Milrinone increased Ca(2+)-ATPase activity more in heart failure than in control (+19% vs. +11%, P<0.05), contributing to the preservation of positive lusitropy.
Absolute Event Rate: 19% vs 11%
p-value: p=<0.05
In tachycardia-induced heart failure (HF), positive lusitropic effects of milrinone or dobutamine were assessed by evaluating the time constant of left ventricular (LV) pressure decay (tau) and Ca(2+)-ATPase activity of the sarcoplasmic reticulum (SR). The peak value of the positive first derivative of LV pressure (+dP/dt) was less increased, either by dobutamine (2-10 microg x kg(-1) x min(-1)) or by milrinone (4-20 microg/kg), in HF than in control (P < 0.05), whereas tau was shortened to an extent similar to that in control with dobutamine P = not significant (NS) and to an even greater extent with milrinone (P < 0.05). Ca(2+)-ATPase activity increased similarly in HF and control with dobutamine (1 microM; +11% in HF vs. +12% in control, P = NS), whereas it increased more with milrinone (1 microM; +19% in HF vs. +11% in control, P < 0.05). Ca(2+)-ATPase activity-cAMP relationships were shifted to the left by milrinone or dobutamine in HF compared with control. Thus, in HF, the sensitivity of Ca(2+)-ATPase activity to cAMP was increased on addition of cAMP-dependent inotropic agents, contributing to the preservation of positive lusitropy.
Tanigawa et al. (Tue,) conducted a other in Tachycardia-induced heart failure. Milrinone or dobutamine vs. Control was evaluated on Increase in Ca(2+)-ATPase activity with milrinone (1 microM) (p=<0.05). Milrinone increased Ca(2+)-ATPase activity more in heart failure than in control (+19% vs. +11%, P<0.05), contributing to the preservation of positive lusitropy.