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自发性高血压大鼠在运动期间体温调节受损与下丘脑神经元激活减少有关。

Impaired thermoregulation in spontaneously hypertensive rats during physical exercise is related to reduced hypothalamic neuronal activation.

机构信息

Laboratório de Endocrinologia e Metabolismo, Departamento de Fisiologia e Biofísica, Universidade Federal de Minas Gerais, Av. Antônio Carlos, 6627., Belo Horizonte, MG, 31270-901, Brazil.

Laboratório de Fisiologia do Exercício, Departamento de Educação Física, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.

出版信息

Pflugers Arch. 2020 Dec;472(12):1757-1768. doi: 10.1007/s00424-020-02474-2. Epub 2020 Oct 10.

Abstract

This study aimed to evaluate the physical exercise-induced neuronal activation in brain nuclei controlling thermoregulatory responses in hypertensive and normotensive rats. Sixteen-week-old male normotensive Wistar rats (NWRs) and spontaneously hypertensive rats (SHRs) were implanted with an abdominal temperature sensor. After recovery, the animals were subjected to a constant-speed treadmill running (at 60% of the maximum aerobic speed) for 30 min at 25 °C. Core (T) and tail-skin (T) temperatures were measured every minute during exercise. Ninety minutes after the exercise, the rats were euthanized, and their brains were collected to determine the c-Fos protein expression in the following areas that modulate thermoregulatory responses: medial preoptic area (mPOA), paraventricular hypothalamic nucleus (PVN), and supraoptic nucleus (SON). During treadmill running, the SHR group exhibited a greater increase in T and an augmented threshold for cutaneous heat loss relative to the NWR group. In addition, the SHRs showed reduced neuronal activation in the mPOA (< 49.7%) and PVN (< 44.2%), but not in the SON. The lower exercise-induced activation in the mPOA and PVN in hypertensive rats was strongly related to the delayed onset of cutaneous heat loss. We conclude that the enhanced exercise-induced hyperthermia in hypertensive rats can be partially explained by a delayed cutaneous heat loss, which is, in turn, associated with reduced activation of brain areas modulating thermoregulatory responses.

摘要

本研究旨在评估控制高血压和正常血压大鼠体温调节反应的脑核内的物理运动诱导的神经元激活。将 16 周龄雄性正常血压 Wistar 大鼠(NWR)和自发性高血压大鼠(SHR)植入腹部温度传感器。恢复后,动物在 25°C 下以 60%最大有氧速度进行 30 分钟的恒速跑步机跑步。在运动过程中,每分钟测量核心(T)和尾巴皮肤(T)温度。运动 90 分钟后,处死大鼠,收集其大脑,以确定调节体温反应的以下区域中的 c-Fos 蛋白表达:视前内侧核(mPOA)、室旁下丘脑核(PVN)和视上核(SON)。在跑步机跑步期间,SHR 组的 T 增加幅度更大,皮肤散热的阈值也更高。此外,与 NWR 组相比,mPOA(<49.7%)和 PVN(<44.2%)中的神经元激活减少,但 SON 中没有。高血压大鼠中 mPOA 和 PVN 中运动诱导的激活减少与皮肤热损失的延迟开始密切相关。我们得出结论,高血压大鼠运动引起的体温升高增强可以部分解释为皮肤热损失延迟,而皮肤热损失延迟与调节体温反应的脑区激活减少有关。

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