the calcium transient were less than control. During the beats exhibiting an increase in twitch, no alteration in the relation between cell length (twitch amplitude) and the intracellular calcium transient was found compared with control conditions. In addition, the temporary increase in twitch amplitude occurred in cells contracting under voltage-clamp control when halothane was introduced, and it was not associated with any increase in the calcium current. The sarcoplasmic reticulum calcium content at the time of the halothane-induced increase in twitch also was not increased.ConclusionsThe short-lived increase in twitch after abrupt exposure to halothane or enflurane is related to increased intracellular calcium during the beat and not to any changes in myofilament sensitivity to calcium. Because these results eliminate most alternative explanations for this phenomenon, the authors conclude that halothane, and probably also enflurane, increases the fraction of calcium released from the sarcoplasmic reticulum with each heart beat. Isoflurane appears to lack this action.