Coronary arteriography in the intact rabbit: demonstration of coronary vasomotor and electrocardiographic effects of ergonovine and indomethacin in rabbits after abrupt cessation of prolonged nitroglycerin treatment.

Abrupt withdrawal of chronic nitroglycerin treatment may predispose the coronary circulation to spasm. To test this hypothesis directly, we developed a technique for performing selective coronary arteriography in the intact rabbit with images obtained by video-based methods or cineangiographic film. Experiments were then conducted in rabbits treated three times daily with topical nitroglycerin ointment for 6 weeks and in age- and sex-matched control animals. Forty hours after cessation of treatment, animals were anesthetized, and ECG and coronary vasoactive effects (determined by coronary arteriography) of ergonovine, 0.2 mg/kg (intravenous) and indomethacin, 25 mg/kg (intravenous) were assessed. Of six nitroglycerin-treated rabbits, one died of ventricular fibrillation prior to arteriographic study. The remaining five developed ECG abnormalities (single ventricular premature beats, nonsustained ventricular tachycardia, and ST segment deviation) upon challenge with ergonovine or indomethacin. Neither agent evoked ECG changes in control rabbits. In contrast, the degree of luminal diameter reduction in epicardial coronary arteries provoked by ergonovine or indomethacin did not differ between control and nitroglycerin-treated animals. Focal coronary artery spasm was not observed in any rabbit. Our results demonstrate that selective coronary arteriography in rabbits is feasible and that changes in vessel caliber may be assessed from images thus obtained. Data from this study indicate that ergonovine- and indomethacin-induced ECG abnormalities observed in nitroglycerin-treated rabbits cannot be ascribed to epicardial coronary artery spasm.

Attenuation of vagal noradrenergic tachycardia by naloxone.

Electrical stimulation of the transected right vagus nerve in anesthetized and atropinized dogs produced tachycardia that was not attenuated by beta-adrenoceptor blockade. Naloxone in intravenous doses of 1 and 4 mg/kg antagonized the tachycardia evoked by nerve stimulation in a dose-dependent manner. However, the attenuation was maximal at approximately 55% of the control response. These results suggest that an endogenous opiate peptide(s) may have a mediator or modulator role in nonadrenergic tachycardia evoked by vagal nerve stimulation in anesthetized and atropinized dogs.