Modeling rapidly adapting pulmonary stretch receptor activity to step-wise and constant pressure inflation of the lungs.

Rapidly-adapting pulmonary stretch receptors (RAPSRs) provide the central nervous system with information regarding the rate of lung inflation, lung compliance and the sensation of dyspnea. Other than satisfying parameters of an adaptation index to constant pressure lung inflation for identification, no mathematical model has been ascribed to the stimulus-response relationship of lung volume-pressure to RAPSR activity. Herein, linear, power, polynomial and non-linear (four parameters logistic) models are tested for the best "goodness of fit" line of RAPSR activity to step-wise lung inflation to four times tidal volume and constant pressure inflation to 10, 20, 30 and 40 cm HO of the lungs of guinea pigs and dogs.

Interaction of tobacco smoke exposure and ovalbumin-sensitization promotes goblet cell and submucosal gland metaplasia in guinea pigs.

Exposure to irritants such as tobacco smoke (TS) causes acute airway inflammation. Chronic exposure may cause airway remodeling contributing to enhanced airway resistance. We hypothesize that combining airway sensitization and inhalation of irritants enhances the number of mucous producing cells beyond either agent alone.

The effect of vasoactive agents on post-pressure hyperemia.

The cutaneous hyperemic response following the release of direct pressure occlusion lasts much longer than the short-term hyperemia that occurs after proximal arterial occlusion. Post-pressure hyperemia may be an important mechanism to prevent pressure induced injury to the skin. The role of vasoactive mediators in modulating post-pressure hyperemia is unknown.

Environmental tobacco smoke exposure and airway hyperresponsiveness.

Environmental tobacco smoke (ETS) exposure is a common health concern despite legislation to limit its presence, especially in public environments. ETS exposure is associated with changes in lung development and morphology, airway hyperresponsiveness and obstruction and development of asthma and its increased severity. However these effects of ETS exposure are not universally supported.