CHLORINE GAS-INDUCED ACUTE LUNG INJURY IN ISOLATED RABBIT LUNG

This study was designed to investigate the pathogenesis of chlorine ga s (CI2) induced acute lung injury and oedema Isolated blood-perfused r abbit lungs were ventilated either with air (n=7) or air plus 500 part s per million (ppm) of CI2 (n=7) for 10 min. Capillary pressure, measu red by analysing the pressure/time transients of pulmonary arterial, v enous and double (both arterial and venous) occlusions, was unchanged in both groups, In CI2-exposed lungs, the fluid filtration rate increa sed from -0.228+/-0.25 to 1.823+/-1.23 mL . min(-1). 100 g(-1) (p<0.00 1) and the filtration coefficient increased from 0.091+/-0.01 to 0.259 +/-0.07 mL . min(-1). cmH(2)O(-1). 100 g(-1) (p<0.001), No changes wer e observed in the control lungs, The extravascular lung water/blood-fr ee dry weight ratio was 8.6+/-1.6 in the CI2 group and 4.0+/-0.5 in th e control group (p<0.001), confirming that the increase in lung weight was related to accumulation of extravascular fluid. Although the alve olar flooding by oedema is explained, in part, by the CI2-induced epit helial injury, our results suggest that CI2 exposure induces acute lun g injury and oedema due to an increased microvascular permeability.