Influence of nicotine in cigarette smoke on acute ventilatory responses in awake dogs

Abstract

To determine whether the acute ventilatory responses to inhaled cigarette smoke are affected by a difference in nicotine level, control cigarettes (low-nicotine research cigarettes) were laced with nicotine to generate an increase of 330% (mean) in nicotine content with little or no change in the levels of other smoke constituents. Acute ventilatory responses to both control and nicotine-laced cigarettes were determined and compared in six awake chronic dogs. Spontaneous inhalation of nicotine-laced cigarette smoke (10% concn, 750 ml vol) via a tracheostomy tube caused distinct and consistent changes in breathing pattern on the first or second breath of inhaled smoke: an apnea in three dogs, an augmented inspiration in two dogs, and rapid shallow breathing in one dog. No significant change in breathing pattern was found immediately following inhalation of control cigarette smoke. Both types of cigarettes caused a delayed hyperpnea. However, the increase in minute ventilation induced by nicotine-laced cigarettes (from a base line of 2.8 to a peak of 25.7 l/min) was significantly greater than that by control cigarettes (from 2.9 to 5.5 l/min). Results of this study suggest that nicotine is responsible for the elicitation of both the immediate and delayed ventilatory responses to inhaled cigarette smoke generated under our experimental conditions.

Tobacco Smoke Induced Cough: Mechanisms Driving Acute and Chronic Cough Pathology

“…Whereas, coughing was absent with inhalation of both low nicotine and gas phase irritants. This corroborated their findings in the dog model (Lee et al, 1983(Lee et al, , 1985(Lee et al, , 1986(Lee et al, , 1989Kou & Lee, 1990. The second study assessed the role of nicotine in TS-associated airway irritation and cough.…”

“…Using single fibre analysis, the authors observed that a single puff of TS generated from high nicotine, but not low nicotine cigarettes triggered action potential generation in bronchopulmonary C-fibres and RARs. Moreover, the competitive selective nACh receptor antagonist hexamethonium inhibited sensory nerve stimulation in response to TS, but had no effect on other tussive stimuli, indicating a role for nicotine in the smokeinduced irritant response in dogs (Lee et al, 1983(Lee et al, , 1985(Lee et al, , 1986(Lee et al, , 1989Kou & Lee, 1990. The ability of nicotine to stimulate airway sensory nerves was corroborated in rat isolated vagal ganglia neurons by assessing calcium influx.…”

Acute Cardiovascular and Sympathetic Effects of Nicotine Replacement Therapy

“…The effects of nicotine on chemoreflex sensitivity in humans are unknown. Some, but not all, [21][22][23] animal studies have been able to show that nicotine increases peripheral chemoreceptor sensitivity to hypoxia. 24 -26 This is likely because of the fact that the effects of exogenous nicotine on chemoreceptors depend on the predominance of nicotinic and muscarinic receptors on the carotid bodies.…”

New Insights Into the Sympathetic, Endothelial and Coronary Effects of Nicotine

“…Nicotinic receptors have been also located on the other side of the chemosensitive synapse 15 but the role of the latter in the carotid body neurotransmission remains unclear. Moreover, several animal studies have shown that nicotine induces an excitatory effect on sympathetic drive mediated by peripheral chemoreflex stimulation 16,17 . However, these results can not be generalized, 18 possibly as a result of differences among species in the predominance of nicotinic receptors on the carotid bodies 14,19 .…”