[The role of protein synthesis in realisation of protective cardiac effects of thyroid hormones during immobilization stress in rats]. / Rol' belkovogo sinteza v realizatsii protektornykh kardial'nykh éffektov tireoidnykh gormonov pri immobilizatsionnom stresse u krys.

A decrease in the protein synthesis by the transcription inhibitor rifampycin prevents myocardial contractile function, protective effect of thyroid hormones and their antioxidant effect under the restraint stress in rats. The findings suggest that the main component of thyroid hormones' protective effect on the heart is related to their specific action realised via the cell genetic apparatus.

[The role of local stress-limiting myocardial systems in the protective cardiac effect of low doses of thyroid hormones during immobilization stress in rats]. / Rol' lokal'nykh stress-limitiruiushchikh sistem miokarda v protektornom kardial'nom éffekte malykh doz tireoidnykh gormonov pri immobilizatsionnom stresse u krys.

Thyroid hormones seem to activate some fundamental cellular protective mechanisms and thus to be an important regulatory factor for local myocardial systems in their stress-limiting activity.

Role of thyroid hormones in stress-induced synthesis of heat-shock proteins in the myocardium.

Thyroxine in near-physiological doses increased the content of heat-shock proteins in the myocardium and stimulated their accumulation during immobilization stress. Blockade of thyroid functions with methimazole decreased the content of heat-shock proteins in rat myocardium during stress and heat shock and prevented their accumulation during adaptation to short-term immobilizations.

[The role of thyroid hormones in prevention of disorders of myocardial contractile function and antioxidant activity during heat stress]. / Znachenie tireoidnykh gormonov v preduprezhdenii narushenii sokratitel'noi funktsii i antioksidantnoi aktivnosti miokarda pri teplovom stresse.

The stress of heat under conditions of immobilisation induced an obvious depression of the cardiodynamic parameters. This correlated well with intensification of lipoperoxydation and a drop in the myocardial antioxydant activity. Small doses of thyroid hormones prevented the decline of the parameters, normalisied myocardial free-radical homeostasis in result of activation of superoxyddysmutase, catalase, and general antioxydant activity.

[The mechanism of stressor suppression of the contractile function and reactivity of aortic smooth muscle]. / K mekhanizmu stressornogo ugneteniia sokratitel'noi funktsii i reaktivnosti gladkoi myshtsy aorty.

Blockade of the NO synthesis did not change the stressor augmentation of the acetylcholine-induced endothelium-dependent relaxation. The immobilisation stress seems to suppress the contractile function and the reactivity of the aorta smooth muscle reactivity as the result of augmentation of the NO basal production in endotheliocytes.

[The mechanism of the action of low doses of thyroid hormones on the stressor-induced changes in rat vascular tonus]. / K mekhanizmu vliianiia malykh doz tireoidnykh gormonov na stressornye izmeneniia tonusa sosudov krys.

Small doses of thyroidine were found to diminish a 6-hr immobilisation-induced decrease of the mean AP and duration of a hypertension response to blockade of NO-synthasa. The thyroidine seems to act on the system of endothelial nitric oxide synthasa.

Influence of the thyroid status of the organism in the realization of the adaptational effect of cold.

The combined three- and six-hour effect of immobilization and cold on euthyroid rats induces suppression of the contractile function and functional reserve of the heart, the death, respectively, of 30 and 80% of the animals, hypothermia, changes in the weight of the adrenals and the spleen, and ulceration of the mucosa of the stomach. Stressing of the hypothyroid rats is accompanied by a substantially more pronounced decrease in the indices of cardiac dynamics and the resistance of the organism after 3 h, and the death of 100% of the animals after 6 h. The periodic effect of cold on euthyroid rats leads to an increase in the strength and speed of contraction and relaxation of the myocardium, as well as to an increase in the relative weight of the spleen. During subsequent stressing, cold adaptation substantially limits the disturbances in contractile function and prevents the decrease in the functional reserve of the heart, increases survival, and decreases the degree of hypothermia, ulcer-formation, and change in the weight of stress-sensitive organs, while the preventive effect of cold adaptation is absent in the hypothyroid animals; this attests to the significance of thyroid status for its realization.

[Importance of thyroid hormones in the realization of the protective effects of cold adaptation]. / Znachenie tireodnykh gormonov v realizatsii zashchitnykh éffektov kholodovoi adaptatsii.

The possibility of limitation of stress-induced changes of lipid peroxidation (LP) and myocardial antioxidant activity (AA) caused by the combined influence of immobilization and cold during 3 hours was studied in experiments on 128 male rats. Cold adaptation was found to reduce death rates up to 10%, the degree of hypothermia, LP activation and myocardial AA depression under combined stress, significantly elevating the concentration of serum thyroid hormones. Hypothyroidism causes a 2.5-fold decrease in thyroid hormones. It also decreased the concentration of LP products and cardiac AA, and stress in hypothyroid rats resulted in as high as 50% increase in death rates and enhanced hypothermia. This also led to less marked LP stimulation and myocardial AA depression. 50% death of animals, lower hypothermia and the same changes in the content of LP products and cardiac AA, as in non-adapted rats were found in cold-adapter hypothyroid rats during combined stress. It is concluded that thyroid hormones determine the efficiency of cold adaptation to a greater extent.

[Changes in the endotheliocyte activity of the coronary vessels under the influence of stress]. / Izmenenie aktivnosti éndoteliotsitov koronarnykh sosudov pod vliianiem stressa.

The effect of saponin and blockade of the nitrogen oxide upon the coronary endothelium was found in rats subjected to a 6-hrs stress. The damage of the endothelium and the blockade abolished the stressor-induced increase in the coronary blood flow velocity. The index of autoregulation and the latter's efficiency, however, remained the same. Preliminary administration of L-arginine prevented the effect of NG-monomethyl-L-arginine upon the coronary flow in the isolated hearts of rats subjected to stress. The post-stressor increase in the coronary blood flow seems to be due to an increase in releasing the nitrogen oxide from the coronary vessels' endotheliocytes.

[The significance of the thyroid status of the body in realizing the adaptive effect of cold]. / Znachenie tireoidnogo statusa organizma v realizatsii adaptatsionnogo éffekta kholoda.

Combined immobilisation and cold for 3 and 6 hrs induced depression of cardiac contractile function and functional reserve, death rate of 30 and 80 per cent resp., hypothermia, alterations in adrenal glands and spleen, gastric mucosa ulceration in euthyroid rats. The changes were more obvious in hypothyroid rats. The cold adaptation significantly reduced the changes in the euthyroid rats whereas this effect was absent in hypothyroid animals. The data obtained corroborate the significance of intact thyroid status for the cold adaptation.

[The autoregulation of the coronary flow of the isolated heart in rats after saponin damage to the endothelium]. / Autoreguliatsiia koronarnogo potoka izolirovannogo serdtsa krys posle povrezhdeniia éndoteliia saponinom.

The damage of the endothelium with saponin completely abolished the autoregulation of the coronary vessels in the Langendorff isolated heart and reduced the volume velocity of the coronary blood flow by 34% at the perfusion pressure 40 mmHg. Indomethacin and verapamil augmented the coronary flow in intact rats. All these agents decreased the distensibility of the coronary vessels by 43-49% on the average. The damage of the endothelium of coronary vessels reduced the maximum reactive hyperemia and, respectively, the coronary vasodilator reserve.

[The role of ultrasonic activation of the thyroid in the development of stress changes in cardiac contractile function]. / Rol' ul'trazvukovoi aktivatsii shitovidnoi zhelezy v razvitii stressornykh izmenenii sokratitel'noi funktsii serdtsa.

Ultrasonic activation of the thyroid is characterized by a rise in T3 concentrations in the serum, acceleration of the rat myocardial contractility under isometric loading. Preliminary activation of the thyroid function restrains stress-related changes in thyroid hormone production and cardiac contractility, prevents reduction of iodized thyroglobulins in thyroid colloid under immobilization.

[The autoregulation of the coronary flow of the isolated rat heart after NO-synthase blockade]. / Autoreguliatsiia koronarnogo toka izolirovannogo serdtsa krys posle blokady NO-sintazy.

The experiments were performed on 67 rat hearts isolated by the Langendorff method. Perfusion pressure (PP) was stepwise increased from 40 to 120 mm Hg. It was found that NO-synthase blockade by NG-monomethyl-L-arginine (NG-MMLA) decreased volume velocity coronary flow (VVCF) at PP 40 and 60 mm Hg, autoregulation index and shifted the onset of effective autoregulation to the right. In cases of high coronary tone, caused by introduction of pituitrine, the autoregulation and its effectiveness was unchanged. The combination of NG-MMLA and pituitrine decreased the autoregulation index again. In cardiac perfusion under constant pressure, the value of maximal hyperemic coronary flow after introduction of NG-MMLA was decreased by 30-57%, and as a result the coronary reserve was decreased by 28.3%. Thus, NO, which released from endothelium of coronary vessels plays a significant role in mechanism of coronary autoregulation.

[Effect of endogenous metabolites on autoregulation and dilational reserve of coronary vessels]. / Vliianie éndogennykh metabolitov na autoreguliatsiiu i rasshiritel'nyi rezerv koronarnykh sosudov.

The experiments have been performed on isolated Langendorff rat's hearts. Perfusion pressure (PP) has been increased from 40 to 120 mm Hg by steps. It has been found out, that captopril, indomethacin and verapamil (blockers of the angiotensin-converting enzyme, eicosanoids synthesis and calcium channels, respectively) increased volume velocity of coronary flow (VVCF) at PP within the range of 80-120 mm Hg, decreased the value of the autoregulation index and the coronary vasodilatory reserve by 28-39%, apparently due to decrease of the basal tone of coronary vessels, while the maximum reactive hyperemia coronary flow was not changed thereby. The blockade of No-synthase by NG-monomethyl-l-arginine (NG-MMLA) caused reduction of VVCF at PP 40 mm Hg by 28.5%, the autoregulation index by 79% and the coronary reserve by 29% due to reduction of reactive hyperemic flow. Captopril and NG-MMLA did not change while verapamil and indomethacin decreased intraventricular pressure. Thus, the decrease of the VVCF, caused by NG-MMLA and its increase caused by addition of inhibitors could be connected with inhibition of the synthesis of substances modulating autoregulation of coronary blood flow, and obviously did not depend on changes in functional activity of myocardium.

[Prevention of disorders of cardiomyocyte ultrastructure in experimental myocardial infarction in immobilization-induced stress by administration of thyroid hormones]. / Preduprezhdenie tireoidnymi gormonami narushenii ul'trastruktury kardiomiotsitov pri éksperimental'nom infarkte miokarda v usloviiakh immobilizatsionnogo stressa.

In the experiment, carried out on 48 non-inbred male rats ultrastructural changes in cardiomyocytes in non-ischemized parts of the heart at experimental infarction of myocardium under conditions of immobilization stress have been studied, as well as possibility to correct these changes by means of thyroid hormones. The stress intensifies dystrophic processes, developed outside the infarction zone, increases the mass of the necrotized tissue, essentially decreases the areas occupied by mitochondria and myofibrils, as well as their ratio in the section area. Small doses of thyroid hormones prevent the heart from the damaging effect of the stressor: decreasing area; occupied by mitochondria, myofibrils and their relation in the section, as well as they stimulate intracellular regenerative processes (accumulation of polymorphous mitochondria with clearly manifested cristae, membranes of the endoplasmic reticulum) and decrease the myocardial necrotized zone). Thus, structural lesions, resulted from the effect of ischemic necrosis and stress, can be prevented by small doses of thyroid hormones+.

[The enhancement of body resistance to combined exposure to immobilization and cold with thyroid hormones]. / Povyshenie ustoichivosti organizma k kombinirovannomu vozdeistviiu immobilizatsii i kholoda tireoidnymi gormonami.

In experiments on 123 male rats have been found that the combination of immobilizing and cold (4 degrees C) stresses during 6 hours results in the formation of 4.5 gastric mucosa ulcers in every rat, marked activation of lipoperoxidation and depression of antioxidant activity of myocardium, significant increase of relative mass of adrenal glands, decrease of spleen mass and death of 80% animals accompanied by the reduction of concentration of thyroid hormones in blood serum and hypothermia (to 28 degrees C). The prestress injection of small doses of thyroidine decreased of mucosa defect rate and the number of ulcers to 2.8, made less marked the changes of relative mass of adrenal glands and spleen and the changes of concentration of thyroid hormones in blood serum, significantly limited the activation of lipoperoxidation, depression of power in antioxidant systems of myocardium, hypothermia (to 32.5 degrees C) and significantly increased the survival rate (to 70%).

[Correction of stress-induced disorders of the ultrastructure of hypertrophied myocardium with thyroid hormones]. / Korrektsiia stressovykh narushenii ul'trastruktury gipertrofiro- vannogo miokarda tireoidnymi gormonami.

In the experiment performed on 25 non-inbred male rats ultrastructural changes in cardiomyocytes of the hypertrophied heart have been studied under conditions of stress caused by immobilization and possibility to correct these changes by means of thyroid hormones. The stress intensifies destructive lesions in a number of organelles++, which develop at a prolonged hypertrophy, decreases essentially the ratio mitochondria/myofibrils in section area. Small doses of the thyroid hormones protect the hypertrophied heart from the damaging effect of the stress: prevent the stress-induced+ decrease in the ratio mitochondria/myofibrils, as well as stimulate development of the regenerative-adaptive processes (increase in size and number of mitochondria and their crists, elements of the sarcoplasmic reticulum, glycogen granules, increase in section areas of their nuclei and chromatin in them). The thyroid hormones restrict essentially decrease in correlation of organelles++, resulted from hypertrophy. Thus, the stress-induced disturbances in ultrastructure of the hypertrophied heart can be prevent by means of the thyroid hormones, administered in small doses.

[The effect of thyroid hormones on the stress-induced changes in the coronary blood flow and contractile function of the hypertrophied heart]. / Vliianie tireoidnykh gormonov na stressornye izmeneniia koronarnogo krovotoka i sokratitel'noi funktsii gipertrofirovannogo serdtsa.

The effect of 6-hour immobilization stress on autoregulation and dilatation of the coronary vessels was studied in 54 hypertrophied hearts of female rats before and after thyroidin treatment. The coronary reserve and autoregulation were found to be decreased. Small doses of thyroidin increased the perfusion index, the gain of autoregulation and coronary reserve, and restricted the effect of stress on the coronary blood flow in hypertrophied heart.

[The dependence of the adaptive effect of brief stress exposures on the thyroid state of the body]. / Zavisimost' adaptatsionnogo éffekta korotkikh stressornykh vozdeistvii ot tireoidnogo statusa organizma.

The effectiveness of adaptation to short-term stresses with regard to the level of thyroid hormones was investigated in experiments on isolated hearts of 94 female rats. Adaptation to stress in euthyroid rats (daily immobilization for 15 days) prevented a 2-fold decrease in the blood concentrations of T3 and thyroxine, caused by 6-hour immobilization stress and determined by radioimmunoassay. In hypothyroid rats multiple sessions of short-term immobilization in itself caused a decrease in the coronary dilating reserve by 29%, in the maximum coronary blood flow developing after 60-second discontinuation of perfusion, by 31%, an increase in intraventricular diastolic pressure; subsequent 6-hour immobilization resulted in a further drop of the coronary reserve, maximum coronary blood flow and an increase in diastolic pressure. Thus the effect of preventing stress changes of the coronary blood flow and myocardial contractility by adaptation to short-term stresses depends on body thyroid function.