Effect of ambient temperature on dexmedetomidine-induced metabolic and cardiorespiratory suppression in spontaneously breathing newborn rats

Newborn animals are known to increase the ventilation–metabolism ratios in hypoxia, particularly at cold environment by decreasing the thermogenesis. We examined whether ambient temperatures and thermoregulatory suppression due to dexmedetomidine, an α₂ adrenoceptor agonist, affect the coupling between ventilation and metabolism in neonatal rats. Wistar rats (3–7 days old) were measured for metabolic and cardiorespiratory indices. Control recordings were made at 34 °C ambient temperature (Ta) and Ta was either kept at 34 °C (Medium), reduced to 27 °C (Low) or increased to 39 °C (High). Once at the desired Ta, the rats were administered normal saline or dexmedetomidine (50 μg∙kg⁻¹) and the indices were again recorded. Control values were comparable between the normal saline and dexmedetomidine groups. Using values relative to the control values in each group, body temperature (Low or High vs. Medium Ta) and heart rate (Low vs. High Ta) were significantly different among the three Ta. At each Ta, the dexmedetomidine group showed significantly lower metabolic rates, minute ventilation, respiratory rate and heart rate, compared to the normal saline group. Despite these changes, the ventilationmetabolism ratios in the dexmedetomidine group were comparable at the Medium and Low Ta, and significantly lower at the High Ta, compared to the normal saline group. Dexmedetomidine plus atipamezole (5 mg∙kg⁻¹, an α₂ adrenoceptor antagonist) did not affect the ventilation–metabolism ratios at the Low and High Ta. Although dexmedetomidine suppresses thermoregulatory responses, the coupling of ventilation and metabolic rates can be preserved through α₂ adrenoceptor activation at cold, but not at hot, ambient temperature. Our results suggest that α₂ adrenoceptor activation impairs control of ventilation at heating or rewarming in newborn rats.