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内源性腺苷活性增强导致老年大鼠耐寒性降低。

Decrease in cold tolerance of aged rats caused by the enhanced endogenous adenosine activity.

作者信息

Wang L C, Jin Z L, Lee T F

机构信息

Zoology Department, University of Alberta, Edmonton, Canada.

出版信息

Pharmacol Biochem Behav. 1992 Sep;43(1):117-23. doi: 10.1016/0091-3057(92)90647-x.

DOI:10.1016/0091-3057(92)90647-x
PMID:1409794
Abstract

During severe cold exposure, old rats (24-28 months) were less capable of maintaining their body temperature compared to young rats (3-6 months) due to lower rate of heat production. Single injection of adenosine deaminase (AD) (converts adenosine to inosine) significantly increased thermogenesis in both young and old rats. However, doubling the dose of AD was required for optimal thermogenic response in old rats. In contrast, the similar enhancements in both thermogenesis and cold tolerance were observed in both young and old rats receiving the same optimal doses of specific adenosine receptor antagonists. These results lead to the suggestion that the lower capability of aged rats to withstand cold exposure could be due to an increase in adenosine stimulation because of the decreased endogenous AD activity rather than an increase in adenosine receptor sensitivity. This notion is further supported by the finding that the AD activity in the neck muscle, a key site for shivering thermogenesis, was significantly lower in old rats as compared to their younger counterparts before and after cold exposure.

摘要

在严重寒冷暴露期间,由于产热率较低,老年大鼠(24 - 28个月)与年轻大鼠(3 - 6个月)相比,维持体温的能力较差。单次注射腺苷脱氨酶(AD)(将腺苷转化为肌苷)显著增加了年轻和老年大鼠的产热。然而,老年大鼠需要将AD剂量加倍才能获得最佳产热反应。相比之下,接受相同最佳剂量特定腺苷受体拮抗剂的年轻和老年大鼠在产热和耐寒性方面都有类似增强。这些结果表明,老年大鼠抵御寒冷暴露能力较低可能是由于内源性AD活性降低导致腺苷刺激增加,而不是腺苷受体敏感性增加。颈部肌肉是颤抖产热的关键部位,在寒冷暴露前后,老年大鼠颈部肌肉中的AD活性明显低于年轻大鼠,这一发现进一步支持了这一观点。

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