Isoflurane increases norepinephrine release in the rat preoptic area and the posterior hypothalamus in vivo and in vitro:: Relevance to thermoregulation during anesthesia
Isoflurane increases norepinephrine release in the rat preoptic area and the posterior hypothalamus in vivo and in vitro:: Relevance to thermoregulation during anesthesia
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DOI：
10.1016/j.neuroscience.2004.11.007
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发表时间：
2005-01-01
期刊：
影响因子：
3.3
通讯作者：
Matsuki, A
中科院分区：
文献类型：
--
作者：
Kushikata, T;Hirota, K;Matsuki, A
全身麻醉剂调节自主神经系统功能，包括体温调节控制，其位于下丘脑前部的视前区。然而，麻醉剂调节下丘脑功能的机制仍不清楚。我们假设异氟醚增加视前区和下丘脑后部去甲肾上腺素的释放，导致体温降低（诱导麻醉）。为了验证这一假设，我们在大鼠中进行了一系列体内和体外研究。体内研究：1）在2%异氟醚麻醉前、麻醉中（30 min）和麻醉后（50 min），通过微透析法测定视前区或下丘脑后部（各n = 9）的去甲肾上腺素释放。2)在五只大鼠中，测量血气和动脉压。3)在视前区注射哌唑嗪（0、0.05、0.5 μ g）、去甲肾上腺素（0、0.1、1.0 μ g）或0.5 μ g哌唑嗪+1.0 μ g去甲肾上腺素后，测量体温变化（各n = 6）。体外研究：从与含Ca 2+缓冲液中的0、1、2或4%异氟烷或含4%异氟烷（n = 10）的无Ca 2+缓冲液孵育的前或后下丘脑切片（各n = 10）中测量去甲肾上腺素释放。数据分析采用重复测量或析因方差分析和Student-Newman-Keuls检验。P < 0.05有显著性差异。麻醉期间，视前区的去甲肾上腺素释放增加约270%，而下丘脑后部的释放保持不变。苏醒时，下丘脑后部去甲肾上腺素释放增加约250%（P < 0.05）。直肠温度变化与视前区去甲肾上腺素释放相关。视前区的去甲肾上腺素增强异氟醚诱导的低温，而哌唑嗪逆转it. Norepinephrine释放从前下丘脑切片增加在所有异氟醚浓度，但只有在最高浓度的后下丘脑切片。在无Ca 2+条件下，4%异氟烷增加了两个区域的去甲肾上腺素。这些结果表明，增加去甲肾上腺素释放的视前区是负责全身麻醉期间体温过低。(C)2005由Elsevier Ltd代表IBRO出版。
General anesthetics modulate autonomic nervous system function including thermoregulatory control, which resides in the preoptic area of the anterior hypothalamus. However, the mechanism by which anesthetics modulate hypothalarnic function remains unknown. We hypothesized that isoflurane increases norepinephrine release in the preoptic area and in the posterior hypothalamus causing hypothermia (luring anesthesia. To test this hypothesis, we performed a series of in vivo and in vitro studies in rats. In vivo studies: 1) Norepinephrine release was measured by microdialysis in the preoptic area or the posterior hypothalamus (n = 9 each) before, during (30 min), and after (50 min) rats were anesthetized with 2% isoflurane. 2) In five rats, blood gases and arterial pressure were measured. 3) Body temperature changes (n = 6 each) were measured after prazosin (0, 0.05, 0.5 mug), norepinephrine (0, 0.1, 1.0 mug), or 0.5 mug prazosin with 1.0 mug norepinephrine injection into the preoptic area. In vitro study: Norepinephrine release was measured from anterior or posterior hypothalamic slices (n = 10 each) incubated with 0, 1, 2, or 4% isoflurane in Ca2+-containing buffer or with 4% isoflurane (n = 10) in Ca2+-free buffer. Data were analyzed with repeated measures or factorial ANOVA and Student-Newman-Keuls tests. P < 0.05 was significant. During anesthesia, norepinephrine release in the preoptic area was increased approximately 270%, whereas the release in the posterior hypothalamus remained unchanged. During emergence, posterior hypothalamic norepinephrine release increased by approximately 250% (P < 0.05). Rectal temperature changes correlated with norepinephrine release from the preoptic area. Norepinephrine in the preoptic area enhanced isoflurane-induced hypothermia, while prazosin reversed it. Norepinephrine release from anterior hypothalamic slices increased at all isoflurane concentrations, but only at the highest concentration in posterior hypothalamic slices. Under Ca2+-free conditions, 4% isoflurane increased norepinephrine from both regions. These results suggest that augmentation of norepinephrine release in the preoptic area is responsible for hypothermia during general anesthesia. (C) 2005 Published by Elsevier Ltd on behalf of IBRO.