[The stress-modulating effects of laser therapy in IHD patients]. / Stress-moduliruiushchie éffekty lazeroterapii u bol'nykh IBS.

Dependence of the response to helium-neon laser therapy (LT) on initial level and changes of blood plasma hydrocortisone (HC), testosterone (T), diene conjugates (DC) concentration, general antioxidant activity (AOA) of blood plasma, TxB and 6-keto-PGF were estimated in 147 patients with ischemic heart disease and stable angina. The response to LT was observed in patients with high levels of HC, T, AOA and 6-keto-PGF1 alpha. A significant increase of DC was noted in these patients too. The minimal level of HC. T and AOA was recorded in patients with negative clinical effect. The treatment only aggravated HC, T and AOA deficiency and raised DC and TxB level. The findings suggest that the effect of LT is based on modulation of nonspecific adaptive mechanisms.

[A morphofunctional study of the hypothalamic postoptic nucleus after hypophysectomy, cooling and immobilization in rats]. / Morfofunktsional'noe issledovanie postopticheskogo iadra gipotalamusa posle gipofizéktomii, okhlazhdeniia i immobilizatsii krys.

Response of the vasopressin (VP) and oxytocin (OT) cells of hypothalamic post optical nucleus (PON) was studied in male Wistar rats under various experimental conditions. Seven days after hypophysectomy, the majority of both VP- and OT-cells became pyknomorphic which seemed to be the result of transsection of the PON-cell axons and indicated that the PON-cells released neurohormones from the posterior pituitary into the blood. When rats were cooled (2 h at 4 degrees C), the size of nucleoli in VP-cells diminished significantly, but in rats stressed by severe immobilization (20 min) these cells revealed clear signs of activation. In contrast to that, no changes were observed in the OT-cells after these treatments. The functional relation of the PON and thyroid gland is discussed.

[The significance of feedback in accomplishing the rat hypothalamic nonapeptidergic center reaction to short-term immobilization stress]. / Znachenie obratnykh sviazei dlia osushcestvleniia reaktsii nonapeptidergicheskikhtsentrov gipothalamusa krys na kratkovremennyi immobilizatsionnyi stress.

Stress response of oxytocin- and vasopressinergic cells in the supraoptic and paraventricular centers of the hypothalamus was studied morphometrically in rats with intact hypophysis and 7 days after hypophysectomy. Severe immobilization (for 20 min.) was applied as an unspecific short-term stress. In nonoperated rats the immobilization resulted in diminution of functional activity of vasopressinergic cells in the paraventricular nucleus exclusively: nucleolar volume of these cells reduced to 80% (P < 0.05). The same pattern of reaction of nonapeptidergic cells was revealed in the hypophysectomized rats under stress immobilization. The stress blood concentration of vasopressin, ACTH, 11-HOCS clearly increased in nonoperated rats but not in the hypophysectomized rats. TSH plasma concentration and the thyroid gland activity did not alter under stress in both groups of rats. Thus, the data evidence for the response of nonapeptidergic hypothalamic centers is not influenced by fluctuations of the hormone level in blood under short-term stress.

[Thyroid stimulating effect of exogenous vasopressin and oxytocin in hypophysectomized rats during immobilization stress]. / Tirostimuliruiushchii éffekt ékzogennogo vazopressina i oksitotsina u gipofizéktomirovannykh krys pri immobilizatsionnom stresse.

Male Wistar rats were hypophysectomized 1 week before restraint stress. The hypophysectomy caused a decrease of blood vasopressin (30%, P less than 0.05) and a diminution of the thyroid activity (the thyrocyte height lowered to 43%, P less than 0.01). The TSH concentration was about normal and remained constant during the experiment. After 20 min of the restraint stress, the vasopressin concentration reached 178% (P less than 0.01), but the thyroid did not response in rats with the intact hypophysis. In the hypophysectomized rats, the restraint stress caused neither essential changes of the blood vasopressin nor the thyroid function as compared with the hypophysectomized control. An injection of vasopressin (5.0 ng/100 g) or oxytocin (15.0 ng/100 g) resulted in a slight activation of the thyroid in the hypophysectomized rats but significantly stimulated in when combined with the restraint stress; vasopressin injection led to an increase of the thyrocyte height to 152% (P less than 0.01), oxytocin--to 126% (P less than 0.05). Thus, in hypophysectomized rats, vasopressin and oxytocin can influence the thyroid directly. Stressful conditions facilitate the thyroid stimulating effect of these nonapeptide neurohormones.

[Reactions of the adrenal cortex and thyroid gland of hypophysectomized rats to hypothermia]. / Reaktsii kory nadpochechnikov i shchitovidnoi zhelezy u gipofizéktomirovannykh krys pri okhlazhdenii.

Male Wistar rats were hypophysectomized 7 days (group 1) and 4-7 weeks (group II) before exposure to hypothermia (4 degrees C for 1 1/2 h). The hypophysectomized rats from group I were devoid of both the posterior lobe and the adenohypophysis, while the rats from group II had the posterior hypophysis but not the adenohypophysis regenerated. A decreased arginine-vasopressin (AVP) blood level in group I (32%) and a very high level of AVP in group II (311%, P less than 0.05) was determined by RIA. The exposure to hypothermia did not influence the AVP plasma level. The thyroid hypofunction was revealed morphometrically in both hypophysectomized groups. Nevertheless, cooling stimulated the thyroid glands in rats of both experimental groups, like it was in the control. Thus, there is no evidence that thyroid gland reaction to hypothermia is affected by AVP. Cooling caused an increase of corticosteroid blood and adrenal cortex content in nonoperated control rats as well as in group II, but not in group I of experimental animals. Hence, it may be assumed that when the adenohypophysis is ablated, a high AVP blood level is necessary to realize the adrenal cortex response to hypothermia.