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Pulmonary hypertension (PH) is a pulmonary vascular disease characterized by increased pulmonary artery pressures. Long standing pulmonary arterial pressure overload leads to right ventricular (RV) hypertrophy, RV failure, and death. RV failure is a major determinant of survival in PH. Oxidative stress has been associated with the development of RV failure secondary to PH. Here we summarize the structural and functional changes in the RV in response to sustained pulmonary arterial pressure overload. Furthermore, we review the pre-clinical and clinical studies highlighting the association of oxidative stress with pulmonary vasculature and RV remodeling in chronic PH. Targeting oxidative stress promises to be an effective therapeutic strategy for the treatment of RV failure.

Microbial samples from the oral cavities of cystic fibrosis (C.F.) patients and 20 age-matched normal control subjects were characterized. Mucoid variant Pseudomonas aeruginosa was isolated from the tongue, buccal mucosa, and saliva of C.F. patients only. Analysis of the data suggests that the oral cavity is a potential reservoir for this organism. Aspiration and cross-contamination from this reservoir may be important in perpetuating chronic pulmonary infection in C.F. patients. Susceptibility testing was performed on 20 mucoid variant P. aeruginosa oral isolates obtained from the patients according to standardized broth dilution procedures. The in vitro antimicrobial effects of sodium fluoride, stannous fluoride, and chlorhexidine were measured. Analysis of the data suggests that clinically safe and achievable levels of chlorhexidine and stannous fluoride may be antimicrobial.

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