Osaka Toshimasa, Kobayashi Akiko, Inoue Shuji
National Institute of Health and Nutrition, Shinjuku 162-8636, Japan.
J Physiol. 2002 Apr 15;540(Pt 2):665-71. doi: 10.1113/jphysiol.2001.013475.
Duodenal infusion of hypertonic solutions elicits osmolality-dependent thermogenesis in urethane-anaesthetized rats. Here we investigated the involvement of the autonomic nervous system, adrenal medulla and brain in the mechanism of this thermogenesis. Bilateral subdiaphragmatic vagotomy greatly attenuated the first hour, but not the later phase, of the thermogenesis induced by 3.6 % NaCl (10 ml kg(-1)). Neither atropine pretreatment (10 mg kg(-1), I.P.) nor capsaicin desensitization had any effect on the osmotically induced thermogenesis, suggesting the involvement of non-nociceptive vagal afferents. Bilateral splanchnic denervation caudal to the suprarenal ganglia also had no effect, suggesting a lack of involvement of spinal afferents and sympathetic efferents to the major upper abdominal organs. Adrenal demedullation greatly attenuated the initial phase, but not the later phase, of thermogenesis. Pretreatment with the beta-blocker propranolol (20 mg kg(-1), I.P.) attenuated the thermogenesis throughout the 3 h observation period. The plasma adrenaline concentration increased significantly 20 min after osmotic stimulation but returned to the basal level after 60 min. The plasma noradrenaline concentration increased 20 min after osmotic stimulation and remained significantly elevated for 120 min. Therefore, adrenaline largely mediated the initial phase of thermogenesis, and noradrenaline was involved in the entire thermogenic response. Moreover, neither decerebration nor pretreatment with the antipyretic indomethacin (10 mg kg(-1), S.C.) had any effect. Accordingly, this thermogenesis did not require the forebrain and was different from that associated with fever. These results show the critical involvement of the vagal afferents, hindbrain and sympathoadrenal system in the thermogenesis induced by osmotic stimulation of the intestines.
向十二指肠灌注高渗溶液会在氨基甲酸乙酯麻醉的大鼠中引发渗透压依赖性产热。在此，我们研究了自主神经系统、肾上腺髓质和大脑在这种产热机制中的作用。双侧膈下迷走神经切断术极大地减弱了由3.6%氯化钠（10 ml kg⁻¹）诱导的产热的第一个小时，但对后期阶段没有影响。阿托品预处理（10 mg kg⁻¹，腹腔注射）和辣椒素脱敏对渗透压诱导的产热均无任何影响，这表明非伤害性迷走神经传入纤维参与其中。双侧肾上腺神经节尾侧的内脏神经去支配也没有效果，这表明脊髓传入纤维和支配主要上腹部器官的交感传出纤维未参与其中。肾上腺髓质摘除术极大地减弱了产热的初始阶段，但对后期阶段没有影响。β受体阻滞剂普萘洛尔（20 mg kg⁻¹，腹腔注射）预处理在整个3小时观察期内减弱了产热。渗透压刺激后20分钟，血浆肾上腺素浓度显著升高，但60分钟后恢复到基础水平。渗透压刺激后20分钟，血浆去甲肾上腺素浓度升高，并在120分钟内保持显著升高。因此，肾上腺素在很大程度上介导了产热的初始阶段，而去甲肾上腺素参与了整个产热反应。此外，大脑切除和退热药吲哚美辛（10 mg kg⁻¹，皮下注射）预处理均无任何影响。因此，这种产热不需要前脑，并且与发热相关的产热不同。这些结果表明，迷走神经传入纤维、后脑和交感肾上腺系统在肠道渗透压刺激诱导的产热中起关键作用。
