The goal of the present investigation was to describe the prevalence of and clinical factors associated with sleep-disordered breathing in children and adolescents. Children and adolescents (3,680 in all, 1-18 years old) attending schools in central Greece were surveyed by questionnaires distributed to parents. We found a similar prevalence of habitual snoring (present every night) among three different age groups (5.3%, 4%, and 3.8% in 1-6-, 7-12-, and 13-18-year-old subjects, P = NS). Several children with an adenoidectomy and/or tonsillectomy were snoring every night (6.1%), whereas sleepiness at school was more common in habitual snorers than in nonhabitual snorers (4.6 vs. 2%, P = 0.03). Seventy randomly selected subjects among 307 snorers without adenoidectomy and/or tonsillectomy underwent polysomnography. The estimated frequency of obstructive sleep apnea-hypopnea among children without adenoidectomy and/or tonsillectomy was 4.3%. Factors associated with snoring were: male gender (odds ratio 1.5 (confidence interval, 1.2-1.9)); chronic rhinitis (2.1 (1.6-2.7)); snoring in father (1.5 (1.2-1.9)), mother (1.5 (1.1-2.0)), or siblings (1.7 (1.2-2.4)); adenoidectomy in mother (1.5 (1.0-2.2)); and passive smoking (1.4 (1.1-1.8)). In conclusion, snoring every night was equally prevalent in younger and older ages, more frequent in males, and present even in some children with a history of adenoidectomy and/or tonsillectomy. Chronic rhinitis, family history of snoring, and exposure to cigarette smoke were associated with an increased frequency of habitual snoring.

Cobalt can mimic hypoxia and has been implicated as a cause of lung defects. However, the effect of cobalt on airway smooth muscle (ASM) cells has not been analyzed in detail. In this article, we use primary cultures of ASM cells from rabbit trachea and show that exposure to cobalt chloride causes a rapid increase of the intracellular levels of hypoxia-inducible factor-1alpha, which is detected predominantly inside the nucleus. With the use of specific inhibitors, we demonstrate that induction of hypoxia-inducible factor-1alpha by cobalt depends on active protein synthesis but not transcription. Furthermore, wortmannin, LY294002, and N-acetyl-L-cysteine inhibit the effect of cobalt, suggesting that it involves the phosphatidylinositol 3 kinase pathway and production of reactive oxygen species. Interestingly, cobalt chloride attenuates the contractile response of rabbit airways induced by potassium chloride, but not by acetylcholine, suggesting a link between the cellular response to hypoxic stimuli and the contractile properties of ASM cells.

The fluid and solute transport properties of pleural tissue were studied by using specimens of intact visceral and parietal pleura from adult sheep lungs. The samples were transferred to the laboratory in a Krebs-Ringer solution at 4 degrees C within 1 h from the death of the animal. The pleura was then mounted as a planar sheet in a Ussing-type chamber. The results that are presented in this study are the means of six different experiments. The spontaneous potential difference and the inhibitory effects of sodium nitroprusside (SNP), ouabain, and amiloride on transepithelial electrical resistance (R(TE)) were measured. The spontaneous potential difference across parietal pleura was 0.5 +/- 0.1 mV, whereas that across visceral pleura was 0.4 +/- 0.1 mV. R(TE) of both pleura was very low: 22.02 +/- 4.1 Omega. cm2 for visceral pleura and 22.02 +/- 3.5 Omega. cm2 for parietal pleura. There was an increase in the R(TE) when SNP was added to the serosal bathing solution of parietal pleura and to the serosal or mucosal bathing solution in visceral pleura. The same was observed when ouabain was added to the mucosal surface of visceral pleura and to either the mucosal or serosal surface of parietal pleura. Furthermore, there was an increase in R(TE) when amiloride was added to the serosal bathing solution of parietal pleura. Consequently, the sheep pleura appears to play a role in the fluid and solute transport between the pleural capillaries and the pleural space. There results suggest that there is a Na+ and K+ transport across both the visceral and parietal pleura.

Background and purpose: Recent studies on blood vessels have provided evidence that testosterone may exert direct effects on smooth muscle. However, an acute effect on airway reactivity has not been shown yet. The aim of this study was to assess the direct effect of testosterone on the responsiveness of male adult rabbit airway smooth muscle (ASM), precontracted with 10 mM acetylcholine, 10mM carbachol or 80 mM KCl. Experimental approach: Contractility studies of rabbit tracheal smooth muscle were performed. Key results: Testosterone at concentrations of or above 1 nM had a significant relaxant effect on ASM precontracted with acetylcholine or carbachol, but did not affect ASM precontracted with KCl. The mechanical removal of airway epithelium as well as the inhibition of NO synthetase (by 100mM L-NAME) reduced the relaxation caused by testosterone. The effect of testosterone was not altered by impairing prostanoid synthesis (by 10mM indomethacin). The nitric oxide donor, sodium nitroprusside, had the same relaxant effect on ASM precontracted with either carbachol or KCl. Inhibitors of androgen receptors (10mM flutamide) or DNA transcription (100mM actinomycin D) did not alter the effect of testosterone. Prolonged incubation of ASM with 100 nM or 100 mM testosterone for 24 or 48 h did not alter their responsiveness to acetylcholine. BSAtestosterone (1pM to 100nM) relaxed significantly ASM precontracted with carbachol. The mechanical removal of airway epithelium abolished the relaxant effect of BSA-testosterone. Conclusions and implications: Testosterone relaxes precontracted ASM via an epithelium and NO-mediated way. This effect is mediated via a non-genomic pathway.