The influence of methyl isocyanate (MIC) inhalation on the gas exchange function of the lungs in guinea pigs was studied by measuring arterial blood gases, pH, and tracheal pressure during constant-volume, artificial ventilation with air or lOO1 02 at 40 and 120 min after exposure. A 15 min exposure to MIC at concentrations of 240 to 628 ppm caused a marked reduction in Pao2 and PHa and an elevated tracheal pressure during artificial ventilation. The low Pao2 was only slightly elevated when the animals were ventilated with 100% 02. Although the dry-wet lung weight ratio was reduced at the highest exposure concentration, the effect was not severe and no significant increase in lung water was found at the lower concentrations. MIC inhalation caused severe pulmonary blood shunting and ventilation/perfusion imbalance. This, in turn, led to hypoxemia, metabolic acidosis, and tissue hypoxia, which could produce death. The pulmonary gas exchange deficit likely resulted from bronchial and bronchiolar obstruction caused by sloughed epithelium and other debris from intra-and extrapulmonary airways.
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