Endocardial endothelium and myocardial performance in rats: effects of changing extracellular calcium and...

It is known that endocardial endothelium (EE) modulates the performance of its subjacent myocardium. However, one species where these effects have been more difficult to describe is the rat. As the rat is a species which is used to evaluate the contractile effects of various pathologic conditions, a better appreciation of the contractile effects of EE and its modulatory role on the contractile effects of inotropic substances is important. In this study, the contractile effects of increasing extracellular calcium concentrations (0.7 mM to 3.25 mM) and phenylephrine (10(-7) to 10(-4) M) on rat papillary muscles with intact endocardial endothelium (EE on) and after endocardial endothelial removal (EE off) were assessed. At 0.7 mM extracellular calcium concentration, endocardial endothelial removal decreased all measured indices of myocardial performance (P < 0.05 EE on v EE off), except for maximum rate of unloaded muscle shortening (Vmax) which did not change, and decreased time to peak tension development (TTPT) as well as shortening of time to half tension decline from peak tension (RT1/2) shortening. Increasing extracellular calcium concentration from 0.7 mM to 3.25 mM caused all indices of myocardial performance and RT1/2 to increase more in muscles without EE, such that at 2.5 mM extracellular calcium all differences between EE on and EE off had disappeared. The only exception was TTPT which decreased with increasing extracellular calcium concentrations in muscles with EE on but increased in muscles with EE off. Again, at 2.5 mM extracellular calcium concentration differences in TTPT between EE on and EE off had disappeared. Except for minor differences on TTPT, increasing phenylephrine concentrations had similar contractile effects on muscles with EE on and EE off. These results indicate that EE modulates rat myocardial contraction and that these effects are best observed at lower extracellular calcium concentrations (0.7 mM). They also indicate that EE does not appear to significantly modulate the myocardial effects of alpha-adrenergic agonists in the rat.