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通过向视前区/下丘脑前部注射β-内啡肽降低兔子的热敏感性。

Reduced thermal sensitivity in the rabbit by beta-endorphin injection into the preoptic/anterior hypothalamus.

作者信息

Rezvani A H, Heath J E

出版信息

Brain Res. 1984 Feb 6;292(2):297-302. doi: 10.1016/0006-8993(84)90765-0.

Abstract

Male New Zealand White rabbits, Oryctolagus cuniculus, were stereotaxically implanted with a guide tube above the preoptic/anterior hypothalamus (PO/AH) for the injection of beta-endorphin (beta-E) or saline at ambient temperatures of 20 and 25 degrees C. Ear skin and PO/AH temperatures were recorded in loosely restrained control and beta-E-pretreated rabbits while radiant heat was applied to the dorsal skin. Without beta-E administration the ear skin temperature (Tear) underwent a rapid increase during back heating. Following beta-E administration there was a marked vasoconstriction along with a large reduction in responsiveness of ear skin temperature to radiant heat. The time to respond to radiant heat for beta-E-pretreated rabbits was significantly longer than that for control rabbits. In control animals, the increase in Tear in response to radiant heat exposure depended upon the initial ear temperatures. However, in beta-E-pretreated rabbits vasodilatation response to radiant heat exposure was nearly the same regardless of the initial Tear. These data suggest that there is a significant reduction in passage of temperature information from cutaneous thermal receptors to the PO/AH in beta-E-pretreated animals and that beta-E-induced reduction in sensitivity of the vasomotor system to radiant heat may account for the effectiveness of this opioid peptide to promote hyperthermia in the rabbit.

摘要

雄性新西兰白兔(穴兔属)被立体定位植入一根导管,置于视前区/下丘脑前部(PO/AH)上方,以便在20摄氏度和25摄氏度的环境温度下注射β-内啡肽(β-E)或生理盐水。在对背部皮肤施加辐射热时,对未受约束的对照兔和经β-E预处理的兔记录耳部皮肤和PO/AH温度。在未给予β-E的情况下,背部受热期间耳部皮肤温度(Tear)迅速升高。给予β-E后,出现明显的血管收缩,同时耳部皮肤温度对辐射热的反应性大幅降低。经β-E预处理的兔对辐射热作出反应的时间明显长于对照兔。在对照动物中,辐射热暴露引起的Tear升高取决于初始耳部温度。然而,在经β-E预处理的兔中,无论初始Tear如何,对辐射热暴露的血管舒张反应几乎相同。这些数据表明,在经β-E预处理的动物中,从皮肤热感受器到PO/AH的温度信息传递显著减少,并且β-E诱导的血管运动系统对辐射热敏感性降低可能解释了这种阿片肽促进兔体温过高的有效性。

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