Sleep-disordered breathing in the healthy elderly. Clinically significant?

We evaluated sleep/wake, medical, and psychological parameters in a cohort of healthy men and women between 50 and 80 years of age. Consistent with previous investigations of sleep-disordered breathing (SDB) in older persons, nocturnal breathing disturbances were quite common in our normal-aged subjects, with more than 15 percent experiencing five or more SDB events per hour of sleep. However, when SDB indices were correlated with comprehensive measures of daytime functioning, the number of statistically significant relationships was at or below expectations from chance alone. Additionally, comparison of high-SDB subjects (AHI greater than or equal to 5) with low-SDB subjects (AHI less than 5) failed to reveal reliable differences on measures of daytime functioning. We conclude that SDB occurring in otherwise healthy older persons is not a cause for immediate concern, although longitudinal studies may yet demonstrate significant long-term sequelae of SDB in this population.

Nicotine is responsible for airway irritation evoked by cigarette smoke inhalation in men.

To determine whether nicotine is involved in evoking the irritant effects of cigarette smoke in airways, we studied the responses to inhalation of a single puff (30 ml) of three types of smoke (high nicotine, low nicotine, and gas phase) in healthy male nonsmokers. After the upper airways were locally anesthetized, the subjects, breathing through a mouthpiece, were instructed to signal the detection and the intensity of airway irritation with a push-button device. Inhalation of high-nicotine smoke consistently triggered an intense airway irritation in the lower neck and upper chest region; the total number of push-button signals generated in the first 5 s was 6.61 +/- 0.87 (mean +/- SE, n = 12), with a detection latency of 0.93 +/- 0.11 s. By contrast, inhalation of low-nicotine and gas phase smoke either was not detected or caused only very mild irritation (0.89 +/- 0.4 and 0.36 +/- 0.22, respectively). In addition, the intensity of smoke-induced airway irritation was markedly reduced after premedication with aerosolized hexamethonium, a nicotinic receptor antagonist (P < 0.01, n = 8). Furthermore, inhalation of nicotine aerosol also immediately evoked intense airway irritation and coughs (n = 5). Thus we conclude that the airway irritation evoked by inhaling cigarette smoke results from an activation of sensory endings located in the central airways and nicotine is the primary agent responsible for this action.

Airway irritation and cough evoked by inhaled cigarette smoke: role of neuronal nicotinic acetylcholine receptors.

In a series of studies carried out in different experimental models, we investigated the type(s) of lung afferents and mechanism(s) underlying the cigarette smoke-induced airway irritation and cough. In healthy non-smokers, the intensity of airway irritation and cough evoked by cigarette smoke was markedly reduced after premedication with hexamethonium. A similar pattern of responses was also triggered by inhalation of nicotine aerosol. These studies in human subjects suggested nicotine as the primary causative agent in cigarette smoke that evokes airway irritation. Indeed, single-fiber recording experiments performed in anesthetized dogs showed that both C-fibers and rapidly adapting receptors in the lungs and airways were stimulated by inhalation of one puff of cigarette smoke, and the intensity of this stimulatory effect was related to the nicotine content in the cigarette and abolished by hexamethonium. To further study the direct effect of nicotine on these sensory nerves, we measured the change in intracellular calcium concentration ([Ca(2+)](i)) of pulmonary sensory neurons isolated from the nodose and jugular ganglia of adult rats. Our results showed that nicotine evoked an abrupt and transient increase in [Ca(2+)](i) in approximately 34% of the 522 neurons tested, and 1,1-dimethyl-4-phenylpiperazinium, a selective agonist of the neuronal nicotinic acetylcholine receptors (NnAChRs), evoked a similar pattern of response as that of nicotine in these neurons. In conclusion, results of these studies show that nicotine exerts a direct stimulatory effect on vagal pulmonary sensory neurons. This stimulatory effect of nicotine is primarily responsible for the airway irritation and cough evoked by inhaled cigarette smoke, and is mediated through an activation of the NnAChRs.

Disseminated Strongyloides stercoralis infection.

A case of disseminated S stercoralis is an immunosuppressed patient manifested with diarrhea, a rash, and progressive respiratory insufficiency. The parasites were eradicated with thiabendazole despite continued steroid therapy, and the patient survived the hospitalization. The characteristics of S stercoralis allow it to be harbored within a host for prolonged periods of time, only to disseminate once cell-mediated immunity is suppressed. A diagnosis of strongyloidiasis should be considered in an immunocompromised patient with a petechial rash. Prompt diagnosis and initiation of thiabendazole therapy provides the greatest opportunity for patient survival. Secondary bacterial infections should be aggressively sought. Mortality from disseminated strongyloidiasis approaches 80%.