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大鼠孤束核电解损伤所致动脉血压的慢性不稳定

Chronic lability of the arterial blood pressure produced by electrolytic lesions of the nucleus tractus solitarii in the rat.

作者信息

Buchholz R A, Nathan M A

出版信息

Circ Res. 1984 Mar;54(3):227-38. doi: 10.1161/01.res.54.3.227.

Abstract

The purpose of this study was to assess the chronic effects of lesions of the nucleus tractus solitarii on the cardiovascular activity of rats. Arterial pressure and heart rate were recorded in conscious, unrestrained rats 7-216 days following placement of electrolytic lesions in the nucleus tractus solitarii. To assess the impact of environmental stimuli on the mean level and lability of the mean arterial pressure, cardiovascular activity was recorded under conditions of controlled and uncontrolled environmental stimulation. Nucleus tractus solitarii lesions abolished the reflex bradycardia to a phenylephrine-induced elevation in arterial pressure. A marked increase in the lability of the mean arterial pressure was produced with nucleus tractus solitarii lesions. The standard deviation of the mean arterial pressure, an index of lability, was 380% greater in rats with lesions than in control rats. The average mean arterial pressure, heart rate and heart rate variability were not significantly different between the lesion and control groups, regardless of the environmental conditions under which the measurements were made. Nucleus tractus solitarii lesions also greatly exaggerated the arterial pressure response to naturally occurring behaviors, such as eating and drinking. Vagal and beta-adrenergic blockade with methyl atropine and propranolol did not alter the average level or lability of the mean arterial pressure, although heart rate responses were similar in both groups. alpha-Receptor blockade with prazosin significantly lowered the mean arterial pressure in both lesion and control rats, but the decrease in mean arterial pressure was significantly greater in rats with nucleus tractus solitarii lesions (42 +/- 6 mm Hg, 38.5%) than in control rats (27 +/- 4 mm Hg, 23.2%). Prazosin also reduced the lability of the mean arterial pressure to control levels in rats with lesions. Thus, the chronic effects of nucleus tractus solitarii lesions in rats are to abolish the cardiomotor component of the baroreflexes and to produce extreme lability of the arterial pressure without altering the average level of the mean arterial pressure. Exaggerated blood pressure responses are seen in association with various behaviors. These effects are mediated primarily by changes in sympathetic discharge to the vasculature and are independent of the ambient level of environmental stimuli.

摘要

本研究的目的是评估孤束核损伤对大鼠心血管活动的慢性影响。在孤束核放置电解损伤后7至216天,对清醒、不受束缚的大鼠记录动脉血压和心率。为了评估环境刺激对平均动脉压的平均水平和易变性的影响,在受控和不受控环境刺激条件下记录心血管活动。孤束核损伤消除了对去氧肾上腺素引起的动脉压升高的反射性心动过缓。孤束核损伤导致平均动脉压的易变性显著增加。作为易变性指标的平均动脉压标准差,损伤大鼠比对照大鼠高380%。无论测量时的环境条件如何,损伤组和对照组之间的平均动脉压、心率和心率变异性的平均值均无显著差异。孤束核损伤还极大地夸大了对自然行为(如进食和饮水)的动脉压反应。用甲基阿托品和普萘洛尔进行迷走神经和β-肾上腺素能阻滞,虽两组心率反应相似,但并未改变平均动脉压的平均水平或易变性。用哌唑嗪进行α-受体阻滞可显著降低损伤大鼠和对照大鼠的平均动脉压,但孤束核损伤大鼠的平均动脉压下降幅度(42±6 mmHg,38.5%)显著大于对照大鼠(27±4 mmHg,23.2%)。哌唑嗪还将损伤大鼠的平均动脉压易变性降低至对照水平。因此大鼠孤束核损伤的慢性影响是消除压力反射的心动运动成分,并在不改变平均动脉压平均水平的情况下产生动脉压的极度易变性。在各种行为时可观察到血压反应过度。这些效应主要由对血管系统的交感神经放电变化介导,且与环境刺激的周围水平无关。

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