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前列腺素E1诱导家兔发热。

Prosaglandin E1 fever induced in rabbits.

作者信息

Stitt J T

出版信息

J Physiol. 1973 Jul;232(1):163-79. doi: 10.1113/jphysiol.1973.sp010262.

Abstract
  1. Micro-injections of prostaglandin E(1) (PGE(1)) into the anterior hypothalamus of the rabbit produced fever which was nearly immediate in onset. The prostaglandin sensitive region appears to be identical to that described as being fever sensitive to leucocytic pyrogen.2. Micro-injections of PGE(1) into the posterior hypothalamus and midbrain reticular formation of the rabbit did not produce fever.3. The febrile response to PGE(1) injected into the anterior hypothalamus was dose dependent over a range of 20-1000 ng.4. Ambient temperature influenced the thermoregulatory mechanism by which PGE(1) fever evolved. In the cold, PGE(1) fever was due to increased heat production while during heat exposure both evaporative and dry heat losses were reduced without significant changes in heat production. Vasoconstriction, confined mainly to the ears, was effective in producing fever in standard room environments (24-25 degrees C) along with a small increase in heat production.5. The preoptic anterior hypothalamic area retained its thermosensitivity during PGE(1) fever; heating this area attenuated, while cooling augmented the fever.6. The results support the view that PGE(1) is a mediator of pyrogen induced fever.
摘要
  1. 向家兔下丘脑前部微量注射前列腺素E(1)(PGE(1))可引起发热,发热几乎立即出现。前列腺素敏感区域似乎与对白细胞致热原敏感的发热区域相同。

  2. 向家兔下丘脑后部和中脑网状结构微量注射PGE(1)不会引起发热。

  3. 向家兔下丘脑前部注射PGE(1)所引起的发热反应在20 - 1000纳克范围内呈剂量依赖性。

  4. 环境温度影响PGE(1)发热所涉及的体温调节机制。在寒冷环境中,PGE(1)发热是由于产热增加,而在热环境中,蒸发散热和干热散失均减少,产热无明显变化。主要局限于耳部的血管收缩在标准室温环境(24 - 25摄氏度)下可有效引起发热,同时产热略有增加。

  5. 在PGE(1)发热期间,视前区下丘脑前部区域仍保持其热敏性;加热该区域可减轻发热,而冷却则会增强发热。

  6. 这些结果支持PGE(1)是致热原诱导发热的介质这一观点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecf3/1350497/d57cbc070565/jphysiol00957-0186-a.jpg

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