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背景:动脉血管平滑肌细胞膜电位的微小变化就可以导致张力的显著性改变,膜去极化与高血压形成有密切关系。目的:研究易卒中型自发性高血压大鼠大脑中动脉平滑肌细胞的静息膜电位(Em)及其对血管活性物质KCl、去甲肾上腺素的反应性。设计:对照分析动物实验。单位:山东省医学科学院药物研究所。材料:雄性卒中型自发性高血压大鼠18只和雄性Wistar大鼠26只。方法:①两组大鼠经乌拉坦(1g/kg)腹腔注射麻醉,迅速取出大脑,剥离出大脑中动脉,应用细胞内微电极记录血管平滑肌细胞膜电位。②分别观察不同浓度的KCl(10,20,50mmol/L),去甲肾上腺素(10-7,10-6,10-5mol/L)对血管平滑肌细胞膜电位的影响。主要观察指标:①两组大鼠血管平滑肌细胞膜电位。②不同浓度的KCl和去甲肾上腺素对血管平滑肌细胞膜电位的影响。结果:①卒中型自发性高血压大鼠膜电位明显低于Wistar大鼠[(-48.2±3.1),(-64.4±4.3)mV]。②KCl(10,20,50mmol/L)和去甲肾上腺素(10-7,10-6,10-5mol/L)均引起大脑中动脉膜电位去极化,且皆呈剂量依赖式特点;与Wistar大鼠比较,卒中型自发性高血压大鼠的大脑中动脉反应性明显增强。结论:卒中型自发性高血压大鼠大脑中动脉血管平滑肌细胞膜电位较低,对KCl和去甲肾上腺素的反应性明显高于Wistar大鼠。
Background: Small changes in the membrane potential of arterial smooth muscle cells can lead to significant changes in tension, and membrane depolarization is closely related to the formation of hypertension. Objective: To study the resting membrane potential (Em) and its reactivity to vasoactive substances (KCl and norepinephrine) in rat middle cerebral artery smooth muscle cells in spontaneously hypertensive rats with stroke. Design: Control analysis of animal experiments. Unit: Institute of Materia Medica, Shandong Academy of Medical Sciences. MATERIALS: Eighteen male spontaneously hypertensive rats and 26 male Wistar rats. Methods: ①The rats in both groups were anesthetized with urethane (1g / kg) intraperitoneally, the brain was removed rapidly, and the middle cerebral artery was dissected out. The intracellular microelectrode was used to record the membrane potential of vascular smooth muscle cells. ② The effects of different concentration of KCl (10,20,50mmol / L), norepinephrine (10-7,10-6,10-5mol / L) on the membrane potential of vascular smooth muscle cells were observed. MAIN OUTCOME MEASURES: ① The membrane potential of vascular smooth muscle cells in two groups. Effects of KCl and norepinephrine at different concentrations on the membrane potential of vascular smooth muscle cells. Results: ①The membrane potential of stroke-induced spontaneously hypertensive rats was significantly lower than that of Wistar rats [(-48.2 ± 3.1), (-64.4 ± 4.3) mV]. ②KCl (10,20,50mmol / L) and norepinephrine (10-7,10-6,10-5mol / L) all caused the depolarization of the middle cerebral artery membrane potential in a dose-dependent manner; and Wistar rats, stroke-induced spontaneous hypertensive rat middle cerebral artery reactivity was significantly enhanced. CONCLUSIONS: Stromal spontaneous hypertensive rats have lower membrane potential of middle cerebral artery smooth muscle cells and higher reactivity to KCl and norepinephrine than those of Wistar rats.