Crandall D L, Ferraro G D, Lozito R J, Cervoni P, Clark L T
American Cyanamid Company, Pearl River, NY 10965.
J Hypertens. 1989 Aug;7(8):683-7. doi: 10.1097/00004872-198908000-00013.
The development of a novel model of human alcoholism has involved the presentation of a 30% alcohol solution to Sprague-Dawley rats via a syringe-feeding needle apparatus. With twice daily intermittent drinking, rats consumed an equivalent of 7-8 g/kg body weight of alcohol, which represented 25% of total daily caloric intake. Alcohol was absorbed rapidly, as significant circulating concentrations were observed within 15 min of gavage, eventually peaking at approximately 200 mg% 1 h later. Hemodynamic recordings in the conscious state after a 10-week drinking program indicated a normotensive blood pressure at peak blood alcohol levels, yet a hypertensive response 24 h after the final drink at a time when blood alcohol was not detected. Alcoholic rats continued to gain weight in parallel with controls fed ad libitum throughout the study, and changes in cardiac size and indices of contractility were not affected by 10 weeks of intermittent drinking. Additionally, no histological evidence of cardiac muscle damage was observed in alcoholic animals. Our animal model closely resembles the clinical situation in terms of the pattern of alcohol consumption, circulating concentrations of alcohol and the percentage of caloric intake in the form of alcohol. The hemodynamic changes observed support the hypothesis that alcoholic hypertension may be a manifestation of withdrawal, as opposed to any direct pressor effect of alcohol itself.
一种新型人类酒精中毒模型的建立,是通过注射器喂食针头装置给斯普拉格-道利大鼠提供30%的酒精溶液。大鼠每天分两次间歇性饮酒,摄入的酒精量相当于7 - 8克/千克体重,占每日总热量摄入的25%。酒精吸收迅速,灌胃后15分钟内即可观察到显著的循环浓度,最终在1小时后达到约200毫克%的峰值。经过10周饮酒方案后,清醒状态下的血流动力学记录显示,在血酒精水平达到峰值时血压正常,但在最后一次饮酒24小时后,尽管未检测到血酒精,却出现了高血压反应。在整个研究过程中,酒精性大鼠的体重继续与自由进食的对照组平行增加,间歇性饮酒10周并未影响心脏大小和收缩性指标的变化。此外,在酒精性动物中未观察到心肌损伤的组织学证据。就酒精消费模式、酒精循环浓度以及酒精形式的热量摄入百分比而言,我们的动物模型与临床情况非常相似。观察到的血流动力学变化支持了这样一种假设,即酒精性高血压可能是戒断的一种表现,而非酒精本身的任何直接升压作用。