Nitric oxide mediates the vagal protective effect on ventricular fibrillation via effects on action potential duration restitution in the rabbit heart.

摘要: We have previously shown that direct vagus nerve stimulation (VNS) reduces the slope of action potential duration (APD) restitution while simultaneously protecting heart against induction ventricular fibrillation (VF) in absence any sympathetic activity or tone. In current study we examined role nitric oxide (NO) effect VNS. Monophasic potentials were recorded from a left epicardial site on innervated, isolated rabbit hearts (n = 7). Standard restitution, effective refractory period (ERP) and VF threshold (VFT) measured at baseline during VNS presence NO synthase inhibitor N(G)-nitro-L-arginine (L-NA, 200 microm) reversing blockade with L-arginine (L-Arg, 1 mm). Data represent mean +/- S.E.M. The curve was shifted upwards became less steep when compared to baseline. L-NA blocked whereas L-Arg restored maximum reduced 1.17 0.14 0.60 0.09 (50 5%, P < 0.0001) control, 0.98 0.93 0.12 (2 10%, NS) 1.16 0.17 0.50 0.10 (41 9%, 0.003) plus L-NA. ERP increased by control 119 6 ms 130 (10 0.045) this increase not affected (120 4 133 ms, 11 3%, 0.0019) (114 123 8 2%, 0.006). VFT 3.0 0.3 5.8 0.5 mA (98 12%, 0.0017) 3.4 0.4 3.8 (13 0.6) perfusion 2.5 6.0 0.7 (175 50%, Direct flattened APD preparation intact autonomic nerves. These effects using reversed replenishing substrate for production L-Arg. This is first demonstrate plays an important anti-fibrillatory ventricle, possibly via restitution.