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[去甲肾上腺素输注引起动脉高血压的代偿机制分析]

[Analysis of compensatory mechanisms of arterial hypertension in norepinephrine infusion].

作者信息

Eremeev V S, Pliss M G, Khrustaleva R S, Tsyrlin V A, Shcherbin Iu I

出版信息

Fiziol Zh SSSR Im I M Sechenova. 1988 Nov;74(11):1571-9.

PMID:2907742
Abstract

The NA infusion induced a raise in the AP, inhibition of sympathetic vasomotor activity and a drop in the heart rate in alert male cats. The hypertensive effect of the NA was weakening during first 90 min of the infusion, a complete inhibition of sympathetic activity persisted during the whole period of infusion as well as a decrease in the heart rate, in anesthetized cats. After deafferentation, the markedness of the arterial hypertension weakening decreased and the effect of the infusion on sympathetic activity and heart rate was abolished. Administration of pentamine during the infusion did not affect the AP in anesthetized cats, increased it in alert animals and decreased the AP in deafferented cats. The organism seems to have no humoral mechanisms of compensation of arterial hypertension induced with the 3-hr infusion of noradrenaline.

摘要

去甲肾上腺素输注可使清醒雄性猫的动脉血压升高、交感缩血管活动受抑制及心率下降。在输注的最初90分钟内,去甲肾上腺素的升压作用减弱,在麻醉猫中,整个输注期间交感活动持续被完全抑制,心率也下降。去传入神经后,动脉高血压减弱的程度降低,输注对交感活动和心率的影响被消除。输注期间给予喷他明对麻醉猫的动脉血压无影响,使清醒动物的动脉血压升高,而去传入神经猫的动脉血压下降。机体似乎不存在对3小时去甲肾上腺素输注所致动脉高血压进行代偿的体液机制。

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