Depression of myocardial force and stiffness without change in crossbridge kinetics: effects of volatile anesthetics reproduced by nifedipine.
Depression of myocardial force and stiffness without change in crossbridge kinetics: effects of volatile anesthetics reproduced by nifedipine.
复制标题
在不改变横桥动力学的情况下抑制心肌力和僵硬度：硝苯地平再现挥发性麻醉剂的作用。
DOI：
10.1097/00000542-198909000-00022
复制
发表时间：
1989
期刊：
影响因子：
8.8
通讯作者：
Berman,MR
中科院分区：
文献类型：
--
作者：
Chung,OY;Blanck,TJ;Berman,MR
作者研究了硝苯地平（一种肌膜慢钙通道阻滞剂）对Ba 2+挛缩家兔右心室小梁和乳头肌动态刚度和力的影响，试图重现氟烷、安氟醚和异氟醚对柴田等人报道的类似制剂的影响。一旦确定了钡挛缩力，用频率范围为0.1-100 Hz的小振幅正弦振荡扰动肌肉长度。然后将硝苯地平1 μ M加入到灌流液中，并再次测量动态刚度。使用额外的钡来确定挛缩力恢复到或超过对照水平。硝苯地平可显著降低挛缩力和高频刚度，但对刚度振幅最小的频率（fmin）无影响（P <0.005）。收缩力和僵硬度可以通过在硝苯地平处理的肌肉中加入额外的钡来恢复。这些结果与柴田等人使用挥发性麻醉剂报告的结果相似。由于硝苯地平特异性作用于肌膜慢Ca 2+通道，以与挥发性麻醉剂相似的方式影响该制剂中的挛缩力和动态刚度，因此作者认为柴田等人研究的麻醉剂可能通过其对肌膜慢Ca 2+通道的作用而发挥其负性肌力活性的重要成分。
The authors examined the effects of nifedipine, a sarcolemmal slow Ca2+ channel blocker, on dynamic stiffness and force of rabbit right ventricular trabeculum and papillary muscle in Ba2+ contracture, in an attempt to reproduce the effects of halothane, enflurane, and isoflurane on a similar preparation as reported by Shibata et al. Once barium contracture force was established, muscle length was perturbed with small amplitude sinusoidal oscillations in the frequency range of 0.1-100 Hz. Nifedipine 1 microM was then added to the superfusate and dynamic stiffness was again measured. Additional barium was used to determine restoration of contracture force to and beyond control levels. Nifedipine produced a significant decrease in contracture force and high-frequency stiffness with no effect on the frequency (fmin) at which stiffness amplitude exhibited a minimum (P less than 0.005). Contracture force and stiffness could be restored by adding additional barium to the nifedipine-treated muscles. These results are similar to those reported by Shibata et al. using volatile anesthetics. Since nifedipine, which acts specifically at the sarcolemmal slow Ca2+ channel, affects contracture force and dynamic stiffness in this preparation in a manner similar to the volatile anesthetics, the authors suggest that the anesthetics studied by Shibata et al. may well exert a significant component of their negative inotropic activity via their action on the sarcolemmal slow Ca2+ channel.