Permeability of the respiratory membrane in healthy, non-smoking controls and patients with sarcoidosis and chronic obstructive lung disease

Abstract

I n pulmonary and/or bronchial circulatory systems the exudation of plasma proteins to lung compartments may be due to increased pcrnieatiility of the respiratory membrane[ 1,2]. Epithelial and endothelial cells DI !lie alveolar lcvcl arc joined by tight junctions in the lungs of normal healthy people. These tight junctions form a barrier to prevent protein cxudation[3]. The permeability of the epithelial layer to proteins is less than that of the endothel layer]3]. In pathologic cases, high nioleculer weight proteins can pass the endothelial barrier easily through the intcrcndothelial gaps[3,4\. Biopsy material taken from the airway mucosa of patients with asthma showed increased epithel obstruction, enlargement of the basal nienibranc, protein exudation and increased permeability of respiratory membrane[S]. There is a strong correlation between respiratory membranc permeability and airway hypcrresponsiveness and airway inflammation[5-7]. Airway hyperresponsiveness is the obstructive reaction of the bronchioles to cold, allergens. dangerous respiratory irritants, fog, dust and occupational exposures[X]. On the other hand the unbalance between the contracting and relaxing effects of adrenergic and cholinergic systems on muscle tonus constitutes another factor[6,9]. The activation of parasympathetic nervous system leads to a release of mediators from mast cells and leukocytes[7-9]. Hypercholinergic response plays an important role in the local bronchial inflammatory reaction. Increased airway epithelial destruction and increased permeability of respiratory membrane occur as a result of neurogenic inflammation[9, lo]. In the recent years the permeability of the respiratory membrane is determined by the concentration gradient of proteins between the serum and the bronchoalveolar lavage fluid (BALF) to understand the pathogenesis of various pulmonary diseases[l1-13]. High molecular weight proteins not formed in the lungs are specially chosen for determination1 11-13]. We examined in this study the permeability of the respiratory membrane in healthy, non-smoking controls (n= l l ) , patients with sarcoidosis (n = 19), and patients with chronic obstructive pulmonary disease (COPD) (n= 12). Venous blood was obtained from each individual and BALF was taken from the right nicdiuni lobe by means of a fiber optic broncoscope. Serum and BALF saniplcs were analyzed for albumin (alb), total protein (Tpr) and urea. Albumin and lotal protein analyses were done by the Fulin-Lowry methodl 141 and urea by the enzymatic methodllS]. From the biochemical data: The concentration gradient across the respiratory membrane (protcinl in BALF [protcinl in serum 0 protein = IlHNl x and