Matsumoto I, Niijima A, Oomura Y, Sasaki K, Tsuchiya K, Aikawa T
Department of Physiology, Nagasaki University School of Medicine, Nagasaki University, Nagasaki 852, Japan.
Am J Physiol. 1998 Oct;275(4):R1003-12. doi: 10.1152/ajpregu.1998.275.4.R1003.
Effects of exogenous acidic fibroblast growth factor (aFGF), which is increased in the brain by food intake, on the plasma levels of catecholamines and on sympathetic efferent outflow were examined in anesthetized rats. A guide cannula was inserted into the cerebral third ventricle, and a vascular indwelling catheter was inserted into the right atrium from the jugular vein. Plasma epinephrine (Epi) and norepinephrine (NE) increased markedly in a dose-dependent manner for up to 120 min after intracerebroventricular or intravenous administration of aFGF (6-667 fmol/rat). Concomitant increases occurred in the efferent activity in the sympathetic nerves supplying the adrenal, spleen, and interscapular brown adipose tissue after the above administrations of aFGF. Both intravenous and intracerebroventricular administration of 10 ng basic FGF (bFGF) also increased sympathetic adrenal efferent activity and plasma Epi and NE concentrations. However, the increases induced by 10 ng bFGF were smaller than those induced by 10 ng aFGF. Bilateral splanchnicotomy completely prevented the increases in Epi induced by intracerebroventricular or intravenous aFGF but had less effect on the increases in NE. Pretreatment with an antibody against corticotropin-releasing factor (CRF), given via the intracerebroventricular route, significantly attenuated the increases in Epi and NE evoked by intracerebroventricular or intravenous administration of aFGF. Hepatic vagotomy also greatly reduced the increases in both catecholamines and the increases in sympathetic efferent firing rates evoked by intravenous administration of aFGF. These findings indicate that 1) aFGF administered intracerebroventricularly activates adrenomedullary secretion and sympathetic outflow via CRF release and 2) aFGF injected intravenously also induces sympathoadrenomedullary activation via centrally released CRF. The idea is discussed that sympathetic activation induced either by endogenous aFGF after feeding or by exogenously administered aFGF may play roles both in energy expenditure after overeating and in the modulation of immune functions.
在麻醉大鼠中，研究了因食物摄入而在脑中增加的外源性酸性成纤维细胞生长因子（aFGF）对儿茶酚胺血浆水平及交感神经传出活动的影响。将引导套管插入大脑第三脑室，并通过颈静脉将血管留置导管插入右心房。脑室内或静脉内给予aFGF（6 - 667 fmol/大鼠）后，血浆肾上腺素（Epi）和去甲肾上腺素（NE）在长达120分钟内呈剂量依赖性显著增加。在上述aFGF给药后，供应肾上腺、脾脏和肩胛间棕色脂肪组织的交感神经传出活动也随之增加。静脉内和脑室内给予10 ng碱性成纤维细胞生长因子（bFGF）也增加了交感肾上腺传出活动以及血浆Epi和NE浓度。然而，10 ng bFGF引起的增加小于10 ng aFGF引起的增加。双侧内脏神经切断术完全阻止了脑室内或静脉内aFGF引起的Epi增加，但对NE增加的影响较小。通过脑室内途径给予促肾上腺皮质激素释放因子（CRF）抗体进行预处理，可显著减弱脑室内或静脉内给予aFGF引起的Epi和NE增加。肝迷走神经切断术也大大降低了静脉内给予aFGF引起的儿茶酚胺增加以及交感神经传出放电率增加。这些发现表明：1）脑室内给予aFGF通过释放CRF激活肾上腺髓质分泌和交感神经传出；2）静脉内注射aFGF也通过中枢释放的CRF诱导交感肾上腺髓质激活。文中讨论了一个观点，即进食后内源性aFGF或外源性给予aFGF诱导的交感神经激活可能在暴饮暴食后的能量消耗以及免疫功能调节中均发挥作用。
