Effects of short-term administration of estradiol on reperfusion arrhythmias in rats of different ages

Little is known about age-related differences in short-term effects of estradiol on ischemia-reperfusion (I/R) insults. The present study was designed to evaluate the effects of short-term treatment with estradiol on reperfusion arrhythmias in isolated hearts of 6-7-week-old and 12-14-month-old female rats. Wistar rats were sham-operated, ovariectomized and treated with vehicle or ovariectomized and treated with 17β-estradiol (E2; 5 µg·100 g-1·day-1) for 4 days. Hearts were perfused by the Langendorff technique. Reperfusion arrhythmias, i.e., ventricular tachycardia and/or ventricular fibrillation, were induced by 15 min of left coronary artery ligation and 30 min of reperfusion. The duration and incidence of I/R arrhythmias were significantly higher in young rats compared to middle-aged rats (arrhythmia severity index: 9.4 ± 1.0 vs 3.0 ± 0.3 arbitrary units, respectively, P < 0.05). In addition, middle-aged rats showed lower heart rate, systolic tension and coronary flow. Four-day E2 treatment caused an increase in uterine weight. Although E2 administration had no significant effect on the duration of I/R arrhythmias in middle-aged rats, it induced a marked reduction in the rhythm disturbances of young rats accompanied by a decrease in heart rate of isolated hearts. Also, this reduction was associated with an increase in QT interval. No significant changes were observed in the QT interval of middle-aged E2-treated rats. These data demonstrate that short-term estradiol treatment protects against I/R arrhythmias in hearts of young female rats. The anti-arrhythmogenic effect of estradiol might be related to a lengthening of the QT interval.

Effects of short-term administration of estradiol on reperfusion arrhythmias in rats of different ages.

Little is known about age-related differences in short-term effects of estradiol on ischemia-reperfusion (I/R) insults. The present study was designed to evaluate the effects of short-term treatment with estradiol on reperfusion arrhythmias in isolated hearts of 6-7-week-old and 12-14-month-old female rats. Wistar rats were sham-operated, ovariectomized and treated with vehicle or ovariectomized and treated with 17ß-estradiol (E2; 5 µg·100 g-1·day-1) for 4 days. Hearts were perfused by the Langendorff technique. Reperfusion arrhythmias, i.e., ventricular tachycardia and/or ventricular fibrillation, were induced by 15 min of left coronary artery ligation and 30 min of reperfusion. The duration and incidence of I/R arrhythmias were significantly higher in young rats compared to middle-aged rats (arrhythmia severity index: 9.4 ± 1.0 vs 3.0 ± 0.3 arbitrary units, respectively, P < 0.05). In addition, middle-aged rats showed lower heart rate, systolic tension and coronary flow. Four-day E2 treatment caused an increase in uterine weight. Although E2 administration had no significant effect on the duration of I/R arrhythmias in middle-aged rats, it induced a marked reduction in the rhythm disturbances of young rats accompanied by a decrease in heart rate of isolated hearts. Also, this reduction was associated with an increase in QT interval. No significant changes were observed in the QT interval of middle-aged E2-treated rats. These data demonstrate that short-term estradiol treatment protects against I/R arrhythmias in hearts of young female rats. The anti-arrhythmogenic effect of estradiol might be related to a lengthening of the QT interval.

The electrocardiogram of rats with an old extensive myocardial infarction

The electrocardiographic alterations of old murine myocardial infarction have not been well characterized. In the present study, adult Wistar rats, of both sexes were infarcted by left coronary artery ligation and the electrocardiogram was recorded 1 to 11 months later. When compared to sham-operated rats, animals with large infarcts, identified on the basis of extensive transmural scars, showed (P<0.01) a marked rightward deviation of the QRS axis (+125.3- ñ 34.3- vs 59.99- ñ 15.9-), a high incidence of Q waves (88% vs 0% in classic lead 1), a decrease in QRS amplitude index (0.66 ñ 0.31 mV vs 1.00 ñ 0.23 mV), a discrete increse in PR interval (58 ñ 7 ms vs 53 ñ 5ms) and greater P wave amplitude. The present results show that the electrocardiogram (EKG) is a reliable tool for diagnosis of old extensive infarctions in rats

Oscillations of cardiac rate induced by acetylcholine in the isolated guinea pig heart

1. The effects of acetylcholine (ACh) on cardiac rate (electrocardiogram), contractile force and coronary flow recorded simultaneously were investigated in isolated guinea pig hearts perfused with Locke solution by the method of Langendorff. 2. Bolus injections of 0.5-550 nmol ACh induced oscillations of cardiac rate. These changes were not directly related to the doses of ACh injected (X**2 test, P > 0.05). 3. The presence of 10 micronM physostigmine in the Locke solution increased the number of heart rate oscillations elicited by ACh. 4. The electrocardiogram showed that the heart rate oscillations were due to wandering pacemakers, such as slow or fast junctional rhythm, and slow or fast indioventricular rhythmy, which were intermingled with sinus rhythym, A - V block or sinus bradycardia. 5. In most experiments, the increase in ventricular rate was associated with an increase in ventricular contractile force ("Bowditch Effect") and a simultaneous reduction of coronary flow. 6. The heart rate oscillations were not prevented bu reserpine or blockade of nicotinic receptors (hexamethonium plus gallamine) but were prevented blockade of muscarinic receptors with atropine. 7. We conclude that the heart rate oscillations induced by ACh are due to several electrophysiological mechanisms (automatism and/or conduction disturbances_ related to activation of muscarinic receptors