Intracoronary injection of nicotine or veratridine into the circumflex artery in dogs resulted in larger decreases in heart rate and arterial pressure compared to injection into the LAD artery.
Sensory endings with vagal afferents that mediate cardioinhibitory and vasodepressor responses are preferentially distributed to the inferoposterior left ventricle in dogs.
The purpose of this study was to determine the relative magnitudes of the reflex effects mediated by sensory endings in the left ventricle activated by intracoronary injection of nicotine or veratridine into left anterior descending (LAD) or circumflex (Cx) coronary arteries in the dog. Injection of nicotine or veratridine into the Cx consistently resulted in larger decreases in heart rate, arterial pressure, and in gracilis perfusion pressure than were observed following injection of the same dose into the LAD. Vagotomy abolished the cardioinhibitory and vasodepressor responses to intracoronary nicotine or veratridine. The weight of left ventricle perfused by LAD or Cx was not different (43.5 +/- 1.65 and 44.5 +/- 2.2 g, respectively. These data indicate that chemical activation of sensory endings with vagal afferents in the inferoposterior left ventricle of the dog results in larger cardionhibitor and vasodepressor responses than result from activation of respects in the anterior left ventricle. Further, these data provide strong evidence that these sensory endings which are chemically activated are preferentially distributed to the inferoposterior left ventricle.
Walker et al. (Tue,) reported a other. Intracoronary injection of nicotine or veratridine into circumflex (Cx) artery vs. Injection into left anterior descending (LAD) artery was evaluated on Decreases in heart rate, arterial pressure, and gracilis perfusion pressure. Intracoronary injection of nicotine or veratridine into the circumflex artery in dogs resulted in larger decreases in heart rate and arterial pressure compared to injection into the LAD artery.