ABSTRACT
BACKGROUND:After acute myocardial infarction(AMI),there is still surviving myocardium in and around the infarcted area,which plays an important role in the occurrence of arrhythmia. OBJECTIVE:To study the alterations of the activities of Na+ channel current(INa),L-calcium current(ICa-L),transient outward K+ current(Ito) and inward rectifying K+ current(IK1) in the cardiomyocytes in the infarcted area after AMI. DESIGN: A randomized controlled study. SETTING:Department of Cardiology,Bethune International Peace Hospital. PARTICIPANTS:The experiment was finished in the Central Laboratory of the Department of Cardiology,Bethune International Peace Hospital from January to June 2003.Twenty New Zealand pure big-ear rabbits were randomly divided into AMI group(n=10) and control group(n=10). INTERVENTIONS:Rabbit AMI models were established by ligation of the left anterior descending coronary artery.The ventricular myocytes were separated with the method of enzymatic dissociation technique,and the changes of the ion currents were recorded with the whole cell patch-clamp techniques. MAIN OUTCOME MEASURES:The changes of INa,ICa-L,Ito and IK1 in the cardiomyocytes taken from the infarcted area of epicardium 24 hours after AMI in both the AMI and control groups. RESULTS:Twenty-four hours after AMI,the peak current densities of INa,ICa-L and IK1 in the AMI group [(28.48± 3.53) pA/pF,n=16;(3.91± 0.95) pA/pF,n=12;(26.93 ± 3.48) pA/pF,n=16]were all significantly reduced as compared with those in the control group [(45.50± 5.33) pA/pF,n=12;(5.58± 1.53) pA/pF,n=10;(34.12± 4.21) pA/pF,n=10] (t=3.026,P< 0.01;t=2.985,P< 0.01;t=2.706,P< 0.05).There was no significant difference in the Ito density between the AMI group and control group (P >0.05). CONCLUSION:The reduce of INa,ICa-L and IK1 caused by AMI can result in the decrease of myocardial conduction velocity,the shortening of action potential-time,abnormal repolarization,which is possibly the ionic mechanism for the reentrant ventricular arrhythmia after AMI.
ABSTRACT
Objective To determine the changes of L-type calcium currents(I Ca-L ) of rabbit ischemic myocytes in peri-infarcted zone.Methods Rabbit AMI models were made by ligation of branches of left coronary artery. After 1 week and 2 months, single pericardial myocytes were isolated enzymatically from ischemic zone adjacent to infarcted area and the normal control cells from similar regions in normal rabbit hearts. I Ca-L were recorded by using patch clamp techniques in the whole cell configuration. Results Peak of I Ca-L density of ischemic cells from the peri-infarcted zone was significantly reduced in AMI onc week later ( 3 52 0 93 pA/pF, n=6) compared to control cells ( 5 58 1 53pA/pF,n=10), P0 05 The steady-state inactivation curves were shifted to the hyperpolarizing direction in ischemic cells,the half-maximal voltage dependence of inactivation(V 1/2 ) in ischemic cells was 25 9 7 0 mV in AMI 1W , 21 3 5 6mV in AMI 2M and 13 1 4 2mV in the control cells(compared with control group,P
ABSTRACT
AIM: To study the current density of transient outward potassium current (I_(to)) in cells from the epicardial zone of the 1-week and 2-month infarcted rabbit heart. METHODS: Rabbits were infarcted by ligation of the left anterior descending coronary artery, 1 week as well as 2 months later, the single ventricular myocytes were isolated enzymatically from the infracted area of 1-week infracted rabbit heart (PMI-1 week) and 2-month infracted heart (PMI-2 months), region remote from the infracted zone of 2-month infracted heart (REM-2 months) and free wall of left ventricule from noninfarcted heart (CON). I_(to) was recorded using whole cell patch-clamp techniques. (RESULTS:) Membrane capacitance of myocytes in REM-2 months group was signifitantly larger than that in CON. I_(to)current density (at +60 mV) was significantly reduced in PMI-1 week [(7.5?2.4) pA/pF, n=12] and PMI-2 months [(10.6?4.1) pA/pF, n=18] compared with CON [(17.4?5.2) pA/pF, n=16], P
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AIM: To study the effect of experimental acute necrotizing pancreatitis (ANP) on sodium and L-type calcium current in rat cardiomyocytes. METHODS: I Na and I Ca-L were recorded using whole cell patch-clamp techniques from left ventricular myocytes in ANP model established by retrograde injection of 3 5% sodium taurocholate 2 5 mL/kg into pancreatic duct. RESULTS: Peak I Na current density (at -30 mV) was significantly reduced in ANP [(12 45?2 26) pA/pF, n =16] compared with sham [(25 32?3 31) pA/pF, n= 14], P
ABSTRACT
AIM: To study the current density and function of Na + channel in cells from the epicardial border zone of the 1-week infarcted rabbit heart. METHODS: Rabbits were infarcted by ligation of the left anterior descending coronary artery. 1 week later, I Na was recorded using whole cell patch-clamp techniques in ventricular myocytes from infarcted heart(IZs) and compared with the I Na from noninfarcted heart(NZs). RESULTS: Peak I Na current density(at -30 mV) was significantly reduced in IZs(22 48?4 62 PA/PF, n= 14) compared with NZs(45 50?5 33 PA/PF, n= 12), P