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谷氨酸钠诱导的肥胖大鼠的压力反射和自主神经调节改变。

Altered baroreflex and autonomic modulation in monosodium glutamate-induced hyperadipose rats.

机构信息

Department of Physiological Sciences, State University of Londrina, Londrina, PR, Brazil.

出版信息

Metabolism. 2012 Oct;61(10):1435-42. doi: 10.1016/j.metabol.2012.03.005. Epub 2012 May 1.

DOI:10.1016/j.metabol.2012.03.005
PMID:22554831
Abstract

We aimed to examine the cardiovascular function by tonic and baroreflex alterations in obese rats induced by monosodium glutamate (MSG). Neonatal male Wistar rats were injected with MSG (4 mg/g body weight) or equimolar saline (control, C). At 90 days, all rats were anesthetized for catheterization of the femoral artery for mean arterial pressure (MAP) and heart rate (HR) recordings in the conscious state. After baseline, we performed IV treatment with hexamethonium (25 mg/kg), or atropine (1 mg/kg) or propranolol (3 mg/kg). We also performed the spectral analysis of heart rate variability (HRV) and baroreflex sensitivity. Baseline comparison showed that obese rats are hypertensive compared with control (C=110±2 mmHg; MSG=: 123±3 mmHg, P<0.05). After ganglionic blockade with hexamethonium the differences in MAP between control and obese rats disappeared. Beta adrenergic blockade with propranolol induced a greater decrease in heart rate compared with control. The analysis of HRV showed that obese rats have increased modulation by both components of the autonomic nervous system compared with control rats. The baroreflex gain showed increased sensitivity for the parasympathetic component in the obese rats (C=-2.41±0.25; MSG=-3.34±0.23 bpm/mmHg) compared with control. Our data suggest that both components of autonomic cardiac tonus and the parasympathetic component of the baroreflex sensitivity are increased in the MSG obese rat. It is possible that the parasympathetic alterations observed in these MSG obese rats may have originated from central areas of cardiovascular control.

摘要

我们旨在通过谷氨酸单钠(MSG)诱导的肥胖大鼠的紧张和压力反射改变来检查心血管功能。新生雄性 Wistar 大鼠注射 MSG(4mg/g 体重)或等摩尔盐水(对照,C)。90 天后,所有大鼠在麻醉状态下进行股动脉导管插入术,以记录清醒状态下的平均动脉压(MAP)和心率(HR)。在基线后,我们进行了 IV 治疗,用六烃季铵(25mg/kg)、阿托品(1mg/kg)或普萘洛尔(3mg/kg)。我们还进行了心率变异性(HRV)和压力反射敏感性的频谱分析。基线比较表明,肥胖大鼠的血压高于对照组(C=110±2mmHg;MSG=:123±3mmHg,P<0.05)。用六烃季铵阻断神经节后,对照组和肥胖大鼠之间的 MAP 差异消失。用普萘洛尔阻断β肾上腺素能可使心率比对照组下降更大。HRV 分析表明,与对照组大鼠相比,肥胖大鼠的自主神经系统两个组成部分的调制都增加了。肥胖大鼠的压力反射增益显示出对副交感成分的敏感性增加(C=-2.41±0.25;MSG=-3.34±0.23bpm/mmHg),与对照组相比。我们的数据表明,MSG 肥胖大鼠的自主心脏紧张的两个组成部分和压力反射敏感性的副交感成分都增加了。在这些 MSG 肥胖大鼠中观察到的副交感改变可能起源于心血管控制的中枢区域。

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