Effects of unilateral castration on the hypothalamic structures involved in the regulation of gonadal function in rat.

This study was undertaken to evaluate the effects of unilateral gonadectomy on the hypothalamic structures involved in the regulation of gonadal function in adult rats of both sexes. Unilateral gonadectomy was performed; 15 days later stereological parameters of cell activity of both the halves of hypothalamic preoptico-suprachiasmatic area (PO-SC) and arcuate nucleus (NA) were analyzed. Under the same experimental conditions the activities of the FSH and LH immunoreactive cells were analyzed separately in both the halves of the adenohypophysis. The results showed that in the rats of both sexes subjected to unilateral gonadectomy the mean diameter of cell nuclei of the contralateral half of PO-SC was significantly greater than that of the ipsilateral half. However, in the control intact or bilaterally gonadectomized rats, there were no significant differences in the values of the same parameter between two halves of PO-SC. On the other hand, neither in the unilaterally gonadectomized nor in the controls, the values of the mean diameter of NA cell nuclei differed significantly between the two halves of this structure. The FSH and LH pituitary cells behaved like NA cells. Therefore, since in the experimental animals compensatory function was developed, and since nervous signaling was different from the sides of the removed and intact gland, the present results suggest involvement of a pure nervous mechanism, besides hormonal control, in the regulation of the compensatory gonadal function. This mechanism seems to be functional in the rats of both sexes. These results also indicate that PO-SC is the anatomical structure involved in this regulation.

The possible mechanism of action of ethanol on rat thymus.

Alcohol is a known suppressant of the immune system and alcoholics frequently have impaired humoral and cell-mediated immunity. The purpose of this study was to investigate the effect of a single dose of ethanol on the thymus and the possible mechanism of its action. Adult female Wistar rats were divided into three groups which were treated with: (a) ethanol (4 g/kg i.p.), (b) naltrexone (5 mg/kg i.p.) and 45 min later with ethanol, (c) naltrexone alone. Untreated rats served as controls. The animals were killed 20 h after administration of alcohol. Thymuses were removed and fixed in Bouin's solution. Paraffin sections were stained with hematoxylin-eosin and analysed using stereological measurements. Our results showed that a single dose of ethanol significantly decreased the volume of the thymus especially affecting the cortex. This effect was blocked by pretreatment with naltrexone. Therefore, it seems that the effect of ethanol on the thymus is mediated by an opioid-dependent mechanism.

Effect of isoproterenol on blood pressure and heart rate in different phases of the oestrous cycle.

The effects of a beta-adrenergic agonist, 1-isoproterenol, on heart rate and systemic blood pressure were examined in female rats in different phases of the oestrous cycle. In addition, the effect of isoproterenol on the same variables was studied in ovariectomized rats and ovariectomized rats treated with either oestradiol or progesterone. To this end, heart rate and blood pressure were monitored for 10 min after i.v. injection of isoproterenol (80 micrograms/kg). After isoproterenol injection, the heart rate was found to be significantly (p less than 0.05) higher in rats in the prooestrous phase of the cycle than in rats in the metaoestrous phase. Furthermore, isoproterenol induced a significantly (p less than 0.05) greater increase in heart rate in ovariectomized rats treated with oestradiol, than in ovariectomized otherwise nontreated animals or ovariectomized rats treated with progesterone. No difference in blood pressure response to isoproterenol was observed between the groups. The results indicate that oestrogens modify cardiovascular response to a beta-adrenergic stimulator, possibly by affecting beta-adrenergic receptors in the heart.