Interaction of the chemoreflex and the pulmonary inflation reflex in the regulation of coronary circulation in conscious dogs.

Abstract

The interaction of chemoreflex and pulmonary inflation reflex control of the coronary circulation was examined in conscious dogs by comparing the responses to chemoreflex stimulation (intracarotid injection of nicotine) when ventilation was allowed to increase with those when ventilation was controlled. The responses were also compared with those elicited by both forced mechanical and spontaneous hyperinflation. When the heart rate was constant, intracarotidly administered nicotine induced an increase in the depth of respiration followed closely by an increase in late diastolic coronary flow from 48 +/- 2 to 106 +/- 8 ml/min and a reduction in late diastolic coronary resistance from 1.62 +/- 0.08 to 0.78 +/- 0.06 mm Hg/ml min-1. After beta-receptor and cholinergic blockade, a similar coronary dilation in response to nicotine occurred only when ventilation was allowed to increase. However, when ventilation was controlled, intracarotidly administered nicotine increased coronary resistance after combined beta-receptor and cholinergic blockade. The reflex coronary dilation was not observed after carotid sinus nerve section or after alpha-receptor blockade. Thus, nicotine stimulation of the carotid chemoreflex results in a striking coronary dilation that has two components. The minor component involves a chemoreflex with its efferent pathway in tthe vagi. The major component of coronary dilation follows an increase in the depth of respiration, and its efferent component appears to involve withdrawal of alpha-adrenergic constrictor tone. An almost identical period of reflex coronary dilation followed either forced mechanical or spontaneous hyperinflation in the conscious dog.

Stimulation of pulmonary C fibres decreases coronary arterial resistance in dogs.

“…The coronary vasodilatation seen in the present study is similar to that which has PULMONARY CHEMOREFLEX AND CORONAR Y RESISTANCE 287 been observed previously during carotid sinus nerve stimulation (Hackett, Abboud, Mark, Schmid & Heistad, 1972), peripheral chemoreceptor stimulation (Hashimoto, Igarashi, Uei & Kumakura, 1964;Vatner & McRitchie, 1975;Vatner, 1983;Murray, Lavallee & Vatner, 1984), carotid sinus baroreceptor stimulation (Ito & Feigl, 1985), and the Bezold-Jarish reflex (Feigl, 1975). Further, the neurohumoral basis for the changes in coronary resistance evoked by capsaicin in the present study is comparable to that seen in previous studies.…”

Control of the Myocardial Contractile State by Carotid Chemo- and Baroreceptor and Pulmonary Inflation Reflexes in Conscious Dogs

“…Thus, it is possible that the increase in coronary flow could have been responsible for the increase in contractility. However, this mechanism seems unlikely in view of the experiments after beta adrenergic blockade where the reflex coronary vasodilatation still occurs (13), but the inotropic response was abolished. If the increase in flow produced the inotropic response, then the response should not have been abolished by beta blockade.…”

“…It is known that stimulation of the carotid chemoreceptor reflex elicits reflex coronary vasodilatation (13). It has also been reported that an increase in coronary flow, per se, may increase myocardial contractility (24).…”

“…As these dogs were not anesthetized, care was taken so as not to perform any intervention or experiment that was not tolerated by the conscious dogs in the absence of succinylcholine, as done previously in conscious rabbits and conscious dogs (4,13,20,21 to calibrate the differentiator directly. Peak responses were compared to control values with the paired t test whereas responses in groups having different numbers were compared with the unpaired t test (22).…”

“…This was accomplished by injecting small quantities of nicotine or cyanide into the carotid artery to stimulate the chemoreceptors. It must be kept in mind that in the conscious dog the carotid chemoreceptor reflex elicits an intense increase in respiratory drive, which couild modif'y the effects of' the carotid chemoreceptor reflex through stimulation of pulmonary inflation af'ferents (4,12,13). Therefore, a secondary goal was to identify the extent to which the effects on contractility would be modified by the concomitant increase in respiration and stimullation of pulmonary inflation afferents.…”