Mingwei Bao | PubMed Health

PubMed2006

Abnormal intracellular calcium handling underlying T-wave alternans and its hysteresis.

AIMS: To investigate the mechanism underlying T-wave alternans (TWA) and its hysteresis under ischemia conditions. METHODS: Transmembrane action potential (AP) from endocardial, M, and epicardial cells and monophasic AP (MAP) from four epicardial sites were recorded in ventricular wedge preparation and in isolated intact rabbit heart, respectively. The AP/MAP duration (APD/ MAPD), effective refractory period (ERP), activation time, and APD/MAPD restitution were determined under control and ischemia conditions. The effects of ryanodine (0.01 and 1 micromol x l(-1)) on TWA, and the effects of low extracellular Ca2+ and 4-aminopyridine on its hysteresis were studied. RESULTS: Ischemia shortened the APD/MAPD and effective refractory period of all recording sites symmetrically, except the APD of M cells, which shortened markedly. In the ischemia group, TWA was induced within a cycle length (CL) range from 160 to 250 ms, which corresponded to a diastolic interval region of 0-70 ms. In this diastolic interval region, the repolarization restitution curve was the steepest (slope > 1.0). All TWA were accompanied by repolarization alternations. Low concentration ryanodine (0.01 micromol x l(-1)) facilitated TWA, high concentration (1 micromol x l(-1)) abolished it. Alternans of calcium transient were observed in myocytes purfused with ischemia solution during rapid stimulation. Ryanodine (0.1 micromol x l(-1)) abolished alternans of calcium transient, and ryanodine (0.01 micromol x l(-1)) facilitated them. After 60 min pacing at a CL of 200 ms, TWA persisted until the initial several beats at a CL of 300 ms at which a TWA was exceptional. The suppression of hysteresis by low extracellular Ca2+ and 4-aminopyridine indicated an underlying role of the intracellular Ca2+ overload and transient outward current (I(to)). CONCLUSION: TWA is principally due to repolarization alternans, which is secondary to steep APD/MAPD restitution, and relates to intracellular calcium cycling. Hysteresis relates to intracellular Ca2+ overload and I(to).

4-Aminopyridine↗

PubMed2004

Differences in the changing trends of monophasic action potential duration and effective refractory period of the ventricular myocardium after myocardial infarction in vivo.

BACKGROUND: The relationship between monophasic action potential duration (MAPD) and effective refractory period (ERP) is poorly understood after myocardial infarction (MI) in vivo. METHODS AND RESULTS: Forty rabbits were randomized into either a sham operation (SO) group (n=10) or MI group (n=30), both of which underwent thoracotomy, but the left anterior descending coronary artery was occluded in the MI group only. The MAPD and ERP of the endocardial, midmyocardial and epicardial cells of the infarction zone were observed at baseline, 2 days after thoracotomy and then 5 min, 15 min, 30 min, 2 days, 14 days and 60 days after coronary occlusion (CO). At baseline, ERP correlated strongly with MAPD90. During the 5-30 min after CO, both MAPD90 and ERP of the 3 layers of the myocardium shortened markedly (eg, MAPD90 Mid) was approximately 50% of the baseline value at 5 min after CO). MAPD90 and ERP recovered gradually over the 2-60 days after MI. ERPMid exceeded MAPD90 Mid and the post repolarization refractoriness phenomenon appeared during the 5-30 min after CO. CONCLUSIONS: The different changing trends of the MAPD and ERP of the mid-myocardial cells may underlie the arrhythmias that occur after MI.

Action Potentials↗