Azithromycin for sarcoidosis cough: an open-label exploratory clinical trial.

Background: Chronic cough is a distressing symptom for many people with pulmonary sarcoidosis. Continuous treatment with a macrolide antibiotic may improve cough. We aimed to assess the potential efficacy of azithromycin in patients with sarcoidosis and self-reported cough.

Quantifying chronic cough: objective versus subjective measurements.

Background And Objective: The assessment of chronic cough has been improved by the development of objective ambulatory cough monitoring systems and subjective quality of life questionnaires. Experimental induction of cough is a useful tool in the assessment of the cough reflex. We wanted to assess the reproducibility of and association between these measurements.

Pulmonary vasodilation in the rat by insulin in vitro could indicate potential hazard for inhaled insulin.

Aims/hypothesis: Hypoxic pulmonary vasoconstriction is an essential mechanism to prevent hypoxaemia in lung diseases. Insulin is known to be a systemic vasodilator but its effect on the pulmonary circulation is not known. Inhaled particulate insulin can generate locally high concentrations in the lung which could be physiologically important.

The effect of the ETA receptor antagonist (CI-1020) in rats with established hypoxic pulmonary hypertension.

ETA receptor antagonists have previously been shown to prevent the development of pulmonary hypertension induced by chronic hypoxia in the rat. Clinically, however, patients present with already established pulmonary hypertension. We have investigated the effects of the ETA receptor antagonist CI-1020 in rats previously adapted to chronic hypoxia.

Plasma levels of atrial natriuretic peptide and brain natriuretic peptide following intravenous saline infusion in oedematous chronic obstructive pulmonary disease and non-oedematous chronic obstructive pulmonary disease.

Some patients with chronic obstructive pulmonary disease (COPD) develop oedematous COPD (oCOPD) with peripheral oedema and have a poor prognosis. The cause of the fluid retention is poorly understood but could be due to defective release of a natriuretic factor. We investigated this hypothesis by measuring levels of brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) before and after a 0.