Stimulation of Epicardial Sympathetic Nerves at Different Sites Induces Cardiac Electrical Instability to Various Degrees

Figures

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  Figure 1. A diagram of the left ventricular anterior (a) and posterior (b) walls of a dog’s heart to show ES and electrophysiology-monitoring sites. LAD, left anterior descending coronary artery; LCX, left circumflex coronary artery; CS, coronary sinus; GCV, great cardiac vein; MCV, middle cardiac vein; SCV, small cardiac vein; LASV, left atrium slanting veins; VPVSC, vena-posterior-ventriculi-sinistri-cordis.

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  Figure 2. The Systolic Blood Pressure (SBP) was monitored after ES and β1-receptor blockade in PB, AS and AP groups. *p < 0.05, compared to NC group.

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  Figure 3. Ventricular effective refractory period (ERP) at the left ventricular anterior and posterior walls were measured after ES in PB, AS and AP groups. The animals in NC group didn’t undergo ES. *p < 0.05, compared to NC group.

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  Figure 4. Ventricular effective refractory period (ERP) at the left ventricular anterior and posterior walls was measured after administration of β1-receptor blocker. #p > 0.05, compared to NC group.

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  Figure 5. Density of sympathetic nerve fibers was demonstrated by IHC. ES at the PB site promoted the cardiac sympathetic nerves regeneration more obviously than other groups. Compared with untreated animals, ES at the AS and AP sites did not affect the density of TH positive nerve fibers in ventricular tissues. The density of sympathetic nerves numbers at PB site was highest among the observed sites. *p < 0.05 compared with NC group. &p < 0.05 compared with PB site. +p < 0.05 compared with AS site. Scale bars, 200 μm.

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  Figure 6. Density of parasympathetic nerve fibers was demonstrated by IHC. There was no difference in fiber density from base to apex. ES had no influence on the cardiac parasympathetic nerves regeneration among all experimental groups. Scale bars, 400 μm.