The Impact Of Vagus On The Monophasic Action Potential Of Ventricular Outflow Tract Myocardium In Dogs

Objective:Idiopathic ventricular tachycardia (IVT) occurs in patients without structural heart disease, metabolic disturbance, electrolyte distur-bance. IVT can seriously threat to human life and health. The most common original site of IVT is ventricular outflow tract. Clinically, vagal stimul-ation can terminate the occurrence of IVT. However, the role of the autonomic nervous on the mechanism of outflow tract ventricular tachy-cardia is still not clear. This study aimed to investigate the impact of vagus on the monophasic action potential (MAP) of ventricular outflow tract myocardium, and further to explaine the mechanism of IVT.Methods:Eight adult mongrel dogs were intubated and ventilated with a constant volume-cycled respirator (O2 saturation was kept above 95%), bilateral vagosympathetic (VS) tunks were decentralized for stimulation. The MAP recording electrode was inserted into the left ventricular outflow tract (LVOT) through the left femoral artery. Another two MAP recording electrodes were inserted into the right ventricular outflow tract (RVOT) and right ventricular apex (RVA) through the right femoral vein. Metoprolol was given to block sympathic effects. MAP and effective refractory period (ERP) were recorded at the LVOT, RVOT, RVA under baseline and vagal stimulation respectively. S2APD90, S2APD50 were measured at LVOT, RVOT and RVA. The sizes of vagal impact on LVOT, RVOT, RVA were difined by the subtraction of MAPD under the baseline and MAPD under the vagal stimulation. Results:1. The comparison of the MAP under vagal stimulation and basic state at the same siteGive decreasing S1S2 stimulus from 350/300ms, S2APD90 under vagal stimulation were significantly lower than S2APD90 under basic state (177.1±12.3ms vs 198.5±12.1ms, P<0.001 at RVOT; 159.1±16.7ms vs 168.5±15.1ms, P<0.001 at RVA; 176.7±6.7ms vs 202.4±7.3ms, P<0.001 at LVOT); S2APD50 under vagal stimulation were significantly lower than S2APD50 under basic state (141.4±10.5ms vs 155.4±11.5ms, P<0.001 at RVOT; 133.4±12.9ms vs 141.6±14.1ms, P<0.001 at RVA; 145.9±14.7ms vs 159.2±8.0ms, P<0.001 at LVOT). Give decreasing S1S2 stimulus from 300/250ms, S2APD90 under vagal stimulation were significantly lower than S2APD90 under basic state (165.4±12.5ms vs 177.8±13.5ms, P<0.001 at RVOT; 145.5±16.6ms vs 155.1±17.8ms, P<0.001 at RVA; 162.9±14.1ms vs 181.4±7.7ms,P<0.001 at LVOT); S2APD50 under vagal stimulation were significantly lower than S2APD50 under the basic state (137.1±11.1ms vs 146.3±11.7ms, P<0.001 at RVOT; 119.1±14.1ms vs 129.7±12.9ms, P<0.001 at RVA; 136.3±7.9ms vs 149.5±6.9ms, P<0.001 at LVOT). They suggested that the MAPD were significantly reduced when vagus was stimulated.2. The differences of the MAP at RVOT, LVOT, RVAGive decreasing S1S2 stimulus from 350/300ms, S2APD90 at RVOT, RVA and LVOT under basic state respectively:198.5±12.1ms,168.5±15.1ms, 202.4±7.3ms; S2APD50:153.3±11.7ms,141.6±14.1ms,159.5±6.9ms. S2APD90 at RVOT, RVA and LVOT under vagal stimulation respectively: 177.1±12.3ms,159.5±16.6ms,176.7±6.7ms; S2APD50:141.4±11.5ms, 132.7±13.6ms,145.8±14.7ms. Give decreasing S1S2 stimulus from 300/250ms, S2APD90 at RVOT, RVA and LVOT under basic state respectively: 177.3±14.1ms,155.7±17.5ms,181.8±7.3ms; S2APD50: 146.3±11.0ms,129.6±13.1ms,149.5±6.9ms. S2APD90 at RVOT, RVA and LVOT under vagal stimulation:165.6±12.3ms,145.5±18.1ms,162.3±12.9ms; S2APD50:137.1±11.5ms,119.1±14.6ms,136.6±7.5ms. The MAPD at RVOT and LVOT had no significant differences (P>0.05), but the MAPD at RVA were significantly different with that at RVOT and LVOT (P<0.05). They pointed out that the MAPD at outflow tract and RVA were significantly different at basic state, because the outflow tract and apex had different electrophysiological characteristics and anatomical structure. On the other hand, they also prompted the regulation of vagus at outflow tract might be different with that at apex.3. The differences in influencial sizes of vagus on the MAP at different positionsGive decreasing S1S2 stimulus from 350/300ms, the influencial sizes of vagus on S2APD90:14.8±5.5ms at LVOT,12.1±3.9ms at RVOT,8.3±4.1ms at RVA; on S2APD50:15.7±6.3ms at LVOT,14.1±3.2ms at RVOT, 9.4±3.9ms at RVA. Give decreasing S1S2 stimulus from 300/250ms, the influencial sizes of vagus on S2APD90:13.9±8.6ms at LVOT,12.6±4.3ms at RVOT,6.6±2.8ms at RVA; on S2APD50:13.6±3.7ms at LVOT,12.3±3.9ms at RVOT,7.1±3.4ms at RVA. The influential size of vagus at the outflow tract was more significant than that at RVA, the influential sizes at LVOT and RVOT had no significantly differences (P>0.05), but the influential sizes at the outflow tract was significant different with that at RVA (P<0.05), it suggested that the regulation of vagus at outflow tract might be stronger than that at apex.Conclusions:The MAPD were significantly reduced at outflow tract and RVA when vagus was stimulated. The impact of vagus on the MAP at ventricular outflow tract is more significant than that at RVA, which suggested that the regulation of the vagus at outflow tract might be stronger than that at apex, and might be related to the occurrence of IVT.