The gastric juice aspiration syndrome (GJA-S,
Mendelson syndrome) was studied experimentally in pigs. Following instillation of gastric juice into the right main bronchus
necrosis of pneumocytes and bronchiolar epithelium occurred with activation of
complement and a
prostaglandin E releasing system (possibly the
kinin system). Cell
necrosis was followed by loss of
surfactant and formation of hyaline membranes, rich in
immunoglobulin M. The alveolar damage organized, resulting in intraalveolar and interstitial
fibrosis. The causative agents were found to be both gastric hydrochloric acid and
pepsin. Pretreatment with H2-, or
acetylcholine-receptor-antagonists (
cimetidine or
pirenzepin) as well as buffering of the gastric juice to a neutral pH did not prevent lung
fibrosis. If a mixture of
aluminium hydroxide, magnesium carbonate and
oxethazaine was added to the aspirate, development of lung
fibrosis was prevented, but severe granulomatous reaction with foreign body giant cells within both lungs evolved.
Kallikrein inhibitor, when administered intravenously not later than 3 min after artificial aspiration, protected the left lung completely and large areas of the right. If infused within 60-90 s complete protection of the left lung and the right upper lobe was achieved. In the majority of the animals a mild focal
fibrosis developed in the right lower lobe; in one experiment both lungs were devoid of fibrotic areas. If
Kallikrein inhibitor was infused 5 min prior to aspiration, lung
fibrosis was not prevented.