| Late sodium current, also known as persistent sodium current, means the voltage clamp after depolarization within a few hundred milliseconds of the activities of sodium channel current. It is in the maintenance of action potential plateau and decided action potential duration and the inter-ventricular dispersion of repolarization play an important role.In recent years a large number of studies have shown that myocardial ischemia and hypoxia in the process, increased late sodium current has a close relationship with the arrhythmia. Late sodium current in the following areas mainly affected by heart rate: First of all, the platform of the increase in Na + influx, and subsequent cell in order to maintain its steady-state balance and stimulate the reverse NCX induced Ca2 + influx, have increased the platform of the net inward current and delayed repolarization, prolong the APD. APD extension and intracellular Ca2 + concentration increased, the ventricular muscle cells EADs provide possible easily lead to reentrant arrhythmias. Second, the increased late sodium current induced by intracellular Ca2 + concentration the increased tension caused by increased cardiac, slow ventricular initiative to relax, thereby increasing myocardial oxygen consumption, resulting in further deterioration of left ventricular function. Third, the ventricular muscle of different cells increased late sodium current in the different levels of normal and ischemic ventricular myocytes increased late sodium current caused by the different levels of inter-regional dispersion of repolarization increased offer for the reentrant arrhythmias conditions.Therefore, anything that can lead to increased late sodium current and caused the regional differences between the late sodium current factors can impact on arrhythmias. Inhibit the late sodium current increased and decreased regional differences between the late sodium current factor can be inhibited to varying degrees from arrhythmia.Membrane phospholipids of biological material is one of the important components of their life activity in the cell plays an important role. sphingosine- 1-phosphate(S1P) is the most recent scholars attach great importance to a phospholipids metabolism, with a wide range of biological effects, including inhibition of apoptosis, induction of vascular endothelial cell proliferation and migration and involved in immune regulation, bone growth and development, regulation of angiogenesis, and metastasis of tumors and so on.Myocardial infarction on the one hand due to increased phospholipase activity of S1P increased cell membrane phospholipid metabolism; the other hand, platelet aggregation and activation, more S1P is released into the local organization. Are reported in the literature, coronary heart disease and serum S1P levels and coronary stenosis severity is positively correlated.This paper uses a variety of experimental methods to study it, to further explore the S1P myocardial cells in ischemia and hypoxia play a biological role, and to find possible S1P heart protection mechanism.1. The effect of S1P to the state of hydrogen peroxide damage in guinea pig cardiac late sodium currentWhole-cell patch clamp technique with different concentrations of S1P on the coronary artery ligation induced myocardial ischemia late sodium current.Infarction ventricular myocytes Department late sodium current compared with the normal myocardial cells had higher (P <0.05), the effect of this increase can be 2μmol / L of TTX inhibited (P <0.05). When given the low concentrations of exogenous S1P to the time of infarction ventricular myocytes Department late sodium current did not affect (P> 0.05), high concentration and the concentration of S1P may inhibit ventricular infarction Department late sodium current increased (P <0.05 ).2. The effect of S1P to two-weeks acute myocardial infarction rat ventricular myocytes late sodium currentWhole-cell patch clamp technique with different concentrations of S1P on the coronary artery ligation induced myocardial ischemia late sodium current.Infarction ventricular myocytes Department late sodium current compared with the normal myocardial cells had higher (P <0.05), the effect of this increase can be 2μmol / L of TTX inhibited (P <0.05). When given the low concentrations of exogenous S1P to the time of infarction ventricular myocytes Department late sodium current did not affect (P> 0.05), high concentration and the concentration of S1P may inhibit ventricular infarction Department late sodium current increased (P <0.05 ). 3. The effect of S1P to hydrogen peroxide damaged guinea pig ventricular myocytes action potentialUsing whole cell patch clamp current clamp mode of different concentrations of S1P on the damage caused by hydrogen peroxide the role of APD.2μmol / L TTX induced by hydrogen peroxide could prolong the APD was significantly shorter (P <0.01), Vmax improve (P <0.05). However, no significant effect on the APA (P> 0.05). High concentrations of S1P can APD further reduced, and so as APD50 and APD90。These results suggest that high concentrations of S1P may inhibit the late sodium current increased, inhibition of plateau Na + influx and increased late sodium current caused by reverse NCX caused by calcium influx, reduced the APD and the consequent possible of EADs might inhibit the incidence of reentrant excited.In addition, when exogenous to the high concentration of S1P, the infarcted part of the late sodium current in cardiac cells and normal cells tend to value close, suggesting that S1P may inhibit the myocardium increased late sodium current, late of myocardial tissue differences tended to increase in the same sodium current, reduces the dispersion of repolarization, resulting in anti-arrhythmic effect.Experimental results show:1. External source to 10μmol / L of S1P and 1μmol / L of S1P may reduce coronary artery ligation in rats caused by ventricular infarction in part of the late sodium current cell.2. External source to 10μmol / L of S1P and 1μmol / L of S1P can reduce hydrogen peroxide induced guinea pig ventricular myocytes in the late sodium current.3. Exogenous to 10μmol / L of S1P and 1μmol / L of S1P induced by hydrogen peroxide can reduce the extension of the APD50 and APD90. This role was to give exogenous late sodium current blocker TTX similar effects.
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