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神经通路对手术创伤发热反应的影响。

Influence of neural pathways on the pyrexial response to surgical trauma.

作者信息

Kirkeby O J, Risöe C

出版信息

Acta Chir Scand. 1985;151(1):7-9.

PMID:3872548
Abstract

Epidural analgesia inhibits several metabolic effects of trauma. Some of these effects are generated by the endogenous fever mediator interleukin-1. Postoperative fever was therefore studied in 52 patients, 25 of whom had had epidural analgesia and 27 general anaesthesia. Transvesical prostatectomy was used as standard surgical trauma. Most of the patients had postoperative temperature rise exceeding 0.5 degree C, but the rise was not influenced by epidural analgesia. These data suggest that the release of endogenous fever mediator is not under control of afferent pathways from the region of trauma. The findings are also consistent with regulation of interleukin-1 release which is independent of adrenal stimulation, cyclic AMP or beta-endorphin, as epidural analgesia prevents postoperative increase of these hormones.

摘要

硬膜外镇痛可抑制创伤的多种代谢效应。其中一些效应是由内源性发热介质白细胞介素-1产生的。因此,对52例患者进行了术后发热研究,其中25例接受硬膜外镇痛,27例接受全身麻醉。经膀胱前列腺切除术被用作标准的手术创伤。大多数患者术后体温升高超过0.5摄氏度,但这种升高不受硬膜外镇痛的影响。这些数据表明,内源性发热介质的释放不受创伤部位传入通路的控制。这些发现也与白细胞介素-1释放的调节一致,该调节独立于肾上腺刺激、环磷酸腺苷或β-内啡肽,因为硬膜外镇痛可防止这些激素在术后增加。

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