Xanthine-Xanthine oxidase ( X-XOD) added to the culture medium of cultured cardiac cells in rats may damage cell membrane. Electrophysiological findings indicated that APA, MDP, OS,Vmax, were decreased and the SDF was increased. Astragalus polysaccharide (APS) could protect the cells from being damaged by X-XOD. APS recoverted all the de-creased cardiac functional parameters in free-radical-damaged rats by X-XOD. APS had anti-free-radical damage action on the cultured my-ocardiocytes and the myocardial contractility of the isolated rat working heart.

Objective:Effects of oxymatrine on the sodium current were studied .Methods:The whole cell voltage clamp technique was used in isolated ventricular cells of guinea-pig.Results:Oxymatrine (0.1,0.3 and 1 mmol/L) showed inhibition to the sodium current in dose-dependence.Conclusion:These results indicate that inhibition of oxymatrine to the sodium current may be one of mechanisms of its antiarrhythmic action.

Objective:To analyse the property of voltage-dependent potassium 〔K(v)〕 channel in healthy people′s peripheral lymphocyte so as to contribute the control for property alteration under some pathological condition,and to try to find the new subset of this channel.Methods:Patch-clamp whole cell recording technique was used.Results:In the recorded 39 cells,activated voltage of the channels was -40.3±2.5 Mv.No inactivation phenomenon appeared under repeated stimulation.The closing time of the channels was 116.3+8.2 ms under the repolarization,and the current could be inhibited by 10 mmol/L TEA.Conclusion:There might be only one type of K(v) channel in human peripheral blood lymphocytes,and its properties quite resumble the type of n K(v) channel in mice.

Objective:To investigate the effect of the BmK-9-(2) on the sodium current in guinea-pigventricular myocytes. Methods:The whole cell patch-clamp technique was used. Results:The BmK-9-(2)increased the magnitude of the peak inward sodium current (27 ％) ,peak sodium conductace (17 %) and theprolong time course of sodium channel inactivation (8％) and there was no effects on calcium channels.Conclusion:BmK-9-(2) can activate sodium channel and prolong the inactivated course of myocytes.

Objective To investigate the effect and mechanism of sphingosine 1-phosphate(S1P)on action potential(AP)and voltage-dependent potassium current(KV)in isolated guinea pig ventricular myocytes.Methods The ventricular myocytes were isolated by using Langendorff perfusion method.The AP and KV were recorded by whole cell patch-clamp recording technique.Results S1P prolonged the 50% and 90% action potential duration(APD50 and APD90)and decreased KV which were blocked by pertussis toxin(PTX)or Calphostin C.Conclusion S1P decreased KV in a PKC pathway and prolonged action potential duration in guinea-pig ventricular myocytes.

OBJECTIVETo study the inhibition of voltage-activated K(+) conductance and cell proliferation by 4-aminopyridine (4-AP) in the human small-cell lung cancer (SCLC).

METHODSInhibition of voltage-activated K(+) current by 4-AP through the whole-cell patch-clamp technique in SCLC cell line was studied. The influence on the cell-cycle by 4-AP was observed by flow cytometry to identify the in vitro inhibition by 4-AP to the cell proliferation of the SCLC cell line.

RESULTSExposure of the tumor cells to 5 mmol/L 4-AP reduced the peak outward K(+) current (evoked by a depolarization to +80 mV) from 1.22 +/- 0.11 nA (n = 30) to 0.59 +/- 0.10 nA (n = 28). Flow cytometry results showed that cell population accumulated in the G(0)/G(1) phase and a significantly reduced proportion in the S phase and G(1)/G(2) phase cells after having been exposed to 4-AP for three days. Incubation of the SCLC cells with 0.1, 5, 10, 15, 20 mmol/L 4-AP resulted in a concentration-and time-dependent reduction in the number of viable cells as compared with the control.

CONCLUSIONThe voltage-activated K(+) channels expressed by SCLC play an important role in SCLC cell proliferation. The proliferation of the SCLC cells is inhibited by K(+) channel antagonists.

4-Aminopyridine ; pharmacology ; Carcinoma, Small Cell ; pathology ; Cell Division ; drug effects ; Humans ; Lung Neoplasms ; pathology ; Potassium Channel Blockers ; pharmacology ; Potassium Channels, Voltage-Gated ; antagonists & inhibitors ; metabolism ; Tumor Cells, Cultured