RESUMEN
Synthetic radioinert androgen methyltrienolone administered daily for 2 weeks to male rats with severe diabetes led to a sharp increase in blood testosterone and was accompanied by reduction in glucose level due to an increase in tissue sensitivity to insulin. Normalization of plasma testosterone concentration contributed to saturation of active androgen receptors in the myocardium with testosterone; the number of free receptors decreased by 1.8 times. Testosterone that diminishes the catabolic effects of glucocorticoids improved the state of the myocardium, which was confirmed by activation of DNA and RNA synthesis.
Asunto(s)
Anabolizantes/uso terapéutico , Diabetes Mellitus Experimental/tratamiento farmacológico , Metribolona/uso terapéutico , Miocardio/metabolismo , Testosterona/sangre , Anabolizantes/farmacocinética , Animales , Glucemia/análisis , Corticosterona/sangre , Replicación del ADN , Diabetes Mellitus Experimental/metabolismo , Diabetes Mellitus Experimental/fisiopatología , Estradiol/sangre , Hormona del Crecimiento/sangre , Corazón/efectos de los fármacos , Insulina/sangre , Resistencia a la Insulina , Masculino , Metribolona/farmacocinética , ARN/biosíntesis , Ratas , Receptores Androgénicos/metabolismo , Testosterona/metabolismo , Distribución TisularRESUMEN
Using 20 male rats the electron microscopic study of conducting system of the heart was performed to assess the effect of fluorouracil--an antineoplastic drug belonging to antimetabolite group. A daily dose of 15 mg/kg of fluorouracil was injected intraperitoneally for 5 days; three courses of injections with the intervals of three weeks were performed. Toxic effect of fluorouracil is demonstrated after the first course of injections and is revealed as a predominant injury of pacemaker cells in sinoatrial and atrioventricular nodes. Latent pacemaker myocytes and Purkinje fibers undergo "calcium injury" during the second and the third courses of fluorouracil injections. The irreversible damage of contractile and specialized myocytes results in fibrosis which develops predominantly in the areas of atrioventricular bundle and its branches.
Asunto(s)
Antimetabolitos Antineoplásicos/toxicidad , Fluorouracilo/toxicidad , Sistema de Conducción Cardíaco/efectos de los fármacos , Sistema de Conducción Cardíaco/ultraestructura , Animales , Nodo Atrioventricular/efectos de los fármacos , Nodo Atrioventricular/ultraestructura , Capilares/efectos de los fármacos , Capilares/ultraestructura , Vasos Coronarios/efectos de los fármacos , Vasos Coronarios/ultraestructura , Citoplasma/efectos de los fármacos , Citoplasma/ultraestructura , Inyecciones Intraperitoneales , Masculino , Microscopía Electrónica , Ramos Subendocárdicos/efectos de los fármacos , Ramos Subendocárdicos/ultraestructura , Ratas , Nodo Sinoatrial/efectos de los fármacos , Nodo Sinoatrial/ultraestructuraRESUMEN
The protective action of the 2nd type neuroleptanalgesia (NLA) preparations on the damaged myocardium in experimental infarction complicated by cardiogenic shock is documented and analysed. The use of NLA within the first 5 days of the infarction complicated by cardiogenic shock decreased the intensity of the myocardial damage in the zone around the infarction and prevented necrotic changes in teh "extra-infarction" myocardium. Consequently, cardiosclerosis developing after the infarction had a smaller size and at a lesser degree decreased the contractile capacity of the heart muscle and its energy supply. The protective influence of NLA on the myocardium in cardiogenic shock is brought about through the action of the preparations on the various pathogenetic components of shock upon which the size of the myocardial damage depends.