Hatton D C, Bukoski R D, Edgar S, McCarron D A
Department of Medical Psychology, Oregon Health Sciences University, Portland 97201-3098.
J Hypertens. 1992 Jun;10(6):529-37. doi: 10.1097/00004872-199206000-00005.
To determine the effect of chronic alcohol consumption upon blood pressure, blood pressure reactivity and vascular contractility in Wistar rats.
Wistar rats were fed a liquid diet containing 36% ethanol; control rats were pair fed.
Rats were maintained on diets for 18 weeks. Indirect systolic blood pressure was measured weekly. Catheters were implanted for assessment of direct arterial pressure and blood pressure reactivity to norepinephrine, angiotensin II and ethanol injections. In a subgroup of rats, contractility of isolated mesenteric resistance vessels was measured.
In comparison with simultaneously pair-fed controls, ethanol-treated rats developed significantly lower blood pressure within 3 weeks of exposure to alcohol; this continued throughout the study. Despite the reduction in blood pressure, in vitro assessment of vascular contractility in mesenteric resistance vessels indicated that ethanol consumption significantly enhanced vascular contractility to norepinephrine and attenuated the vasodepressive effects of ethanol. Measurement of blood pressure reactivity to infused pressor agents showed no difference between controls and ethanol-treated rats in response to norepinephrine but a significantly attenuated pressor response to angiotensin II was observed in ethanol-treated rats.
The blood pressure results contrast with reports of elevated blood pressure in Wistar rats given ethanol in drinking water. This disparity may be due to nutritional factors. Increased vascular contractility combined with hypotension suggests that cardiovascular regulatory systems offset the direct effects of ethanol upon the vasculature. This view is reinforced by the lack of difference between groups in blood pressure reactivity to norepinephrine. The attenuated angiotensin II responses in the ethanol-treated rats suggests altered levels of circulating angiotensin II in this group.
确定长期饮酒对Wistar大鼠血压、血压反应性及血管收缩性的影响。
给Wistar大鼠喂食含36%乙醇的液体饮食;对对照大鼠进行配对喂食。
大鼠维持饮食18周。每周测量间接收缩压。植入导管以评估直接动脉压及对去甲肾上腺素、血管紧张素II和乙醇注射的血压反应性。在一组大鼠中,测量离体肠系膜阻力血管的收缩性。
与同时期配对喂食的对照大鼠相比,乙醇处理的大鼠在接触酒精3周内血压显著降低;这种情况在整个研究过程中持续存在。尽管血压降低,但肠系膜阻力血管血管收缩性的体外评估表明,饮酒显著增强了血管对去甲肾上腺素的收缩性,并减弱了乙醇的血管舒张作用。对注入升压剂的血压反应性测量显示,对照大鼠和乙醇处理的大鼠对去甲肾上腺素的反应无差异,但在乙醇处理的大鼠中观察到对血管紧张素II的升压反应显著减弱。
血压结果与给Wistar大鼠饮用含乙醇的水后血压升高的报道相反。这种差异可能是由于营养因素。血管收缩性增加与低血压并存表明心血管调节系统抵消了乙醇对血管系统的直接作用。去甲肾上腺素血压反应性在两组之间缺乏差异进一步支持了这一观点。乙醇处理的大鼠中血管紧张素II反应减弱表明该组循环血管紧张素II水平发生了改变。