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The Syrian (golden) hamster has provided the most extensively studied model of pineal physiology, and in the species the pineal gland has a potent suppressive effect on the reproductive system and on serum free thyroxim (T4) concentration. The pineal's suppressive effect on the gonads and T4 is classically evoked by subjecting the hamsters to a short photoperiod (less than 12-h light/day) or to blinding by bilateral orbital enucleation. Additional pinealectomy prevents the regression of the reproductive system and the reduction of T4. Burn injury of humans results in depressed serum concentrations of free triiodothyroxine (T3) and T4, reduced serum binding of T4, and low testosterone concentrations. Burned male Syrian hamsters (burn size 23% of body surface) exhibited reduced total (T4) and free (FT4) serum concentrations, a defect in T4 binding to serum proteins manifested by the T4 dialyzable fraction but not the in vitro T3 charcoal uptake, and reduced serum testosterone concentration. These changes are similar to those noted previously in burned humans. Unlike such patients, burned hamsters did not exhibit reduced serum T3 nor elevated rT3 concentrations in a reproducible manner. Pinealectomy performed before burning in hamsters did not prevent the burn-induced depression in serum T4 and testosterone.

Rats with a cutaneous burn exhibited a burn-size-related depression of serum thyroid hormones 2 weeks after injury. Thyroidectomized rats had a marked rise in brain in vitro T4 deiodination to T3 and in serum TSH concentration compared to controls. These normal responses to depressed thyroid hormones were not seen in burned rats. The depression of serum thyronines and thyrotrophin suggests that the burned rat may be a model for human burn injury and other nonthyroidal illness. In this model it appears that the brain and pituitary do not respond as in thyroidectomy, suggesting lack of true hypothyroidism in burn injury.

A single subcutaneous injection of melatonin to rat or mouse pups on the day of birth inhibited the compensatory ovarian hypertrophy response to unilateral ovariectomy at six weeks of age. The body weights of melatonin-treated female mice were significantly depressed as compared to the body weights of control animals and failed to increase after castration. Compensatory adrenal hypertrophy failed to occur in mice treated with melatonin on the day of birth. Inhibition of ovarian and adrenal compensatory growth was not apparent in mice treated with melatonin on day 17 of life. It is concluded that melatonin may influence the differentiating gonadal and adrenal CNS control centers during the critical neonatal period of organizational endocrine function in the mouse and rat. (Modified author abstract)