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Impaired thermoregulation in spontaneously hypertensive rats during physical exercise is related to reduced hypothalamic neuronal activation
Pflügers Archiv - European Journal of Physiology ( IF 4.5 ) Pub Date : 2020-10-10 , DOI: 10.1007/s00424-020-02474-2
Lucas Rios Drummond 1 , Helton Oliveira Campos 1 , Paulo Marcelo de Andrade Lima 1 , Cletiana Gonçalves da Fonseca 2 , Ana Cançado Kunstetter 2 , Quezia Teixeira Rodrigues 1 , Raphael Escorsim Szawka 1 , Antônio José Natali 3 , Thales Nicolau Prímola-Gomes 3 , Samuel Penna Wanner 2 , Cândido Celso Coimbra 1
Affiliation  

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 (Tcore) and tail-skin (Tskin) 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 Tcore 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.



中文翻译:

自发性高血压大鼠在体育锻炼期间体温调节受损与下丘脑神经元激活减少有关

本研究旨在评估体育锻炼诱导的脑核神经元激活,控制高血压和正常血压大鼠的体温调节反应。16 周大的雄性血压正常 Wistar 大鼠 (NWRs) 和自发性高血压大鼠 (SHRs) 被植入腹部温度传感器。恢复后,动物在 25°C 下进行恒速跑步机跑步(以最大有氧速度的 60%)30 分钟。核心(T)和尾皮(T皮)) 运动期间每分钟测量一次体温。运动后 90 分钟,对大鼠进行安乐死,并收集它们的大脑以确定以下调节体温调节反应区域的 c-Fos 蛋白表达:内侧视前区 (mPOA)、室旁下丘脑核 (PVN) 和视上核(儿子)。在跑步机跑步过程中,SHR组表现出更大的T增加和相对于 NWR 组的皮肤热损失增加的阈值。此外,SHR 在 mPOA (< 49.7%) 和 PVN (< 44.2%) 中显示出神经元激活减少,但在 SON 中没有。高血压大鼠 mPOA 和 PVN 中较低的运动诱导激活与皮肤热量损失的延迟发生密切相关。我们得出结论,高血压大鼠运动诱发的体温过高可以部分解释为延迟的皮肤散热,这反过来又与调节体温调节反应的大脑区域的激活减少有关。

更新日期:2020-10-11
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