RESUMO
A limited number of studies have reported respiratory muscle strength as an early indicator of pulmonary dysfunction in younger age groups. Hence this study was carried out to analyze the same in young Saudi males. The objective of the study was to assess the effect of smoking habits on respiratory muscle strength in young Saudi males. A total of 376 young subjects were inducted. The respiratory muscle strength was studied through PI[max], PE[max] and MVV. Dynamic lung volumes included FVC, FEV[1], FEV[1] / FVC ratio and FEF[25-75]. Smoking was quantified by estimating the total number of cigarettes smoked and the smoking behavior of subjects was categorized as: [1] never smoked; [2] smoking < 15 cigarettes a day; and [3] smoking > 15 cigarettes a day. The non-smokers formed the control group. Former smokers were not included. Respiratory muscle strength and dynamic lung volumes were measured by a dry electronic spirometer. Deteriorating effect of smoking was found on respiratory muscle strength, lung volumes and airflow parameters in our sample. Mild smokers showed a 5.39% decrease in FEF[25-75] whereas a 01% increase in FEV[1] / FVC ratio compared to non-smokers. In heavy smokers both FEF[25-75%] and FEV[1] / FCV% were decreased by 14.7% and 3.1% respectively. PI max was insignificant in mild smokers and heavy smokers whereas PE max was significant in heavy smokers p > 0.03. Smoking was related to decline in respiratory muscle strength, lung volumes and airflow obstruction as well. This study indicated a positive dose response relationship of smoking and pulmonary dysfunction
RESUMO
The present study deals with the chronotropic effects of Sildenafil citrate [Viagra] on right atrial contracctility of mammalian isolated heart muscle. Effects of Sildenafil citrate on rat isolated heart in-vitro using right atrial samples, in comparison with nor-adrenaline, revealed that Sildenafil at 10[-7] M and above produced dose related increases in contractility. The maximum observed increase at 10[-4] M represented a 126% +/- 31% increase above control amplitude. Nor-adrenaline produced similar dose-related increases in contractility and was appoximately three times more potent than Sildenafil citrate. Dimaprit also produced similar responses to the Sildenafil but was less potent. These results indicated that rat responds to Sildenafil citrate, which increases contracility and enhances atrial automaticity, with sensitivity comparable to that for nor-adrenaline. The selective antagonism of the Sildenafil contractility response by cimetidine indicated that this response is mediated via histamine H [2]-receptors and not H [1] noradrenergic beta receptors. The involvement of histamine H [2]- receptors is confirmed by the similarity of the response to dimaprit. The production of spontaneous contractions by dimaprit further suggests that Sildenafil citrate-induced enhancement of atrial automaticity is mediated via modified histamine H [2]-receptors