[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.

[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+.

[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.

[Thyroid hormones and the poststress changes in the contractile function and ultrastructure of the hypertrophic heart]. / Tireoidnye gormony i poststressornye izmeneniia sokratitel'noi funktsii i ul'trastruktury gipertrofirovannogo serdtsa.

The effect of thyroid hormones on stress-induced changes of contractility and ultrastructure of hypertrophied heart, was studied. Small doses of thyroid hormones enhanced the contractility of hypertrophied heart both under stress and without it, and decreased the changes of the Smch/Smf ratio during hypertrophy, preventing these changes during hypertrophy associated with stress.

[Disorders of cardiac contractile function and myocardial adrenoreactivity during stress depending on the thyroid hormone level]. / Narusheniia sokratitel'noi funktsii serdtsa i adrenoreaktivnost' miokarda pri stresse v zavisimosti ot urovnia tireoidnykh gormonov.

An effect of the administration of thyroid hormones at small doses (on the one hand) and hypothyroidism (on the other hand) on stress-induced changes of myocardial contractility and adrenoreactivity was studied in experiments on 86 random bred male rats. The use of thyroid hormones at small doses irrespective of a drug form prevents stress-induced decrease of cardiac contractility and preserves a sufficiently high level of myocardial adrenoreactivity. The suppression of thyroid function of the thyroid gland led to a decrease in adrenoreactivity and caused more profound disorder of contractility in stress. All these data suggest that physiological doses of thyroid hormones prevent cardiac contractility disorders and preserve sufficiently high myocardial adrenoreactivity.

[Thyroid hormone prevention of disorders of cardiac contractile function during stress]. / Preduprezhdenie tireoidnymi gormonami narushenii sokratitel'noi funktsii serdtsa pri stresse.

The depression of cardiac contractility has been observed in rats during the immobilized stress in state of relative physiological rest and maximal load. In the animals pretreated with thyroid after stress the indexes of intensity and rate of myocardial contraction and relaxation didn't differ from the control, and during the maximal load the myocardium was characterized by the less expressed decrease of the structure functioning intensity and the higher rate of relaxation. The data obtained show that the physiological doses of thyroid hormones prevent the myocardium from contractile disorders during stress.

[Myocardial damage during immobilization stress and the protective effect of thyroid hormones]. / Povrezhdenie miokarda pri immobilizatsionnom stresse i zashchitnyi éffeckt tireoidnykh gormonov.

In the experiments performed on 30 white inbred male rats, the stress produces an essential increase of dilated canals in the T-system and sarcoplasmic reticulum, lesions of sarcolemma and nucleolemma, fragmentation and homogenization of mitochondrial cristae; there are many pinocytic vesicles in the capillary walls. Preliminary injection of thyroid hormones in small doses, that do not result in any noticeable influence on the body mass, cardiac contraction rate and thyrotoxin concentration in blood serum, at the stress causes less pronounced changes in ultrastructure of cardiomyocytes, demonstrating as a poor swelling of the T-system elements, preservation of the sarcolemmic integrity at its larger length; besides, large mitochondria with compact arrangement of cristae appear, amount of the sarcoplasmic reticulum elements increases, chromatin margination becomes evident, i. e. a complex of adaptive processes develops. The data presented demonstrate a defensive role of physiological concentrations of the thyroid hormones under the stress.

[Stress-induced changes in the area ratio or the quantitative ratio of myocardial mitochondria and myofibrils and their correction with thyroid hormones]. / Stressornye izmeneniia sootnosheniia ploshchadei ili kolichestvennogo sootnosheniia mitokhondrii i miofibrill miokarda i ikh korrektsiia tireoidnymi gormonami.

An experimental study performed on 30 male white rats has demonstrated that immobilization stress was associated with a decrease in mitochondrial to myofibril area ratio (Smch/Smf) in the left ventricle and interventricular septum by 34.6% and 46.9%, respectively. Pretreatment with small doses of thyroid hormones which did not influence body weight, heart rhythm or serum thyroxin level prevented the decrease and caused Smch/Smf increase in the left ventricle and interventricular septum by 68.7% and 45.8%, respectively. The doses of thyroid hormones applied caused a more marked increase of mitochondrial to myofibril area ratio in the control rats.