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Depressed cardiac sarcoplasmic reticulum calcium transporter activity at low temperature may lead to high cytosolic free Ca 2+ in cold-sensitive species, contributing to the loss of cardiac function at low temperature ( Liu et al., 1997). Rat left ventricle was significantly weaker (greater reduction in maximum developed pressure generated against a balloon) and more slowly contracting (reduced peak d P/d t) when acutely cooled, compared with that of hibernators such as ground squirrel ( Caprette and Senturia, 1984). For example, a 6-fold decrease in guinea pig papillary muscle contractile strength was noted after 3 weeks at 5☌, but a 30% increase in time to peak tension ( Takagi et al., 1999). In response to cooling, cardiac performance is impaired as a result of alteration in sinoatrial pacemaker activity, adrenergic sensitivity, myocyte calcium handling and, hence, contractility. One challenge is to identify which of the suite of presumed adaptive responses to cold exposure reflects species-specific characteristics, and which are capable of physiological modification. Other mammals, however, accommodate more direct exposure to extreme and varying thermal environments, though surprisingly little is known about cardiovascular adaptation to low temperatures ( Gordon, 1993). Cold acclimation (CA) reduces sensitivity to the adrenergic pressor response, but does not elicit any change in heart rate ( f H) ( Budd et al., 1993), although the pattern of haemodynamic responses may vary between cold acclimation and cold exposure ( De Lorenzo et al., 1999). Epidemiological studies have shown an increase in acute myocardial infarctions in colder weather, probably involving elevated haemostatic risk factors, hypertension and sustained tachycardia. The normal limit is around 25☌, after which ventilation may cease and ventricular fibrillation leads to circulatory arrest, but even moderate cooling can lead to significant pathology if prolonged. Further drops in T b lead to impaired ventilation and circulatory decline, in turn leading to hypoxaemia and acidosis ( Cossins and Bowler, 1987). Mammals are generally sensitive to hypothermia, with the first pathological symptoms occurring at a core temperature ( T b) as high as 34☌ in humans. 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. While CA involved an increased capacity for β-oxidation, there was a paradoxical reduction in developed pressure as a result of adrenergic down-regulation. Ex vivo cardiac performance revealed no change in intrinsic heart rate, but a mechanical impairment of cardiac function at low temperatures following CA. However, PSA showed maintenance of cardiorespiratory coupling on acute cold exposure in both groups. Cold acclimation (CA) induced only partial compensation for this challenge, including increased coronary flow at T b=37☌ (but not at T b=25☌), 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. In vivo, acute cold exposure (core temperature, T b=25☌) resulted in hypotension (approximately –20%) due to low cardiac output (approximately –30%) accompanying a bradycardia (approximately –50%). Wistar rats were held at a 12 h:12 h light:dark (L:D) photoperiod and room temperature (21☌ 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☌ over 4 weeks. 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.
The consequences of acute hypothermia include impaired cardiovascular performance, ultimately leading to circulatory collapse.