title: Cold-impaired cardiac performance in rats is only partially overcome by cold acclimation.
abstract: The consequences of acute hypothermia include impaired cardiovascular performance, ultimately leading to circulatory collapse. We examined the extent to which this results from intrinsic limitations to cardiac performance or physiological dysregulation/autonomic imbalance, and whether chronic cold exposure could ameliorate the impaired function. Wistar rats were held at a 12 h:12 h light:dark (L:D) photoperiod and room temperature (21°C; euthermic controls), or exposed to a simulated onset of winter in an environmental chamber by progressive acclimation to 1 h:23 h L:D and 4°C over 4 weeks. In vivo, acute cold exposure (core temperature, T(b)=25°C) resulted in hypotension (approximately -20%) due to low cardiac output (approximately -30%) accompanying a bradycardia (approximately -50%). Cold acclimation (CA) induced only partial compensation for this challenge, including increased coronary flow at T(b)=37°C (but not at T(b)=25°C), maintenance of ventricular capillarity and altered sympathovagal balance (increased low:high frequency in power spectral analysis, PSA), suggesting physiological responses alone were insufficient to maintain cardiovascular performance. However, PSA showed maintenance of cardiorespiratory coupling on acute cold exposure in both groups. Ex vivo cardiac performance revealed no change in intrinsic heart rate, but a mechanical impairment of cardiac function at low temperatures following CA. While CA involved an increased capacity for β-oxidation, there was a paradoxical reduction in developed pressure as a result of adrenergic down-regulation. These data suggest that integrated plasticity is the key to cardiovascular accommodation of chronic exposure to a cold environment, but with the potential for improvement by intervention, for example with agents such as non-catecholamine inotropes.
authors.affiliation: Centre for Cardiovascular Sciences, School of Clinical and Experimental Medicine, University of Birmingham, Birmingham B15 2TT, UK.
authors.forename: David
authors.initials: D
authors.lastname: Hauton
authors.forename: Shaun
authors.initials: S
authors.lastname: May
authors.forename: Rasna
authors.initials: R
authors.lastname: Sabharwal
authors.forename: Durmus
authors.initials: D
authors.lastname: Deveci
authors.forename: Stuart
authors.initials: S
authors.lastname: Egginton
mesh_terms: D000064:Acclimatization / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D003080:Cold Temperature; D004562:Electrocardiography; D006321:Heart / Q000503:physiopathology*; D006334:Heart Function Tests; D006339:Heart Rate / Q000502:physiology; D007035:Hypothermia / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009929:Organ Size; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar