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下丘脑室旁核对于体温升高引起的肾血管收缩至关重要。

Hypothalamic paraventricular nucleus is critical for renal vasoconstriction elicited by elevations in body temperature.

作者信息

Cham Joo Lee, Badoer Emilio

机构信息

School of Medical Sciences, Royal Melbourne Institute of Technology University, Melbourne, Victoria, Australia.

出版信息

Am J Physiol Renal Physiol. 2008 Feb;294(2):F309-15. doi: 10.1152/ajprenal.00488.2007. Epub 2007 Dec 12.

Abstract

Redistribution of blood from the viscera to the peripheral vasculature is the major cardiovascular response designed to restore thermoregulatory homeostasis after an elevation in body core temperature. In this study, we investigated the role of the hypothalamic paraventricular nucleus (PVN) in the reflex decrease in renal blood flow that is induced by hyperthermia, as this brain region is known to play a key role in renal function and may contribute to the central pathways underlying thermoregulatory responses. In anesthetized rats, blood pressure, heart rate, renal blood flow, and tail skin temperature were recorded in response to elevating body core temperature. In the control group, saline was microinjected bilaterally into the PVN; in the second group, muscimol (1 nmol in 100 nl per side) was microinjected to inhibit neuronal activity in the PVN; and in a third group, muscimol was microinjected outside the PVN. Compared with control, microinjection of muscimol into the PVN did not significantly affect the blood pressure or heart rate responses. However, the normal reflex reduction in renal blood flow observed in response to hyperthermia in the control group ( approximately 70% from a resting level of 11.5 ml/min) was abolished by the microinjection of muscimol into the PVN (maximum reduction of 8% from a resting of 9.1 ml/min). This effect was specific to the PVN since microinjection of muscimol outside the PVN did not prevent the normal renal blood flow response. The data suggest that the PVN plays an essential role in the reflex decrease in renal blood flow elicited by hyperthermia.

摘要

血液从内脏重新分配至外周血管系统是在体核温度升高后旨在恢复体温调节稳态的主要心血管反应。在本研究中,我们探究了下丘脑室旁核(PVN)在热应激诱导的肾血流量反射性减少中的作用,因为已知该脑区在肾功能中起关键作用,且可能参与体温调节反应的中枢通路。在麻醉大鼠中,记录了随着体核温度升高时的血压、心率、肾血流量和尾皮肤温度。对照组双侧向PVN微量注射生理盐水;第二组,微量注射蝇蕈醇(每侧100 nl中含1 nmol)以抑制PVN中的神经元活动;第三组,在PVN外微量注射蝇蕈醇。与对照组相比,向PVN微量注射蝇蕈醇对血压或心率反应无显著影响。然而,对照组中热应激时观察到的肾血流量正常反射性减少(从静息水平11.5 ml/min减少约70%),在向PVN微量注射蝇蕈醇后被消除(从静息水平9.1 ml/min最大减少8%)。由于在PVN外微量注射蝇蕈醇并不阻止正常的肾血流量反应,所以该效应是PVN特有的。这些数据表明,PVN在热应激引起的肾血流量反射性减少中起重要作用。

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