This study evaluated right ventricular (RV) and left ventricular (LV) diastolic tolerance to afterload and SERCA2a, phospholamban and sodium-calcium exchanger (NCX) gene expression in Wistar rats. Time constant and end diastolic pressure-dimension relation (EDPDR) were analyzed in response to progressive RV or LV afterload elevations, induced by beat-to-beat pulmonary trunk or aortic root constrictions, respectively. Afterload elevations decreased LV-, but increased RV-. Whereas LV- analyzed the major course of pressure fall, RV- only assessed the last fourth. Furthermore, RV afterload elevations progressively upward shifted RV EDPDR, whilst LV afterload elevations did not change LV-EDPDR. SERCA2a and phospholamban mRNA were similar in both ventricles. NCX-mRNA was almost 50 % lower in RV than in LV. Left ventricular afterload elevations, therefore, accelerated the pressure fall and did not induce diastolic dysfunction, indicating high LV diastolic tolerance to afterload. On the contrary, RV afterload elevations decelerated the late RV pressure fall and induced diastolic dysfunction, indicating small RV diastolic tolerance to afterload. These results support previous findings relating NCX with late Ca2+ reuptake, late relaxation and diastolic dysfunction.
The left ventricular isovolumic pressure decay, obtained by cardiac catheterization, is widely characterized by the time constant τ (tau) of the exponential regression p(t)= P¥+(P0–P¥)exp(–t/τ). However, several authors prefer to prefix P¥=0 instead of coestimating the pressure asymptote empirically; others present τ values estimated by both methods that often lead to discordant results and interpretation of lusitropic changes. The present study aims to clarify the relations between the τ estimates from both methods and to decide for the more reliable estimate. The effect of presetting a zero asymptote on the τ estimate was investigated mathematically and empirically, based on left ventricular pressure decay data from isolated ejecting rat and guinea pig hearts at different preload and during spontaneous decrease of cardiac function. Estimating τ with preset P¥=0 always yields smaller values than the regression with empirically estimated asymptote if the latter is negative and vice versa. The sequences of τ estimates from both methods can therefore proceed in reverse direction if τ and P¥ change in opposite directions between the measurements. This is exemplified by data obtained during an increasing preload in spontaneously depressed isolated hearts. The estimation of the time constant of isovolumic pressure fall with a preset zero asymptote is heavily biased and cannot be used for comparing the lusitropic state of the heart in hemodynamic conditions with considerably altered pressure asymptotes.