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沙鼠热适应诱导心动过缓的机制

Mechanism of heat acclimation induced bradycardia in the sand rat.

作者信息

Horowitz M, Meiri U

机构信息

Division of Physiology, Hadassah School of Dental Medicine, Hebrew University, Jerusalem, Israel.

出版信息

J Basic Clin Physiol Pharmacol. 1993 Apr-Jun;4(1-2):37-46. doi: 10.1515/jbcpp.1993.4.1-2.37.

DOI:10.1515/jbcpp.1993.4.1-2.37
PMID:8679508
Abstract

The effect of heat acclimation on chronotropic response of the heart under normothermic and hyperthermic conditions was studied in the sand rat, Psammomys obesus, a diurnal desert species. All animals were acclimated at 34 degrees C for 0, 5, 14, 30 or 60 days; heat stress was achieved by exposure at 38 degrees C. Continuous measurements of heart rate (HR) were carried out on conscious animals, using chronic subcutaneous electrodes. Atropine (0.1 mg/100 g) and propranolol (1 mg/100 g) were administered to evaluate the para-sympathetic (V) and sympathetic (S) influences on HR. Intrinsic HR (HRi) was measured following administration of both drugs simultaneously. P. obesus developed bradycardia from day 5 of the acclimation. This bradycardia was induced solely by decreased HRi, overriding partial vagal withdrawal. During hyperthermia apparent thermal insensitivity of HR was observed. This was attained by partial sympathetic withdrawal compensating for the increase in HRi due to body temperature rise. It can be concluded that in P. obesus, heat acclimation induced bradycardia is attained by intrinsic changes in the pacing cells. It also emerges that the hyperthermic response is independent of and is not affected by heat acclimation.

摘要

在昼行性沙漠物种肥尾心颅跳鼠中研究了热适应对正常体温和高温条件下心脏变时反应的影响。所有动物在34摄氏度下适应0、5、14、30或60天;通过暴露在38摄氏度下实现热应激。使用慢性皮下电极对清醒动物的心率(HR)进行连续测量。给予阿托品(0.1毫克/100克)和普萘洛尔(1毫克/100克)以评估副交感神经(V)和交感神经(S)对心率的影响。在同时给予两种药物后测量固有心率(HRi)。肥尾心颅跳鼠从适应的第5天开始出现心动过缓。这种心动过缓完全是由HRi降低引起的,超过了部分迷走神经的撤离。在高温期间,观察到心率明显的热不敏感性。这是通过部分交感神经撤离来实现的,以补偿由于体温升高导致的HRi增加。可以得出结论,在肥尾心颅跳鼠中,热适应诱导的心动过缓是由起搏细胞的内在变化引起的。还发现高温反应独立于热适应且不受其影响。

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