Chlorine gas induced acute lung injury in isolated rabbit lung

• Published in: The European respiratory journal Vol. 10; no. 5; pp. 1100 - 1107
• Main Authors: Menaouar, A, Anglade, D, Baussand, P, Pelloux, A, Corboz, M, Lantuejoul, S, Benchetrit, G, Grimbert, FA
• Format: Journal Article
• Language: English
• Published: Leeds Eur Respiratory Soc 01.05.1997; Maney
• Subjects: Animals; Biological and medical sciences; Capillary Permeability - physiology; Chemical and industrial products toxicology. Toxic occupational diseases; Chlorine - administration & dosage; Chlorine - toxicity; Edema - chemically induced; Edema - diagnosis; Edema - physiopathology; Gas, fumes; Gases - administration & dosage; Gases - toxicity; In Vitro Techniques; Lung - pathology; Medical sciences; Pulmonary Artery - physiology; Pulmonary Veins - physiology; Pulmonary Wedge Pressure - physiology; Rabbits; Respiratory Distress Syndrome, Adult - chemically induced; Respiratory Distress Syndrome, Adult - physiopathology; Toxicology; Edema; Respiratory disease; Pathogenesis; Toxicity; Lung; Chlorine Chlorine; Rabbit; Exploration; Lagomorpha; Inhalation; Gases; Vertebrata; Mammalia; Animal; Pneumopathy
• ISSN: 0903-1936; 1399-3003
• DOI: 10.1183/09031936.97.10051100

This study was designed to investigate the pathogenesis of chlorine gas (Cl2) induced acute lung injury and oedema. Isolated blood-perfused rabbit lungs were ventilated either with air (n=7) or air plus 500 parts per million (ppm) of Cl2 (n=7) for 10 min. Capillary pressure, measured by analysing the pressure/time transients of pulmonary arterial, venous and double (both arterial and venous) occlusions, was unchanged in both groups. In Cl2-exposed lungs, the fluid filtration rate increased from -0.228+/-0.25 to 1.823+/-1.23 mL min(-1) x 100 g(-1) (p<0.001) and the filtration coefficient increased from 0.091+/-0.01 to 0.259+/-0.07 mL x min(-1) x cmH2O(-1) x 100 g(-1) (p<0.001). No changes were observed in the control lungs. The extravascular lung water/blood-free dry weight ratio was 8.6+/-1.6 in the Cl2 group and 4.0+/-0.5 in the control group (p<0.001), confirming that the increase in lung weight was related to accumulation of extravascular fluid. Although the alveolar flooding by oedema is explained, in part, by the Cl2-induced epithelial injury, our results suggest that Cl2 exposure induces acute lung injury and oedema due to an increased microvascular permeability.