Effect Of Autonomic Nervous System On The Transmural Dispersion Of Effective Refractory Period Of Acute Myocardial Infraction Across The In Vivo Rabbit Left Ventricular Wall

Arrhythmia is the common clinical manifestation of angiocardiopathy . It can cause hemodynamic compromise and thromboembolism in arrhythmia, even lead to death in direct . In recent years ,it has been paid increasingly attention in arrhythmia .People realize that ANS release many neurothransmitters to affect corresponding and regulate the activity of some ion channels which influence the electricity activity of the cardiac myocytes induce the arrhythmia by reentry and trigger activity or enhanced automaticity.Electrophysiological heterogeneity of the ventricular myocytes or transmural heterogeneity of the ventricular electrophysiology play on important role in the occurrence and maintenance of the re-entrant ventricular arrthythmias .This heterogeneous electrophysiology of ventricular myocytes mainly originates from the differences in the action potential configuration .Ion currents and response to the varions pathologic physiologic factors.Ventricular epicardial,midmyocardial and endocardia myocytes,leading to among the formation of the transmural dispersion of repolarization.Then 2-phase reentry happens easily under the ischemic or other pathologic status and induces arrhythmia.Besides ventricular myoeletric heterogeneity is another important arrhythmogenic factor.Its primary contributor is the distribution and portial dysfunction of autonomic nerve in myocardium,especidlly adrenergic nerve. For example,the regional dysfunction of autonomic nerve ending by the acute myocardium ischemia leads to the heterogeneity of the local cardiac electricity.Aim : To investigate the effect of autonomic nerves on the transmural dispersion of effective refractory period(TDERP)of acute myocardium infraction across the left ventricular free wall on vivo rabbit.METHODS: With the programmed stimulation method,the effective refaractory periods of epicardium, midmyocardium and endocardium were measured during stimutatingt sympathetic and parasympathetic nerves before acute myocardial Infraction and 30 minutes after acute myocardial infraction in 20 open-chest rabbits.RESULTS: The ERP of Epi ,Mid and Endo was shortened during sympathetic stimulation under normal condition ,and that of the Mid was shortened most .The TDERP was increased from 21±17 ms to 30±16 ms( P < 0. 05).The ERP of Epi ,Mid and Endo was prolonged during sympathetic stimulation in acute myocardial infraction ,and that of Mid was prolonged most.The TDERP was increased from 28±16 ms to 24±18 ms ( P < 0. 05) . The ERPs of Epi ,Mid and Endo was prolonged during parasympathetic stimulation under normal condition ,and that of Endo was prolonged most.The TDERP was from 30±16 ms to 38±11 ms ( P <0. 05) ;The ERP of Epi,Mid and Endo was changed little during parasympathetic stimulation in acute myocardial Infraction ,the TDERP was not significantly different from that of the control.CONCLUSION: Sympathetic stimulation can increase the TDERP under normal condition and under acute myocardial Infraction;parasympathetic stimulation dose not significantly affect the TDERP.