Responses of heat stressed chickens to exogenous reverse triiodothyronine (rT(3))

Heat stress is accompanied by a decrease in basal metabolic rate and plasma thyroid hormones. Unlike 3,5,3'-triiodothyronine (T-3) and thyroxine (T-4), 3,3',5'-triiodothyronine (rT(3)) displays hypometabolic properties and antagonizes the hypermetabolic effect of T-3. This study analyses the role of rT(3) in heat (38-39 degrees C) stressed immature chickens. Two experiments which differed in frequency of rT(3) injections (one or two times a day), duration of heat stress (72 or 48 h) and blood sampling were performed. The dose was 14 mu g rT(3)/100 g b.wt./injection (s.c.). It has been shown that rT(3) treatment aggravates heat stress symptoms (enhances circulating corticosterone, catecholamines and free fatty acids) and increases mortality. The critical survival time of the rT(3) treated and heated birds was at first 24 h of stress. No more chickens died during the nest days of the experiment despite the continuation of rT(3) injection, suggesting that rT(3) might disturb the adaptation to heat. Reverse T-3 in heat stressed chickens led to the highest reduction in food consumption (69.9%) and body weight gain (14.0% compared to initial weight). The opposite effect in water consumption (216.9%) was observed. In a neutral environment, rT(3) significantly suppressed body temperature 6 h after injection (40.4; control: 41.1 degrees C), confirming its hypometabolic properties. However, at the same time rT(3) significantly enhanced body temperature in heat stress (43.03 versus heated control 42.56 degrees C). In addition, in rT(3) treated birds decreased plasma triglycerides (TG; 24.3%) and increased plasma free fatty acids (FFA; neutral temperature: 26.4%; heat stress: 57%) were demonstrated. A correlation between corticosterone and FFA (r = 0.52) shows that some of the FFA may originate from lipolysis since hormones of the pituitary-adrenocortical axis accelerate lipolysis. The remaining part of the increased FFA appears to be due to suppressed utilization of FFP, as a consequence of hypometabolic properties of rT(3). Low and negative relation between TG and FFA (r -0.26; P < 0.05) may support such an assumption. The two times higher peak of corticosterone in the rT(3) and the overheated group, as compared to the heated control, occurred at 6 h of heat stress and indicates that rT(3) increases the unfavourable effect of high temperature. This was also confirmed by elevated plasma adrenaline and noradrenaline in rT(3)-injected and heated chickens (55.5 and 123%, respectively). However, a single and two times higher peak of adrenaline at 24 h of heat stress was observed in saline treated birds, but not in rT(3) supplemented animals, suggesting that this difference might explain one of the factors responsible for high mortality. In conclusion, the results obtained demonstrate that physiological doses of rT(3), a hypometabolic hormone, enhance the unfavourable effect of heat stress in chickens.