Endocrine effects of repeated sauna bathing.

Ten healthy male and seven female volunteers were exposed to dry heat (in a Finnish sauna 80 degrees C) 1 h twice a day for 7 days. The levels of ACTH in plasma, cortisol, TSH, thyroid hormones, testosterone, gonadotropins, prolactin and GH in serum and urinary excretion of catecholamines were determined before the experiment, and on the first, third and seventh days. Females participated only in prolactin studies. During the experiments there were no statistically significant changes in serum thyroid hormones, TSH, testosterone, FSH and LH levels. Serum cortisol and plasma ACTH decreased and urinary catecholamine increased slightly at the end of the experiment (P less than 0.05). Serum GH and prolactin in males exhibited 16- and 2.3-fold increases (P less than 0.01), respectively. In females serum prolactin rose over four-fold (P less than 0.01). The GH rise in response to hyperthermia declined after the third day but prolactin remained elevated at the end of the experiments in males. The release of prolactin in females was also high and may be associated with the transient amenorrhoea that occurred in five out of seven subjects after the experiment. The increased release of prolactin and perhaps that of GH may be associated to the heat-exposure-induced dehydration.

Hypothalamic and serum catecholamines in ethanol and acetaldehyde treated guinea-pigs. Relation to moderate short-term cold exposure.

Adult guinea-pigs were treated with ethanol (2.5 g/kg, IP) or acetaldehyde (100 mg/kg, IP) and exposed to moderate cold (+4 degrees C) for 50 minutes. Controls were given 0.9% NaCl solution. The hypothalamic catecholamines norepinephrine (NE) and dopamine (DA) and also norepinephrine and epinephrine (E) in the serum were analyzed by high-performance liquid chromatography with an electrochemical detector. Blood glucose, free fatty acids and glycogen in the liver and skeletal muscle were also measured. Acetaldehyde caused a similar drop in colon temperature as did ethanol, but neither could prevent cold-induced vasoconstriction in the ear lobe. Ethanol significantly reduced the concentration of NE in the hypothalamus compared to the controls. Acetaldehyde had a tendency to lower hypothalamic NE. There was no significant difference between drug-treated groups in NE concentration. Neither ethanol nor acetaldehyde had any effect on hypothalamic DA. In the ethanol group serum E and glucose were significantly elevated compared to the acetaldehyde group. Serum glucose was also higher compared to the controls, and the difference in serum E concentration near the level of significance. No significant differences were found between the groups in serum NE, FFA or skeletal muscle and liver glycogen concentration. The results point to a possible central effect of ethanol during a short-term moderate cold exposure. The effects of acetaldehyde on neuronal tissue remain speculative, but a possible effect on noradrenergic neurons cannot be ruled out. Although the hypothermic effect of acetaldehyde corresponded that of ethanol, further experiments are required to elucidate the role of acetaldehyde in ethanol-induced hypothermia.

Release of norepinephrine from the rat's hypothalamus perfused with alcohol: relation to body temperature.

The activity of norepinephrine (NE) within the thermosensitive region of the anterior hypothalamic, pre-optic area (AH/POA) of the rat was examined in relation to changes in core temperature produced by ethyl alcohol. Following stereotaxic implantation of push-pull guide tubes, a specific site in the AH/POA, reactive or non-reactive to NE, was labeled with 1.0 microliter of [3H]-NE. Alcohol in a concentration of 2.75% or 5.5% was then perfused locally at the same site by push-pull cannulae or administered peripherally in a dose of 2.0 g/kg. In control experiments, artificial CSF was perfused alone. The perfusion of alcohol enhanced or delayed the release of [3H]-NE in AH/POA or failed to alter the efflux of the catecholamine, with the specific response dependent principally on the: (1) anatomical site of hypothalamic perfusion, (2) concentration of alcohol, and (3) interval of perfusion itself. During the perfusion of alcohol within a very circumscribed region in the AH/POA, vasodilatation, as reflected by an increase in skin temperature, and a hypothermia of short latency, occurred. The change in core temperature was usually accompanied by a delay in the efflux of [3H]-NE. After the peripheral administration of 2.0 g/kg alcohol, an alteration in NE efflux from the AH/POA was also induced during the course of a hypothermic response accompanied by vasodilatation. These results suggest that alcohol exerts a direct central effect on nerve cells comprising the thermoregulatory mechanism located within the hypothalamus. Further, the well-known thermolytic effect of alcohol could be mediated in part by noradrenergic synapses within AH/POA, by means of their phasic release of NE.

Hypothalamic catecholamines and tolerance for severe cold in ethanol-treated guinea-pigs.

1 The effect of ethanol (2g/kg) on hypothalamic catecholamines in guinea-pigs kept at room temperature (20 degrees C) and in severe cold (-20 degrees C) for 1.5 h was determined. Serum glucose, triacyl-glycerols and free fatty acids (FFAs), glycogen in liver and skeletal muscle and total lipid and triacyglycerols in the interscapular adipose tissue were also determined. 2 Ethanol increase the noradrenaline and adrenaline content of the hypothalamus at 20 degrees C and reduced ther rectal temperature by about 2 degrees C. The hypothalamic noradrenaline content of the ethanol-treated guinea-pigs exposed to cold, in which the fall in rectal temperature was about 8 degrees C, was higher than in the controls, whose rectal temperature decreased only by about 2 degrees C. 3 Cold exposure increased FFA concentration in serum and reduced skeletal muscle glycogen and serum glucose concentrations in both groups, but no significant differences were found in the carbohydrate and lipid values between the groups at -20 degrees C. 4 It is possible that the diminished cold tolerance in the ethanol-treated guinea-pigs might be due, at least in part, to the effect of ethanol on the catecholamines in the hypothalamus.