大鼠腹主动脉收缩后血流动力学和神经体液的变化。

B Hwang, T Y Qu, C T Hu, H I Chen
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引用次数: 0

摘要

观察6组SD大鼠腹主动脉收缩后心脏负荷、神经体液反应及继发性心肌肥厚的变化。我们发现腹主动脉在肾动脉上方的收缩降低了心率和心输出量,增加了脉压。这些异常会在收缩结束后恢复正常。卡托普利、普萘洛尔和普唑嗪均能降低腹缩大鼠脉压升高,但仍能降低心输出量。主动脉收缩也增加了主动脉阻抗和心脏负荷,但降低了主动脉顺应性。卡托普利、心得安和哌唑嗪也能减轻这些变化。我们已经证实主动脉收缩可引起继发性心肌肥厚,但其发病机制可能是由多种因素引起的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hemodynamic and neurohumoral changes after abdominal aortic constriction in rats.

Cardiac after-load, neurohumoral reaction and the secondary cardiac hypertrophy were studied in six groups of Sprague-Dawley (SD) rats with abdominal aortic constriction. We found that abdominal aortic constriction above the renal arteries decreased the heart rate and cardiac output, and increased the pulse pressure. These abnormalities would return to normal after constriction ended. Captopril, propranolol and prazosin could reduce the increase of pulse pressure but still had decreased in cardiac output of rats with abdominal constriction. Aortic constriction also increased the aortic impedance and cardiac load but decreased aortic compliance. These changes could also be lessened by captopril, propranolol and prazosin. We have confirmed that aortic constriction can induce secondary cardiac hypertrophy, but the pathogenesis might be due to multiple factors.

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