Effect of cold exposure on electrophysiological properties of rat heart

Abstract

Male rats exposed to the cold (4 degrees C) for five or ten days exhibited modifications in their thyroid state, as documented by increases in serum thyroid hormone levels, to which differently graded modifications of heart weight/body weight ratio, heart rate, and resting metabolic rate were associated. The values of the above mentioned thyroid state indicators returned to those of the control when the animals, kept at cold for ten days, were re-exposed to room temperature (24 degrees C) for an additional 10 days. The configuration of action potentials, recorded in vitro at 26 degrees C from fibres of anterior papillary muscles, was different in control rats of different age and was affected by prolonged cold exposure. In fact, the action potential duration (APD) increased after ten days of cold exposure. In the re-exposed group the APD was not different from that of the controls. Such a pattern was not significantly modified when the stimulation frequency increased from 1 Hz to 5 Hz. The above results suggest that in cold exposure, as in experimental hyperthyroidism, thyroid hormone might exert a cardiac chronotropic effect by modifying heart electrophysiological properties. Thus thyroid hormone should play a basic role during the exposure to cold environment, stimulating the body metabolism and increasing heart rate as a response to the requirement for greater tissue perfusion.

Thyroid hormone-induced oxidative stress

“…This idea seemed to be supported by the observation that the extent of oxidative damage found following thyroid hormone treatment [7], cold exposure [77], exercise [77] and caloric restriction [78] was related to the organism's metabolic state. In effect, the hyperthyroid functional state induced in mammals by cold exposure, like experimental hyperthyroidism, leads to enhancement of their basal metabolic rate [79], which reflects increases in the cellular respiration of target tissues as BAT [77], liver, and cardiac and skeletal muscles [80]. However, a recent report has shown that during both pyruvate/malate and succinate-supported state 4 respiration, H 2 O 2 generation by liver mitochondria from cold-exposed rats is accelerated without any change in the O 2 consumption rate [81].…”

Cold defence responses the role of oxidative stress

“…Thyroid hormone-mediated processes are elevated during long-term cold exposure appearing as a hyperthyroid state. Venditti and colleagues have shown that the hyperthyroid functional state induced in mammals by cold exposure, like experimental hyperthyroidism, led to enhancement of their basal metabolic rate, which reflects an increase in the cellular respiration of target tissues including BAT, liver and cardiac and skeletal muscles (35,99,100). There are data indicating that in hyperthyroid tissues increased ROS and RNS production, as well as the decrease in antioxidant capacity and susceptibility to oxidative damage occurs (101).…”