Mechanical effects of liriodenine on the left ventricular-arterial coupling in Wistar rats: pressure-stroke volume analysis

1 In a recent in vivo study, liriodenine, an aporphine alkaloid, has been i dentified as a prominent anti-arrhythmic agent that can prevent rats' sudde n deaths, even at the dose as low as 10(-7) g kg(-1) The aim of this study was to determine whether liriodenine at its effective anti-arrhythmic dose of 10(-7) g kg(-1) had effects on the left ventricular (LV)-arterial coupli ng in Wistar rats. 2 LV pressure and ascending aortic flow signals were recorded to construct the ventricular and arterial end-systolic pressure-stroke volume relationsh ips to calculate LV end-systolic elastance (E-es) and effective arterial vo lume elastance (E-a), respectively. The optimal afterload (Q(load)) determi ned by the ratio of E-a to E-es was used to measure the optimality of energ y transmission from the left ventricle to the arterial system. 3 Liriodenine at the dose of 10(-7) g kg(-1) showed no significant changes in basal heart rate (HR), cardiac output (CO), LV end-systolic pressure (P- es), E-a, E-es, and Q(load). 4 By contrast, liriodenine at the dose of 10(-6) g kg(-1) produced a signif icant fall of 2.0% in HR and a significant rise of 5.8% in CO, but no signi ficant change in P-es. Moreover, liriodenine administration of 10(-6) g kg( -1) to rats significantly decreased E-es by 8.5% and E-a by 10.6%, but did not change Q(load). 5 We conclude that liriodenine at the dose of 10(-7) g kg(-1) has no effect s on the mechanical properties of the heart and the vasculature and the mat ching condition for the left ventricle coupled to its vasculature in rats. Even at 10 times the effective anti-arrhythmic dose, liriodenine shows no e ffects on the efficiency of energy transferred from the left ventricle to t he arterial system.