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血管加压素介导了妊娠晚期大鼠对前列腺素E1给药的发热反应减弱。

AVP mediates the attenuated febrile response to administration of PGE1 in rats near term of pregnancy.

作者信息

Eliason H L, Fewell J E

机构信息

Department of Physiology and Biophysics, The University of Calgary Health Sciences Centre, Calgary, Alberta, Canada T2N 4N1.

出版信息

Am J Physiol. 1998 Sep;275(3):R691-6. doi: 10.1152/ajpregu.1998.275.3.R691.

DOI:10.1152/ajpregu.1998.275.3.R691
PMID:9728064
Abstract

Rats have an attenuated febrile response to intracerebroventricular injection of PGE1 near the term of pregnancy, the mechanism of which is unknown. The present experiments were carried out to test the hypothesis that arginine vasopressin (AVP), functioning as an endogenous antipyretic substance in the central nervous system, mediates this attenuated febrile response. The febrile response to intracerebroventricular injection of 0.2 microg PGE1 was determined in pregnant and nonpregnant rats after an intracerebroventricular injection of either vehicle or a vasopressin V1-receptor antagonist. After intracerebroventricular administration of vehicle, intracerebroventricular administration of 0.2 microg PGE1 produced significant increases in core temperature in both nonpregnant and pregnant animals. The increase in core temperature, however, was attenuated both in magnitude and duration in pregnant compared with nonpregnant animals. After intracerebroventricular administration of a vasopressin V1-receptor antagonist, intracerebroventricular administration of 0.2 microg PGE1 produced significant increases in core temperature that were similar in nonpregnant and pregnant animals. Our data support the hypothesis that a pregnancy-related activation of AVP as an endogenous antipyretic substance in the central nervous system attenuates the febrile response to intracerebroventricular administration of PGE1 near term of pregnancy in rats.

摘要

在妊娠晚期,大鼠对脑室内注射前列腺素E1(PGE1)的发热反应减弱,其机制尚不清楚。本实验旨在验证以下假说:精氨酸加压素(AVP)作为中枢神经系统中的内源性解热物质,介导了这种减弱的发热反应。在脑室内注射赋形剂或血管加压素V1受体拮抗剂后,测定妊娠和未妊娠大鼠对脑室内注射0.2微克PGE1的发热反应。在脑室内给予赋形剂后,脑室内注射0.2微克PGE1可使未妊娠和妊娠动物的核心体温显著升高。然而,与未妊娠动物相比,妊娠动物的核心体温升高幅度和持续时间均减弱。在脑室内给予血管加压素V1受体拮抗剂后,脑室内注射0.2微克PGE1可使未妊娠和妊娠动物的核心体温显著升高,且二者相似。我们的数据支持以下假说:在大鼠妊娠晚期,作为中枢神经系统内源性解热物质的AVP的与妊娠相关的激活减弱了对脑室内注射PGE1的发热反应。

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