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肥胖犬心率的副交感神经控制减弱。

Reduced parasympathetic control of heart rate in obese dogs.

作者信息

Van Vliet B N, Hall J E, Mizelle H L, Montani J P, Smith M J

机构信息

Division of Basic Medical Science, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Canada.

出版信息

Am J Physiol. 1995 Aug;269(2 Pt 2):H629-37. doi: 10.1152/ajpheart.1995.269.2.H629.

Abstract

We investigated why resting heart rate is elevated in dogs fed a high saturated fat diet for 12.7 +/- 1.8 wk. Obese dogs exhibited elevated body weight (59%), blood pressure (14%), and heart rate (25%). Differences in resting heart rate (control, 58 +/- 5 beats/min; obese, 83 +/- 7 beats/min) were abolished after hexamethonium, indicating an autonomic mechanism. Hexamethonium also reduced blood pressure in obese (20 +/- 4 mmHg) but not control (9 +/- 6 mmHg) animals. Propranolol did not affect heart rate in either group, excluding a beta-adrenergic mechanism. Subsequent administration of atropine increased heart rate more in control than in obese dogs (110 +/- 9 vs. 57 +/- 11 beats/min). The sensitivity of the cardiac limb of the baroreflex (Oxford method) was reduced by 46% in the obese group, confirming impairment of the parasympathetic control of heart rate. The standard deviation of blood pressure measurements was normal when expressed as a percentage of the mean arterial blood pressure (control, 11.2 +/- 0.4%; obese, 11.2 +/- 0.5%). Our results indicate that the development of obesity in dogs fed a high saturated fat diet is accompanied by an attenuated resting and reflex parasympathetic control of heart rate.

摘要

我们研究了喂食高饱和脂肪饮食12.7±1.8周的犬只静息心率升高的原因。肥胖犬只体重增加(59%)、血压升高(14%)、心率升高(25%)。六甲铵给药后,静息心率差异消失(对照组,58±5次/分钟;肥胖组,83±7次/分钟),提示存在自主神经机制。六甲铵还降低了肥胖动物的血压(20±4 mmHg),但对对照动物无效(9±6 mmHg)。普萘洛尔对两组心率均无影响,排除了β-肾上腺素能机制。随后给予阿托品后,对照犬只心率升高幅度大于肥胖犬只(110±9次/分钟对57±11次/分钟)。肥胖组压力反射心脏支(牛津法)的敏感性降低了46%,证实了心率的副交感神经控制受损。以平均动脉血压的百分比表示时,血压测量的标准差正常(对照组,11.2±0.4%;肥胖组,11.2±0.5%)。我们的结果表明,喂食高饱和脂肪饮食的犬只肥胖的发展伴随着静息和反射性副交感神经对心率控制的减弱。

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