论文部分内容阅读
AIM: To investigate the effect of β-blockers on spatial dispersion of ventricular repolarization following acute myocardial ischemia. METHODS: Twenty sheep were randomized into control (normal saline, iv) and atenolol (1.5 mg/kg, iv) group. Acute myocardial ischemia was induced by occlusion of the obtuse marginal coronary artery. Unipolar ECG was simultaneously acquired from 64 epicardial sites in both ischemic and non-ischemic regions. Activation-recovery intervals (ARI), an index of ventricular repolarization, was determined from the epicardial ECG. The difference between the longest and shortest ARI was defined as ARI dispersion. RE-SULTS: Ischemic zone in atenolol group was less than that of control group (13 % ± 2 % vs 19 % ± 3 % , P - 0.04). In the control group, pooled ARI dispersion was increased by (18 ± 21), (27 ± 21), and (16 ± 10) ms at 30, 60, and 90 min of coronary artery occlusion respectively (P < 0.01), whereas in the atenolol group, ARI dispersion was only increased by (6 ± 4),
A: To investigate the effect of β-blockers on spatial dispersion of ventricular repolarization following acute myocardial ischemia. METHODS: Twenty sheep were randomized into control (normal saline, iv) and atenolol (1.5 mg / kg, iv) was induced by occlusion of the obtuse marginal coronary artery. Unipolar ECG was simultaneously acquired from 64 epicardial sites in both ischemic and non-ischemic regions. Activation-recovery intervals (ARI), an index of ventricular repolarization, was determined from the epicardial ECG. The difference between the longest and shortest ARI was defined as ARI dispersion. RE-SULTS: Ischemic zone in atenolol group was less than that of control group (13% ± 2% vs 19% ± 3%, P - 0.04). In the control group, pooled ARI dispersion was increased by (18 ± 21), (27 ± 21), and (16 ± 10) ms at 30, 60, and 90 min for coronary artery occlusion respectively atenolol group, ARI dispersion was only incre ased by (6 ± 4),