The Inhibitory Effects Of PNS On Cardiac Hypertrophy And Its Nervus Mechanism

Aim: To study the effect of total saponins of panax notoginseng (PNS) on Stellate ganglion (SG) ' s synaptic transmission, investigate the antagonistic action of PNS on cardiac hypertrophy and its nervus mechanism. Method: (1) Noradrenaline(NA) was induced in the primary culture of neonatal rat cardiac myocyte , 0. 1 10-3g/ml, 0. 5 10-3g/ml PNS were given in the cultured cardiac myocyte at the same time, a week later , the cell surface area and protein content (used as the index of cardiac myocyte hypertrophy) were measured with or without PNS . (2)An animal model of rat with cardiac hypertrophy was established by constricting of abdominal aorta for three weeks. The control group are sham operated , the other three groups are aorta-constricted group, low PNS concentration group(lOOmg/kg/d) and high PNS concentration group(150mg/kg/d) .three weeks later , measured the body-weights of all the rats , then killed the rats and took out their hearts immediately to measure the heart-weight(HW), left ventricular weight(LVW) , the ratio of HW/BW and LVW/BW (LVI).then after dyeing by HE color , measured the cardiomyocyte diameters (MD). (SHntracellular recording techniques were used to investigate the effects of PNS on the fast excitatory postsynaptic potential(f-EPSP), after hyperpolarization potential (AHP), membrane depolarization by application of acetylcholine (Ach) ,. membrane potential and membrane resistance in SG. Result: (1) PNS reduce the increasings of cell surface area and protein content induced by Noradrenaline. (2)The LVI and MD of aorta-constricted group were significantly higher than that of the control group, so the animal model with cardiac hypertrophy wasestablished successfully. The LVI and MD of high PNS concentration groupwere significantly lower than that of the aorta-constricted group, so PNS could depress cardiac myocyte hypertrophy of abdominal aorta -constricted rats at the concentration of 150mg/kg/d. (3)At the concentration of 0.1 10-3~0.16 10-3g/mL, PNS reversibly depressed the fast excitatory postsynaptic potential (f-EPSP) and the after hyperpolarization potential(AHP) , but not altered the membrane depolarization by application of acetylcholine (Ach), The membrane potential and membrane resistance were not significantly altered by PNS. Conclusion: PNS can prevent cardiac myocyte hypertrophy of rat, the effects may be related to its action of inhibition on synaptic transmission in SG via blocking plasma membrane calcium influx.