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本文引用的文献

1
Drastic food restriction; effect on cardiovascular dynamics in normotensive and hypertensive conditions.严格的食物限制;对正常血压和高血压状态下心血管动力学的影响。
J Am Med Assoc. 1948 Aug 28;137(18):1569-74. doi: 10.1001/jama.1948.02890520001001.
2
HYPERTENSION AND CARDIOVASCULAR ABNORMALITIES IN STARVED-REFED SWINE.饥饿再喂养猪的高血压与心血管异常
J Nutr. 1964 Feb;82(2):173-82. doi: 10.1093/jn/82.2.173.
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Effect of fasting and re-alimentation with diets high in carbohydrate or protein on blood pressure and heart rate of sympathectomized dogs.
Am J Physiol. 1957 Oct;191(1):103-7. doi: 10.1152/ajplegacy.1957.191.1.103.
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Height, weight, and their ratio in the accelerated form of primary hypertension.原发性高血压加速型的身高、体重及其比例
AMA Arch Intern Med. 1957 Aug;100(2):263-5. doi: 10.1001/archinte.1957.00260080089017.
5
Prevention of renal hypertension and of the central pressor effect of angiotensin by ventromedial hypothalamic ablation.通过下丘脑腹内侧核损毁预防肾性高血压及血管紧张素的中枢升压作用。
Brain Res. 1981 Feb 2;205(2):255-64. doi: 10.1016/0006-8993(81)90337-1.
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Inhibition of the pathogenesis of spontaneous hypertension in spontaneously hypertensive rats by feeding a high fat diet.
Endocrinology. 1981 Mar;108(3):981-9. doi: 10.1210/endo-108-3-981.
7
The effect of refeeding after semistarvation on catecholamine and thyroid metabolism.
Int J Obes. 1980;4(2):95-100.
8
Hypothalamic paraventricular nucleus lesions produce overeating and obesity in the rat.下丘脑室旁核损伤会导致大鼠暴饮暴食和肥胖。
Physiol Behav. 1981 Dec;27(6):1031-40. doi: 10.1016/0031-9384(81)90366-8.
9
Paraventricular--suprachiasmatic lesions prevent salt-induced hypertension in Dahl rats.室旁核 - 视交叉上核损伤可预防 Dahl 大鼠盐诱导的高血压。
Clin Sci (Lond). 1981 Dec;61 Suppl 7:49s-51s. doi: 10.1042/cs061049s.
10
Oxygen consumption and locomotor activity during restricted feeding and realimentation.限制进食和再喂养期间的耗氧量及运动活动
Am J Physiol. 1981 Nov;241(5):R392-7. doi: 10.1152/ajpregu.1981.241.5.R392.

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.

DOI:10.1152/ajpregu.1988.254.1.R47
PMID:3337269
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2943142/
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)