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饮食性肥胖中的再喂养高血压

Refeeding hypertension in dietary obesity.

作者信息

Ernsberger P, Nelson D O

机构信息

Neuroscience Program, Northwestern University Medical School, Chicago, Illinois 60611.

出版信息

Am J Physiol. 1988 Jan;254(1 Pt 2):R47-55. doi: 10.1152/ajpregu.1988.254.1.R47.

Abstract

A novel model of nutritionally induced hypertension in the rat is described. Dietary obesity was produced by providing sweet milk in addition to regular chow, which elicited a 52% increase in caloric intake. Despite 54% greater body weight gain and 139% heavier retroperitoneal fat pads, 120 days of overfeeding failed to increase systolic pressure in the conscious state (125 +/- 8 vs. 121 +/- 4 mmHg in chow-fed controls) or mean arterial pressure under urethan anesthesia (71 +/- 4 vs. 63 +/- 3 mmHg). In contrast, mild hypertension developed in intermittantly fasted obese animals (a 21-mmHg increase in systolic blood pressure measured in the conscious state and a 16-mmHg increase in mean arterial pressure under anesthesia relative to chow-fed controls). The first 4-day supplemented fast was initiated 4 wk after the introduction of sweet milk, when the animals were 47 g overweight relative to chow-fed controls. Thereafter, 4 days of starvation were alternated with 2 wk of refeeding for a total of 4 cycles. A rapid fall in systolic blood pressure (12 +/- 2 mmHg at 2 days) accompanied the onset of supplemented fasting and was maintained thereafter (2.7 +/- 2.6 mmHg further decrease during the latter half of the fast). With refeeding, blood pressure rose precipitously (13 +/- 3 mmHg in the 1st 2 days), despite poststarvation anorexia. Blood pressure tended to rise slightly over the remainder of the realimentation period (5.2 +/- 2.8 mmHg). After the 4th supplemented fast, hypertension was sustained during 30 days of refeeding. Cumulative caloric intake in starved-refed rats fell within 2% of that in chow-fed controls.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本文描述了一种新型的大鼠营养性高血压模型。除常规饲料外,通过提供甜牛奶诱导饮食性肥胖,热量摄入增加了52%。尽管体重增加了54%,腹膜后脂肪垫重了139%,但120天的过度喂养未能使清醒状态下的收缩压升高(喂食普通饲料的对照组为125±8 mmHg,过度喂养组为121±4 mmHg),也未使乌拉坦麻醉下的平均动脉压升高(对照组为63±3 mmHg,过度喂养组为71±4 mmHg)。相比之下,间歇性禁食的肥胖动物出现了轻度高血压(清醒状态下收缩压相对于喂食普通饲料的对照组升高21 mmHg,麻醉下平均动脉压升高16 mmHg)。在引入甜牛奶4周后,即动物比喂食普通饲料的对照组超重47 g时,开始了为期4天的补充禁食。此后,4天饥饿与2周再喂养交替进行,共4个周期。补充禁食开始时,收缩压迅速下降(第2天下降12±2 mmHg),此后一直维持(禁食后半期进一步下降2.7±2.6 mmHg)。再喂养时,尽管饥饿后出现厌食,但血压急剧上升(最初2天上升13±3 mmHg)。在再喂养期的剩余时间里,血压往往略有上升(5.2±2.8 mmHg)。第4次补充禁食后,在30天的再喂养期间高血压持续存在。饥饿-再喂养大鼠的累积热量摄入比喂食普通饲料的对照组低2%。(摘要截短于250字)

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