Heat stroke: opioid-mediated mechanisms.
Heat stroke: opioid-mediated mechanisms.
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热射病：阿片类药物介导的机制。
DOI：
10.1152/jappl.1996.81.6.2565
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Blatteis,CM
中科院分区：
文献类型：
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作者：
Romanovsky,AA;Blatteis,CM
Romanovsky、Andrej A. 和 Clark M. Blatteis。热射病：阿片类药物介导的机制。应用。 Physiol.81(6): 2565–2570, 1996.—在我们之前对豚鼠的研究中，强烈和长时间的腹腔内加热 (IPH) 会导致中暑，其特点是高死亡率，并伴有两种矛盾的现象：高体温 (Tb) 下的耳部皮肤血管收缩（高热引起的血管收缩）和 IPH 后在环境温度下的 Tbfall (Ta) 低于热中性（高热引起的低体温）。在这项研究中，我们测试了以下假设：这两种现象的机制涉及内源性阿片类激动剂。实验在 24 只未麻醉、轻度约束的豚鼠中进行，每只豚鼠均长期植入腹膜内热电极和下丘脑内热电偶。研究了广谱阿片受体拮抗剂纳曲酮（NTX；50 或 0 μmol/kg sc）对 IPH 诱导的热射病和正常条件下的体温调节作用。通过热电极灌注（50 毫升/分钟；80 分钟）水（45°C）来完成 IPH。 Tawas 保持在~24°C。 IPH 发作时皮肤血管舒张，但随后变为血管收缩，尽管高 Tband 持续 IPH。 IPH 引起的体温过高 (1.8 ± 0.1°C) 之后是 IPH 后 Tbfall (-5.1 ± 0.7°C；仅针对幸存者计算)。 48小时死亡率为50%。 NTX 可防止高热引起的血管收缩，并减弱高热引起的体温过低 (-1.8 ± 0.4°C)。接受 NTX 治疗的动物均未死亡。正常情况下，NTX 对 Tb 调节的影响很小。这些结果表明，高热引起的血管收缩和高热引起的体温过低的现象都是阿片类药物依赖性的。据推测，后者反映了阿片类药物介导的代谢抑制；前者被认为是由阿片类药物引起的血流动力学改变引起的。因为这两种现象在 NTX 治疗的幸存者中都没有发生，所以高 Tb 时的皮肤血管收缩可以被视为热射病严重程度的标志。这表明阿片类拮抗剂可能对热引起的疾病具有治疗潜力。
Romanovsky, Andrej A., and Clark M. Blatteis.Heat stroke: opioid-mediated mechanisms.J. Appl. Physiol.81(6): 2565–2570, 1996.—In our previous study in guinea pigs, intensive and prolonged intraperitoneal heating (IPH) caused heat stroke characterized by high mortality and accompanied by two paradoxical phenomena: ear skin vasoconstriction at a high body temperature (Tb) (hyperthermia-induced vasoconstriction) and a post-IPH Tbfall at an ambient temperature (Ta) below thermoneutrality (hyperthermia-induced hypothermia). In this study, we tested the hypothesis that the mechanisms of the two phenomena involve endogenous opioid agonists. Experiments were conducted in 24 unanesthetized, lightly restrained guinea pigs, each chronically implanted with an intraperitoneal thermode and intrahypothalamic thermocouple. The thermoregulatory effects of a wide-spectrum opioid-receptor antagonist, naltrexone (NTX; 50 or 0 μmol/kg sc), were studied in IPH-induced heat stroke and under normal conditions. IPH was accomplished by perfusing (50 ml/min; 80 min) water (45°C) through the thermode. Tawas maintained at ∼24°C. Skin vasodilation occurred at the onset of IPH but later changed to vasoconstriction despite high Tband continuing IPH. IPH-induced hyperthermia (1.8 ± 0.1°C) was followed by a post-IPH Tbfall (−5.1 ± 0.7°C; calculated for the survivors only). The 48-h mortality rate was 50%. NTX prevented the hyperthermia-induced vasoconstriction and attenuated the hyperthermia-induced hypothermia (−1.8 ± 0.4°C). None of the NTX-treated animals died. The effects of NTX on Tbregulation under normal conditions were minor. These results indicate that the phenomena of both hyperthermia-induced vasoconstriction and hyperthermia-induced hypothermia are opioid dependent. The latter is speculated to reflect opioid-mediated inhibition of metabolism; the former is thought to result from opioid-induced hemodynamic alterations. Because both phenomena did not occur in the NTX-treated survivors, the skin vasoconstriction at high Tband the posthyperthermia Tbfall may be viewed as markers of the severity of heat stroke. It is suggested that opioid antagonists may have therapeutic potential in heat-induced disorders.