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中枢给予蛙皮素、缓激肽和甲硫氨酸脑啡肽的体温调节作用。

Thermoregulatory effects of centrally administered bombesin, bradykinin, and methionine-enkephalin.

作者信息

Francesconi R, Mager M

出版信息

Brain Res Bull. 1981 Jul;7(1):63-8. doi: 10.1016/0361-9230(81)90099-x.

Abstract

Bombesin (BO, 100 ng), bradykinin (BR, 10 microgram), or methionine-enkephalin (EN, 10 microgram) was administered intracerebroventricularly to adult male rats at an environmental temperature of 4 degrees C, 22 degrees C, or 35 degrees C, and rectal (Tre) and tail-skin (Tsk) temperatures were monitored for 5 hours. At 4 degrees C and 22 degrees C BO-treated animals developed acute hypothermia (max delta Tre=-3.25 degrees C and -2.71 degrees C, respectively) which persisted for 2 hours (p less than 0.05). At 22 degrees C and at 300 min post-injection, BO-treated animals became significantly (p less than 0.05) hyperthermic (deltaTre = +1.28 degrees C) when compared to controls. While BR had no effects at 22 degrees C, en-injected rats demonstrated significant (p less than 0.05) hyperthermia from 180 min through 300 min (delta Tre=+1.40 degrees C). At 22 degrees C both BO and, surprisingly, EN increased Tsk (e.g. delta Tsk =+ 3.49 degrees C and + 2.01 degrees C at 60 min). At 35 degrees C EN elicited hyperthermia which was significantly (p less than 0.05) increased from time 0 at all sampling time (mean delta Tre =+ 1.85 degrees C) and from control levels at 300 min (delta Tre =+1.07 degrees C, p less than 0.05). BO again caused a significant (p less than 0.05, BO vs control, 30 min) decrement (delta Tre =-1.22 degrees C) followed by increments (p less than 0.05) from 12-0-300 min. We conclude that the hypothermic effect of BO is dependent upon environmental temperature, partially caused by vasodilation, and possible biphasic in nature; EN treatment generally elicits hyperthermia under these conditions while BR produced no effects on thermoregulation.

摘要

在环境温度为4℃、22℃或35℃的条件下,向成年雄性大鼠脑室内注射蛙皮素(BO,100纳克)、缓激肽(BR,10微克)或甲硫氨酸脑啡肽(EN,10微克),并监测直肠温度(Tre)和尾皮温度(Tsk)5小时。在4℃和22℃时,接受BO治疗的动物出现急性体温过低(最大体温变化量ΔTre分别为-3.25℃和-2.71℃),持续2小时(p<0.05)。在22℃且注射后300分钟时,与对照组相比,接受BO治疗的动物体温显著升高(p<0.05)(ΔTre = +1.28℃)。虽然BR在22℃时无作用,但注射EN的大鼠在180分钟至300分钟期间体温显著升高(p<0.05)(ΔTre = +1.40℃)。在22℃时,BO和令人惊讶的是EN均使Tsk升高(例如在60分钟时,ΔTsk分别为+3.49℃和+2.01℃)。在35℃时,EN引起体温升高,在所有采样时间点体温均显著高于0时刻(平均ΔTre = +1.85℃),且在300分钟时高于对照组水平(ΔTre = +1.07℃,p<0.05)。BO再次导致显著的体温下降(p<0.05,BO与对照组相比,30分钟时,ΔTre = -1.22℃),随后在12 - 300分钟期间体温升高(p<0.05)。我们得出结论,BO的体温过低效应取决于环境温度,部分由血管舒张引起,且可能具有双相性;在这些条件下,EN治疗通常会引起体温升高,而BR对体温调节无影响。

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