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首页> 外文期刊>Life sciences >The protective action of amlodipine on cardiac negative inotropism caused by prolonged incubation in vitro.
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The protective action of amlodipine on cardiac negative inotropism caused by prolonged incubation in vitro.

机译：氨氯地平对长时间体外培养引起的心脏负性肌力的保护作用。

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The mechanism of the antihypertensive action of the 1,4-dihydropyridine Ca2+ antagonist amlodipine was studied in isolated ventricular strips and aortic rings from Wistar rats after oral treatment with amlodipine 15 mg/kg/day for one week. The contractions evoked by electrical stimulation of isolated strips from right ventricles pretreated with amlodipine (5 nM) were unaffected during the first hour after mounting, but they decreased in magnitude after prolonged incubation (4 hr). However, the decrease in response of these preparations after prolonged incubation was less than that observed in strips prepared from untreated rats. A negative inotropic effect of amlodipine was observed at concentrations higher than 300 nM. In the presence of lower concentrations of amlodipine (5 nM-30 nM) after prolonged incubation, the contractions of ventricular strips were significantly more sustained than in the absence of amlodipine. Likewise, the decrease in contractility evoked by increasing the stimulation frequency from 1 to 3 Hz was reduced in amlodipine treated rats. The recovery of contractility was improved when stimulation frequency was returned to 1 Hz. On the other hand, when rat ventricular strips pretreated with amlodipine (5 nM) were exposed to isoprenaline (3 microM), the contractions evoked by isoprenaline were enhanced. The isoprenaline effect was not altered with 300 nM amlodipine, but with 3 microM became weak and was significantly lower than in strips treated with isoprenaline alone. In addition, treatment with amlodipine produced a marked decrease in the contractions evoked by 100 mM KCl solution in isolated aortic rings when compared to untreated rats. This inhibition was produced in a time-dependent manner with an IC50 equal to 30 and 3 nM after 2 and 45 min of contraction, respectively. Ex vivo results show that amlodipine treatment decreased aortic contractility without producing a negative inotropic effect although there was an occupation of cardiac Ca2+ channels. These results suggest that a protective effect of amlodipine on cardiac negative inotropism is produced by prolonged incubation in vitro.
机译：在口服Wistar大鼠15 mg / kg / day持续1周后，在Wistar大鼠分离的心室带和主动脉环中研究了1,4-二氢吡啶Ca2 +拮抗剂氨氯地平的降压作用机理。在安装后的第一小时内，通过电刺激从用氨氯地平（5 nM）预处理的右心室分离的条带引起的收缩未受到影响，但在延长的孵育时间（4 hr）后它们的大小降低了。然而，长时间温育后，这些制剂的响应降低小于从未经处理的大鼠制备的条中观察到的响应降低。在高于300 nM的浓度下观察到氨氯地平的负性肌力作用。长时间孵育后存在较低浓度的氨氯地平（5 nM-30 nM），与不使用氨氯地平的情况相比，心室带的收缩明显更持久。同样，在氨氯地平治疗的大鼠中，通过将刺激频率从1 Hz增加到3 Hz引起的收缩力降低也有所减少。当刺激频率恢复到1 Hz时，收缩力的恢复得到改善。另一方面，将氨氯地平（5 nM）预处理的大鼠心室片暴露于异丙肾上腺素（3 microM）时，异丙肾上腺素引起的收缩增强。 300 nM氨氯地平不会改变异丙肾上腺素的作用，但3 microM的作用会减弱，并且显着低于单独使用异丙肾上腺素治疗的条带。此外，与未经治疗的大鼠相比，用氨氯地平治疗可明显减少分离的主动脉环中100 mM KCl溶液引起的收缩。收缩2分钟和45分钟后，IC50分别以时间依赖性方式产生这种抑制作用，IC50分别为30和3 nM。离体结果显示，氨氯地平治疗可降低主动脉收缩力，但不会产生负性肌力作用，尽管存在心脏Ca2 +通道的占用。这些结果表明，氨氯地平通过长时间的体外温育产生了对心脏负性肌力的保护作用。

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