Kenney Michael J, Fels Richard J
Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas 66506, USA.
J Appl Physiol (1985). 2003 Nov;95(5):1986-93. doi: 10.1152/japplphysiol.00438.2003. Epub 2003 Jul 25.
Acute heating in young rats increases visceral sympathetic nerve discharge (SND); however, renal and splanchnic SND responses to hyperthermia are attenuated in senescent compared with young Fischer 344 (F344) rats (Kenney MJ and Fels RJ. Am J Physiol Regul Integr Comp Physiol 283: R513-R520, 2002). Central mechanisms by which aging alters visceral SND responses to heating are unknown. We tested the hypothesis that forebrain neural circuits are involved in suppressing sympathoexcitatory responses to heating in chloralose-anesthetized, senescent F344 rats. Renal and splanchnic SND responses to increased (38 degrees C-41 degrees C) internal temperature were determined in midbrain-transected (MT) and sham-MT young (3-mo-old), mature (12-mo-old), and senescent (24-mo-old) F344 rats and in cervical-transected (CT) and sham-CT senescent rats. Renal SND remained unchanged during heating in MT and sham-MT senescent rats but was increased in CT senescent rats. Splanchnic SND responses to heating were higher in MT vs. sham-MT senescent rats and in CT vs. MT senescent rats. SND responses to heating were similar in MT and sham-MT young and mature rats. Mean arterial pressure (MAP) was increased during heating in MT but not in sham-MT senescent rats, whereas heating-induced increases in MAP were higher in sham-MT vs. MT young rats. These data suggest that in senescent rats suppression of splanchnic SND to heating involves forebrain and brain stem neural circuits, whereas renal suppression is mediated solely by brain stem neural circuits. These results support the concept that aging alters the functional organization of pathways regulating SND and arterial blood pressure responses to acute heating.
对幼年大鼠进行急性加热会增加内脏交感神经放电(SND);然而,与幼年费希尔344(F344)大鼠相比,衰老的大鼠对热疗的肾和内脏SND反应减弱(肯尼·MJ和费尔斯·RJ。《美国生理学杂志:调节、整合与比较生理学》283:R513 - R520,2002)。衰老改变内脏SND对加热反应的中枢机制尚不清楚。我们检验了这样一个假设,即在前脑神经网络参与抑制水合氯醛麻醉的衰老F344大鼠对加热的交感兴奋反应。在中脑横断(MT)和假MT的幼年(3月龄)、成年(12月龄)和衰老(24月龄)F344大鼠以及颈横断(CT)和假CT的衰老大鼠中,测定肾和内脏SND对内部温度升高(38摄氏度至41摄氏度)的反应。在MT和假MT衰老大鼠加热过程中,肾SND保持不变,但在CT衰老大鼠中升高。MT衰老大鼠与假MT衰老大鼠相比,以及CT衰老大鼠与MT衰老大鼠相比,内脏SND对加热的反应更高。MT和假MT的幼年和成年大鼠对加热的SND反应相似。MT衰老大鼠加热过程中平均动脉压(MAP)升高,而假MT衰老大鼠则不然,而加热引起的MAP升高在假MT幼年大鼠中比MT幼年大鼠更高。这些数据表明,在衰老大鼠中,抑制内脏SND对加热的反应涉及前脑和脑干神经网络,而肾抑制仅由脑干神经网络介导。这些结果支持了衰老改变调节SND和动脉血压对急性加热反应的通路功能组织这一概念。