Hypothermia induced by inhibition of fatty acid metabolism in anesthetized rats: contributions of the forebrain and vagal afferents.
Hypothermia induced by inhibition of fatty acid metabolism in anesthetized rats: contributions of the forebrain and vagal afferents.
复制标题
麻醉大鼠脂肪酸代谢抑制引起的体温过低：前脑和迷走神经传入的贡献。
DOI：
10.1139/cjpp-2016-0195
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Osaka T
中科院分区：
文献类型：
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作者：
Kubota T;Furuta M;Fukushima A;Kakehashi C;Funabashi T. Akema T.;高瀬堅吉・柳井修一・山口哲生監訳;Osaka T
2-巯基乙酸酯(MA)是一种抑制脂肪酸作为能源利用的抗代谢药物。静脉注射MA(1.2mmol.kgNaCl1)可引起乌拉坦-氯醛糖麻醉、神经肌肉阻滞、人工呼吸的大鼠尾部皮肤温度升高和体温下降，而同等剂量的−不能引起尾部皮肤温度升高和体心温度下降。MA给药后呼吸交换率明显高于生理盐水处理后。另一方面，无论是MA还是氯化钠的注射都增加了产热，这表明了溶液的高渗透压所引起的非特异性效应。这些结果表明，MA引起的体温降低是由热损失增加引起的，而不是由产热量减少引起的。隔夜禁食的大鼠对MA的热损失反应的幅度明显小于进食的大鼠，提示禁食状态下抑制热损失的机制之一。迷走神经切断、辣椒素诱导的感觉神经纤维脱敏或去大脑预处理的大鼠没有表现出MA诱导的低温反应。MA引起的热损失和体温降低可能是由迷走神经传入介导的，需要前脑才能充分表达这种反应。
2-Mercaptoacetate (MA) is an antimetabolic drug that inhibits the utilization of fatty acids as an energy source. The intravenous injection of MA (1.2 mmol·kg−1) elicited an increase in tail skin temperature and a decrease in body core temperature in urethane–chloralose-anesthetized, neuromuscularly blocked, artificially ventilated rats, although administration of the same amount of NaCl did not. The respiratory exchange ratio was significantly higher after administration of MA than that after the saline treatment. On the other hand, heat production was increased by either the MA- or NaCl-injection, suggesting a nonspecific effect caused by the hyperosmolality of the solutions. These results indicate that the MA-induced hypothermia was caused by an increase in heat loss but not by a decrease in heat production. The amplitudes of heat loss responses to MA in rats fasted overnight were significantly smaller than those in fed ones, suggesting a mechanism for suppression of heat loss in the fasted state. Rats pretreated with vagotomy, capsaicin-induced desensitization of sensory nerve fibers or decerebration did not exhibit the MA-induced hypothermic responses. It is possible that the MA-induced heat loss and hypothermia were mediated by the vagal afferents and required the forebrain for the full expression of the responses.