Sex differences in susceptibility to epinephrine-induced arrhythmias.

Gender differences in incidence of cardiac arrhythmias have been documented. It is generally believed that cardiac pathology provides an arrhythmogenic substrate but that a trigger such as sympathetic nervous system activation is required to initiate arrhythmias. This study was done to determine whether there is a sex difference in susceptibility to epinephrine-induced arrhythmias in healthy rats without preexisting pathology and to determine whether gonadal hormones play a role in development of arrhythmias. Untreated, sham-operated, and gonadectomized male and female rats were anesthetized and given IV boluses of epinephrine. ECG, heart rate, and blood pressure were measured continuously for 1 minute and intermittently over a period of 30 minutes. Male rat hearts have a higher occurrence and frequency of epinephrine-induced premature ventricular contractions, missed beats, and blocks than female rat hearts. Ovariectomy increases arrhythmias, thereby abolishing the female advantage. Castration has no effect on occurrence and frequency of premature ventricular contractions but attenuates missed beats and blocks. Sex differences and effect of gonadectomy on epinephrine-induced alterations in heart rate and blood pressure implicate baroreceptor reflex in the dimorphic arrhythmogenic response. Male rat hearts are more susceptible than female hearts to epinephrine-induced arrhythmias, and gonadal hormones play a role in this disparity.

Metabolism of angiotensin I in the coronary circulation of normal and diabetic rats.

Formation of metabolites from angiotensin I that passed the coronary vessels in the isolated working rat hearts of normal and streptozotocin-induced diabetes was evaluated. HPLC analysis showed that the levels of angiotensin II and angiotensin 1-7 were unaltered in the diabetic hearts, but the perfusates of the diabetic hearts contained smaller amounts of angiotensin 1-9. It is not clear why the perfusates of diabetic hearts contain less amount of angiotensin 1-9. It is possible that the peptide is metabolized faster or greater internalization takes place in the diabetic heart. The amount of angiotensin II in the perfusates of normal hearts was 5.8 times greater at the perfusion rate of 2 than at 10 ml/min/g wet heart weight. At such conditions, the amount of angiotensin 1-9 and angiotensin 1-7 in the perfusates were increased 2.4 and 1.5 times, respectively. A higher amount of angiotensin II during myocardial hypoperfusion may lead to constriction of the coronary vessels. As a result, myocardial damage may be facilitated.