It is well known that tobacco consumption causes a respiratory disease called chronic obstructive pulmonary disease (COPD), characterized by formation of emphysema and progressive destruction of the lung.When pulmonary vessels are altered in this disease, life expectancy of the patients worsens. It has not been possible to establish the cause, but it has been attributed to low oxygen concentration in the blood.
However, changes in the pulmonary vessels have also been found in COPD patients with normal oxygen concentrations. These abnormalities mainly consist of the thickening of the internal coat of pulmonary arteries, resulting in a decrease of the arterial lumen size.
The cellular and extracellular components that are involved in this enlargement are unknown.
A study published in this month's European Respiratory Journal (ERJ) by Prof. J.A. Barbera of the Servei de Pneumologia Hospital Clinic in Barcelona, Spain, and colleagues was designed to characterize the changes occurring in pulmonary arteries of patients with mild COPD and in smokers who have not yet developed the disease.
The researchers found that the thickening of the wall is mainly due to the proliferation of smooth muscle cells with synthetic capacity, as well as elastin and collagen deposition.
These alterations occur in both groups of patients to the same degree.
These findings indicate that cellular and extracellular changes of pulmonary vessels may be originated at an early stage in cigarette smoke-induced respiratory disease, suggesting that tobacco consumption is possibly the direct cause of these changes.
[Contact: Prof. J.A. Barbera]
02-Apr-2002
