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[腹内侧下丘脑损伤的肥胖大鼠内源性高胰岛素血症的血流动力学后果]

[Hemodynamic consequences of endogenous hyperinsulinism in obese rats with lesions of the ventromedial hypothalamus].

作者信息

Doaré L, Mesangeau D, Adli H, Germack R, Perret G, Valensi P

机构信息

Centre de recherche LIPHA, Chilly-Mazarin.

出版信息

Arch Mal Coeur Vaiss. 2000 Aug;93(8):1015-8.

PMID:10989748
Abstract

The rat with ventromedian hypothalamus lesions (VMH) is characterized by massive obesity, hyperinsulinemia, increase in parasympathetic tonus and sympathetic depression. The aim of this study was to examine in this model the hemodynamic changes and the baroreflex response and to compare the data with the evaluation of beta adrenergic sensitivity. In VMH rats and Sham operated rats hemodynamic parameters were followed until 8 weeks after operation. Heart rate (HR) and blood pressure (BP) were monitored each week during 24 hours by a telemetric system, a catheter being implanted in aorta. In VMH, HR was significantly lower by the first week (p = 0.02) and until the last measurement. Systolic BP increased progressively in the two groups but was higher in VMH only at 8 weeks (p = 0.03). Compared with Sham rats, 5 days after operation, the percentage of HR acceleration in response to atropine and isoprenaline was significantly higher in VMH, whereas HR response to sodium nitroprussiate was similar in the two groups. Plasma epinephrine and norepinephrine levels were significantly higher in VMH rats. The density of cardiac beta receptors decreased from 15 days to 3 months after operation, similarly in VMH and Sham rats. The affinity of cardiac beta receptors remained stable during the same period and very similar in VMH and Sham rats. This study suggests that in VMH rats 1. bradycardia results mainly from an increase in parasympathetic tone; 2. the increase in reflex tachycardia described in normal rats after insulin infusion needs a normal activity of the sympathetic nervous system; 3. catecholamine levels may be increased despite sympathetic depression, probably as a result of an increase in adrenomedullary secretion possibly due to endogenous hyperinsulinemia; 4. the lack of hypertension in this model including a massive obesity is likely to result from the proper vasodilatory effect of insulin.

摘要

下丘脑腹内侧核损伤(VMH)的大鼠表现为重度肥胖、高胰岛素血症、副交感神经张力增加和交感神经抑制。本研究的目的是在该模型中研究血流动力学变化和压力反射反应,并将数据与β肾上腺素能敏感性评估进行比较。在VMH大鼠和假手术大鼠中,术后8周内监测血流动力学参数。通过遥测系统每周在24小时内监测心率(HR)和血压(BP),将导管植入主动脉。在VMH大鼠中,第一周时HR显著降低(p = 0.02),直至最后一次测量。两组的收缩压均逐渐升高,但仅在8周时VMH组更高(p = 0.03)。与假手术大鼠相比,术后5天,VMH大鼠对阿托品和异丙肾上腺素的HR加速百分比显著更高,而两组对硝普钠的HR反应相似。VMH大鼠的血浆肾上腺素和去甲肾上腺素水平显著更高。术后15天至3个月,VMH大鼠和假手术大鼠心脏β受体密度均降低。在此期间,心脏β受体的亲和力保持稳定,VMH大鼠和假手术大鼠非常相似。本研究表明,在VMH大鼠中:1. 心动过缓主要源于副交感神经张力增加;2. 正常大鼠胰岛素输注后描述的反射性心动过速增加需要交感神经系统的正常活动;3. 尽管交感神经抑制,儿茶酚胺水平可能升高,可能是由于内源性高胰岛素血症导致肾上腺髓质分泌增加;4. 该模型中包括重度肥胖在内的高血压缺乏可能是由于胰岛素适当的血管舒张作用。

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[Hemodynamic consequences of endogenous hyperinsulinism in obese rats with lesions of the ventromedial hypothalamus].[腹内侧下丘脑损伤的肥胖大鼠内源性高胰岛素血症的血流动力学后果]
Arch Mal Coeur Vaiss. 2000 Aug;93(8):1015-8.
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Cardiovascular vagosympathetic activity in rats with ventromedial hypothalamic obesity.腹内侧下丘脑性肥胖大鼠的心血管迷走交感神经活动
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