Changes in myocardial action potential of rabbit with myocardial ischemia exposed to repeated positive acceleration (+Gz)

Objective　To explore the possible mechanism of arrhythmia caused by ischemic coronary vessel lesion through parallel analysis of the monophasic action potential (MAP) changes in normal and ischemic myocardium under positive acceleration (+Gz) exposure. Methods　Sixty New Zealand white rabbits were randomly divided into 4 groups (15 each): control group (group A), acceleration group (group B), ischemia group (group C) and myocardial ischemia undergoing positive acceleration group (group D). The changes in each group were recorded and analyzed, including MAP amplitude (MAPA, mV), maximum rate of 0 phase (Vmax, mV/s), 50% MAP repolarization (MAPD50) and 90% MAP repolarization (MAPD90) by using monophasic action potential method after +Gz exposure and myocardial ischemia. The incidence of arrhythmia was then observed by S1S1 programmed stimulation. Results　No significant changes were found in MAPA and Vmax among the 4 groups (P>0.05). Compared with group A, MAPD50 and MAPD90 were shortened evidently in group B, C and D (P<0.05), most marked in group D, as it was significantly shortened than that of group B and C (P<0.05). The incidence of arrhythmia by S1S1 programmed stimulation was higher in groups B, C and D (P<0.05) than in group A, and it was highest in group D (P<0.05). Conclusions　The duration of action potential will be shortened in myocardial cell after exposure to +Gz or ischemia, and the probability of occurrence of tachyarrhythmias will be increased significantly. +Gz and ischemia are found to have cumulative effect, implying that the functional abnormality of related ion channels existed in the course of repolarization. DOI: 10.11855/j.issn.0577-7402.2014.07.14