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在清醒大鼠中,经脑室内注射促肾上腺皮质激素(ACTH)和促肾上腺皮质激素释放因子(CRF)后出现的升压、心动过速及行为兴奋反应,可被纳洛酮预处理所阻断。

Pressor, tachycardic and behavioral excitatory responses in conscious rats following ICV administration of ACTH and CRF are blocked by naloxone pretreatment.

作者信息

Saunders W S, Thornhill J A

出版信息

Peptides. 1986 Jul-Aug;7(4):597-601. doi: 10.1016/0196-9781(86)90033-1.

Abstract

Experiments were conducted to compare the blood pressure and heart rate responses of conscious rats given intracerebroventricular (ICV) injections of adrenocorticotropin (ACTH 1-24) and corticotropin releasing factor (CRF). Under sodium pentobarbital anaesthesia, rats were implanted with a stainless-steel cannula into the lateral cerebral ventricle and had their right femoral artery and vein cannulated. Upon recovery (24-48 hr later) conscious, unrestrained rats were given ICV injections (total volume 5 microliter by gravity flow) of sterile saline, ACTH (1-24) (0.85 and 1.7 nmoles) or CRF (0.55 and 1.1 nmoles) and blood pressure and heart rate were monitored over the next 2 hr (from the abdominal aorta via the femoral arterial catheter). Both ACTH and CRF caused mean arterial pressure (MAP) to increase, which was paralleled with increases in mean heart rate (MHR). Moreover, these elevations in MAP and MHR were temporally associated with excessive grooming (for ACTH) and locomotor activity (for CRF), which occurred before and lasted as long as MAP and MHR were enhanced. Intravenous (IV) pretreatment whereby naloxone was given 10 min before ICV administration of ACTH (1.7 nmoles) or CRF (1.1 nmoles), showed that naloxone blocked the behavioral, pressor and tachycardic effects of both ACTH and CRF. The results demonstrate that the pressor, tachycardic and locomotor effects evoked in conscious rats by ICV administration of ACTH or CRF are antagonized by naloxone and that their hemodynamic changes may, in part, be mediated by prior behavioral activation.

摘要

进行实验以比较经脑室内(ICV)注射促肾上腺皮质激素(ACTH 1-24)和促肾上腺皮质激素释放因子(CRF)的清醒大鼠的血压和心率反应。在戊巴比妥钠麻醉下,将大鼠植入一根不锈钢套管至侧脑室,并将其右股动脉和静脉插管。恢复(24-48小时后)清醒后,对无拘束的大鼠经脑室内注射(通过重力引流总体积5微升)无菌生理盐水、ACTH(1-24)(0.85和1.7纳摩尔)或CRF(0.55和1.1纳摩尔),并在接下来的2小时内(通过股动脉导管从腹主动脉)监测血压和心率。ACTH和CRF均导致平均动脉压(MAP)升高,同时平均心率(MHR)也升高。此外,MAP和MHR的这些升高在时间上与过度梳理行为(对于ACTH)和运动活动(对于CRF)相关,这些行为在MAP和MHR升高之前出现并持续至其升高结束。静脉内(IV)预处理是在经脑室内给予ACTH(1.7纳摩尔)或CRF(1.1纳摩尔)前10分钟给予纳洛酮,结果显示纳洛酮可阻断ACTH和CRF的行为、升压和心动过速作用。结果表明,经脑室内给予ACTH或CRF在清醒大鼠中诱发的升压、心动过速和运动作用可被纳洛酮拮抗,并且它们的血流动力学变化可能部分由先前的行为激活介导。

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