The effect of estrous cycle on ischemia reperfusion induced arrhythmias in rats

Arrhythmia caused by coronary artery occlusion is a major cause of sudden death both in women and men. Ventricular tachycardia and fibrillation are lethal arrhythmias that may cause sudden death due to ischemia-reperfusion injury. The incidences of these arrhythmias show differences in women and men. There is a cardioprotective difference between women and men. Women are more resistant to heart attack than men. However the cardioprotective effect disappears after menopause in women. Since estrogen diminishes after menopause in women, and it is well known that the administration of estrogen have a cardioprotective effect against ischemia-reperfusion induced arrhythmias, it is thought that the cardioprotective effect in pre-menopausal women is caused by estrogen levels. However, the estrogen levels are fluctuating during menstrual cycle in women and during the estrous cycle in rats. It was shown that there is a difference between phases of estrous cycle in the maintaining of cardiac function after injury. That is why in the present study the effect of estrous cycle on ischemia-reperfusion induced arrhythmias and the role of endogenous estrogen were researched. In the present study 6-7 months old 28 female Sprague Dawley rats were used. The phases of estrous cycle were determined by the observation of the cells present in the vaginal smears. Four groups were created according to the phases of estrous cycle; proestrus, estrus, metestrus, diestrus. Left anterior descending coronary artery was occluded to create ischemia for 6 minutes, and the artery was released for reperfusion for 6 minutes. Electrocardiogram and blood pressure are recorded during ischemia and reperfusion. Blood samples were collected after reperfusion, and serum 17ß-Estradiol levels were determined. After occlusion, blood pressures decreased and ST segment elevation or depression were observed in all animals. There were no differences in arrhythmia score, the incidences of arrhythmias, and arrhythmic periods among the groups. Higher blood pressures were observed in proestrus group, however the difference was not statistically significant. Lower heart rates were observed in estrus group during 6 minutes of ischemia and 6 minutes of reperfusion (P<0.05). 17ß-Estradiol level of proestrus was found higher than the other groups (P<0.05). In conclusion, in the present study it was found that the estrous cycle and endogenous estrogen do not have an effect on ischemia-reperfusion induced arrhythmias, however they may have an effect on the heart rate and blood pressure during ischemia-reperfusion.