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Activation of arterial blood pressure has been shown to influence higher central nervous activity. In animals, induction of sleep-like states and increases of seizure and pain thresholds in response to baroreceptor stimulation have been reported. In certain human groups, mechanical stimulation of the carotid baroreceptors also increases pain thresholds. The present paper examines the hypothesis that smokers show baroreceptor dependent antinociception as compared to non-smokers. It is speculated that one effect which rewards smoking is the nicotine induced phasic blood pressure increase which leads to baroreceptor stimulation and dampens pain perception. One hundred and twenty subjects were investigated using a recently developed mechanical baroreceptor stimulation technique and an electrical pain stimulus. The group of heavy smokers showed the predicted effect: their pain thresholds were enhanced during conditions of increased baroreceptor activity as compared to the control condition. The group of medium, light and non-smokers, however, did not show this effect. Neither blood lipid levels nor diastolic or systolic blood pressure paralleled the group differences on baroreceptor dependent antinociception. In heavy smokers, the nicotine induced phasic blood pressure increase might have baroreceptor dependent pain dampening effects, which might be among the reinforcing qualities of smoking.

Abstract: Recent research on the role of classical conditioning in homeostatic regulation (Dworkin, 1993; Siegel, Krank & Hinson, 1987) has underscored the potential importance of the work of earlier Eastern-European work on physiological conditioning. The present article is a translation and discussion of a paper on blood glucose conditioning, first published in 1954 by the Russian physiologist M.I. Mityushov. Dr. Mityushov was able to demonstrate conditioned hypoglycemia in humans and dogs after using an injection procedure as the CS and intravenous glucose as the UCS. The translation is preceded by a general introduction and followed by a reanalysis and discussion of Mityushov’s results.

BGP-15 reduces ventilation-induced diaphragm dysfunction by improving diaphragm fiber and myosin function and enhancing mitochondrial activity.