Electromechanical effects of urea on the isolated rat heart

Langendorff-perfused isolated hearts and left ventricle papillary muscles from 3-month old albino rats of both sexes were studied before and after a 30-min treatment with 17 mM urea added to the medium, a of urea were produced by an increase in tonicity, the study was repeated using 17 mM sucrose. Mechanical studies on the papillary muscles showed that isometric force development and its first time derivative decreased after washing out urea from the bath (F=9.73 ñ 1.02 g/mm2 to 7.47 ñ 0.72 and dF/dt=66.8 ñ 6.43 to 56.7 ñ 4.60 g (mm2)-1 s-1, respectively; P<0.05). Inotropic responses to isoproterenol and increased extracellular calcium after urea treatment reached values similar to those obtained before urea treatment. Thus, the effect of isoproterenol and calcium was stronger than that obtained before urea treatment. In Langendorff-perfused hearts, the spontaneous heart rate did not change after urea or sucrose treatment. Urea promoted a decrease in the left ventricle isovolumetric systolic pressure (39.7 ñ 4.05 to 26.1 ñ 2.69 mmHg, P<0.05) and a reduction of total QRS amplitude. In both papillary muscles and isovolumetric perfused hearts, contractile responses resulting from changes in extracellular sodium concentration were reduced after urea treatment. The increased osmolarity due to sucrose did not produce any changes in electromechanical activities. Although 17 mM, which reduces isometric force and isovolumic pressure development and modifies the ECG, is well below the concentration required to modify protein conformation in vitro, the present results suggest that its action could be explained by an effect at the sarcolemmal level

Propanolol reduces myocardial hypertrophy in the right cardiac chambers after infarction in rats

The effects of chronic propanolol (Prop) therapy on the post infarction myocardial hypertrophy of infarction rats were studied by histological techniques. male albino rats were submitted to left coronary artery ligation to produce infarction or to sham surgery (Con, N=6)., Infarction rats (Inf) were divided into 2 groups receiving Prop (2.5 mg/kg, twice a day, N+6) or saline (N=6) for one month, respectively. Myocyte diameters were measured in longitudinally oriented sections in the four heart chambers (60 cells/chamber). inf produced a significant increase in mean diameter of myocytes from the right atrium and ventricle and from the left atrium. In the right ventricle, myocyte diameter increased from 8.9 ñ 0.5 um in the Con group to 12.5 ñ 0.6 um in the the Inf group (P<0.05). Under Prop, myocyte diameter was reduced (P<0.05) to 9.8 ñ 0.9 um. Similar values were observed in the right atrium. In the left atrium, Prop produced only a partial reversion of the postinfarction hypertrophy. In the left ventricle, myocyte diameter was not significantly changed after Inf or Prop therapy. These data show that beta blockers reduce the myocardial hypertrophy in the right heart chambers after experimental infarcts in rats. This effect can be secondary to reduction of pulmonary hypertension or to blockade of direct effects of catecholamines on myocardial fibers or both