Is cold acclimation of benefit to hibernating rodents?

Abstract

SUMMARYThe thermal challenge associated with cold acclimation (CA) and hibernation requires effective cardio-respiratory function over a large range of temperatures. We examined the impact of acute cooling in a cold-naïve hibernator to quantify the presumed improvement in cardio-respiratory dysfunction triggered by CA, and estimate the role of the autonomic nervous system in optimising cardiac and respiratory function. Golden hamsters (Mesocricetus auratus) were held at a 12h:12h light:dark photoperiod and room temperature (21°C euthermic control) or exposed to simulated onset of winter in an environmental chamber, by progression to 1h:23h light:dark and 4°C over 4weeks. In vivo acute cooling (core temperature T b =25°C) in euthermic controls led to a hypotension and bradycardia, but preserved cardiac output. CA induced a hypertension at normothermia (T b =37°C) but on cooling led to decreases in diastolic pressure below euthermic controls and a decrease in cardiac output, despite an increase in left ventricular conductance. Power spectral analysis of heart rate variability suggested a decline in vagal tone on cooling euthermic hamsters (T b =25°C). Following CA, vagal tone was increased at T b =37°C, but declined more quickly on cooling (T b =25°C) to preserve vagal tone at levels similar to euthermic controls at T b =37°C. For the isolated heart, CA led to concentric hypertrophy with decreased end-diastolic volume, but with no change in intrinsic heart rate at either 37 or 25°C. Mechanical impairment was noted at 37°C following CA, with peak developed pressure decreased by 50% and peak rate-pressure product decreased by 65%; this difference was preserved at 25°C. For euthermic hearts, coronary flow showed thermal sensitivity, decreasing by 65% on cooling (T=25°C). By contrast, CA hearts had low coronary flow compared with euthermic controls, but with a loss of thermal sensitivity. Together, these observations suggest that CA induced a functional impairment in the myocardium that limits performance of the cardiovascular system at euthermia, despite increased autonomic input to preserve cardiac function. On acute cooling this autonomic control was lost and cardiac performance declined further than for cold-naïve hamsters, suggesting that CA may compromise elements of cardiovascular function to facilitate preservation of those more critical for subsequent rewarming. Supplementary material available online at

Pharmacologically induced hypothermia attenuates traumatic brain injury in neonatal rats

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“…Therefore, anesthesia has to be used in patients to combat the cold defense response, which has the potential to lead to infection and possibly other side effects due to prolonged hypothermia (Schwab et al, 1998), while NTR compounds lead to a lack of shivering (Gu et al, 2015). Also, physical cooling has associated complications such as hypotension, arrhythmia and change of fluid pH (Gröger et al, 2013; Mohr et al, 2013; Stuart et al, 2013). It seems that pharmacological reagent-induced controlled hypothermia, which targets the brain thermoregulatory center, has emerged as an efficient and considerably safer treatment for patients, with a further benefit being that a lot of choices of drug are provided.…”

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