ABSTRACT
Effect of aspirin (1.2 mg/100 g body wt orally for 30 days) on myocardial infarction induced by isoproterenol (200 mg/kg body wt, subcutaneously for 2 days) has been studied in rats using activities of creatine kinase, aspartate amino transaminase, alanine amino transaminase and lactate dehydrogenase and levels of lipid peroxides as standard markers. Aspirin treatment is found to counteract the effect of isoproterenol on lipid peroxide formation and associated enzyme changes in serum and heart.
Subject(s)
Administration, Oral , Animals , Aspirin/administration & dosage , Creatine Kinase/analysis , Isoproterenol/antagonists & inhibitors , L-Lactate Dehydrogenase/analysis , Lipid Peroxides/analysis , Male , Myocardial Infarction/chemically induced , Myocardium/enzymology , Pilot Projects , Rats , Transaminases/analysisABSTRACT
The circulatory effects of norepinephrine (4 * g/kg) and phenylephrine (20 */kg) were determined in anesthetized dogs withnormal plasma magnesium and with induced hypermagnesemia. Norepinephrine caused a 24% increased in heart rate by 103% increase in the systemic vascular, resistance index in normomagnesemic dogs, while with hypermagnesemia the variations were of 13% and 1%, respectively. Isoproterenol increased heart rate by 485 and 185 in dogs with normo- and hypermagnesemia, respectively.Phenylephrine increased the systemic vascular resistance index (74%) only in the normomagnesemic state.The effects of all the drugs were significantly defferent (P<0.01), without and with the simultaneous administration of magnesium sulfate (plasma magnesium, 1.3ñ0.2mEq/l and 6.8ñ1.1 mEq/l, respectively).We conclude that acute induced hypermagnesemia antagonizes the circulatory effects of adrenergic stimulation, a fact that may explain its antiarrhythmic and hemodynamic effects during acute myocardial ischemia
Subject(s)
Dogs , Animals , Hemodynamics/drug effects , Isoproterenol/antagonists & inhibitors , Magnesium/blood , Norepinephrine/antagonists & inhibitors , Phenylephrine/antagonists & inhibitors , Calcium/metabolism , Coronary Disease/physiopathologyABSTRACT
Mediante la desaferentación sinoaórtica (DSA) se obtiene un adecuado modelo de hipertensión neurógena en el que ocurren cambios del tono simpático que determinan una hipertensión considerada lábil. Se estudió la respuesta de los receptores beta cardiovasculares luego de la DSA por estimulación con el agonista beta adrenérgico isoproterenol en ratas despiertas. La DSA no afectó significativamente la hipotensión desarrollada por el isoproterenol a las pocas horas o a los 7 días de la operación en presencia o no de hexametonio. En cambio, el aumento de frecuencia cardíaca producido por isoproterenol a las pocas horas de la DSA es significativamente menor que en los animales sham; a la semana la respuesta es similar a la de las seudooperadas. El pretratamiento con hexametonio previene el efecto observado a las pocas horas de la operación y no modifica la respuesta cronotrópica del isoproterenol a los 7 días. Se postula que la menor respuesta al agonista beta adrenérgico en ratas con DSA en las primeras horas postoperatorias se debería a una subsensibilidad de los receptores beta adrenérgicos miocárdicos causada por el aumento del tono simático y adrenal, ya que el bloqueo del mismo con hexametonio previene el efecto. La DSA subsensibilizaría, los receptores beta adrenérgicos cardíacos, sin afectar los vasculares
Subject(s)
Rats , Animals , Male , Female , Hexamethonium Compounds/pharmacology , Hypertension/etiology , Isoproterenol/pharmacology , Sinus of Valsalva/innervation , Sympathectomy , Blood Pressure/drug effects , Denervation , Efferent Pathways/drug effects , Heart Rate/drug effects , Isoproterenol/antagonists & inhibitorsABSTRACT
Lauric, Myristic and Palmitic acids had no appreciable effect whereas Stearic, Oleic and Linoleic acids caused some reduction in dog blood pressure. Pressor responses to epinephrine and nor-epinephrine were potentiated whereas the depressor response to isoproterenol was reduced during the infusion of fatty acids in dogs. ACTH alone, which causes mobilization of free fatty acids had no appreciable effect on blood pressure responses to catecholamines, however, its administration followed by salicylate produced marked potentiation of the pressor responses to epinephrine and nor-epinephrine; the depressor response to isoproterenol was reduced.