Mechanism of heat acclimation induced bradycardia in the sand rat.

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.