To investigate the effect of sea anemone toxin anthopleurin-Q (AP-Q) on potassium currents in isolated rats and guinea pig ventricular myocytes.Methods The ventricular cells of guinea pigs and SD rats were obtained by enzymatic dissociation method.Whole cell patch clamp technique was used to record potassium currents (Ito,IK,and IK1).Results AP-Q 3-100 nmol/L increased Ito in a concentration-dependent manner,with an EC50 value of 12.7 nmol/L.At a potential of +50mV,AP-Q 10nmol/L increased Ito from (13.3±3.4) pA pF-1 to (19.46±4.3) pA pF-1.AP-Q 0.1-100 nmol/L increased IK and IK tail in a concentration-dependent manner with EC50 values of 4.7 nmol/L and 5.0 nmol/L,respectively.AP-Q 1 pmol/L-100 nmol/L increased IK1 in dose-dependent manner,with an EC50 of 0.2 nmol/L.Conclusions The effect of AP-Q on Ito,IK and IK1 may partly explain its mechanism in shortening APD and increasing RP.(J Geriatr Cardiol 2008;5:243-247)

Objective To observe the effect of carvedilol on the expression of Cx43 in rabbits with myocardial infarction and its association with ventricular arrhythmia.Method Thirty-six rabbits were randomly divided into three groups in equal number(n=12),namely,myocardial infarction(MI)group,carvedilol group and sham MI group.Rabbits of carvedilol group were administered with carvedilol 5 mg kg~(-1)?d~(-1)after MI induced,while no carvedilol was administered to the MI group.The following observations were made:(1)Cx43 density of the epicardial border zone measured by quantitative immnuoconfocal laser scanning,and(2)cx43 protein expression analyzed by western blot.Results(1)Under immunoconfocal laser microscope,the relative density of Cx43 was(0.16?0.06)% in the infarction group and was(0.32?0.11)% in the sham MI group [(0.68?0.15)%,both P