Abstract: AIM: To investigate the electrophysiological alteration of ventricular myocardium in goats with acute stress and metoprolol intervention and to explore the mechanism and prophylactic method of stressful ventricular arrhythmia. METHODS: Fifteen male goats were randomly divided into control group, acute stress group and metoprolol group. Complex stimuli were used to induce acute stressful reactions in goats. Plasma epinephrine and norepinephrine concentrations were measured by high-performance liquid chromatography. Monophasic action potential (MAP) of three slices of left ventricular myocardium was recorded with self-made complex electrodes. MAP90 and MAPd90 (transmural dispersion of repolarization) were also measured. RESULTS: Compared with those in control goats, plasma epinephrine and norepinephrine concentrations in acute stress and metoprolol group increased progressively with elongation of the stimulation. MAP90 of left ventricular mid-myocardium displayed an elongating trend in contrast to epimyocardium and endomyocardium in all groups. MAPd90 of left ventricular myocardium significantly increased in acute stress goats (P<0.01). However, MAPd90 of left ventricular myocardium of metoprolol group decreased significantly in contrast with acute stress goats (P<0.01). CONCLUSION: Complex stimuli induced significant acute stress reaction in goats. Myocardium of left ventricular mid-myocardium displays some unique electrophysiological properties. Acute stress significantly increases the transmural dispersion of repolarization, which may be correlated with ventricular arrhythmia. β adrenergic receptor antagonist can counteract the effect.