Physiological Effects of Cold Stress On Cardiac Function

Cold stress is an important environmental factor which may
interfere with the physiological stability in mammals, especially in small
animals like rabbits. Rabbits are very sensitive to low temperatures because
of the high surface-area to volume ratio, and insulated area, leading to
complex thermoregulatory and cardiovascular responses, to maintain the
core body temperature. The review is a summary of existing scientific
findings on the physiological and molecular actions of cold stress on the
cardiac system in rabbit models. Exposure to cold causes significant
sympathetic response that causes the heart rate to rise, blood pressure to
increase, and the myocardial oxygen demand to increase. Hemodynamic
changes, such as raised systemic vascular resistance, and variations in the
cardiac output exert heavy burden to the myocardium. Moreover, cold stress
has a considerable impact on electrophysiological stability, leading to
slowing conduction, QT prolongation, and an excessively high risk of
arrhythmias. At the molecular level, low temperatures increase oxidative
stress, activate inflammatory signals, impair calcium transluctions, and
induce apoptosis, which plays a role in structural and functional cardiac
changes. Edema, vascular congestion and initial signs of myocardial
remodeling are established in histological studies when exposed over a long
period. The rabbits are a useful translational model because they have
physiological similarities to human beings on autonomic regulation and
cardiac electrophysiology. Given these mechanisms, it is possible to mention
that the research of environmental cold stress on heart health offers valuable
insights into the effect of cold stresses and conditions future studies on
protective measures and adaptive mechanisms.