Prostaglandin cytoprotection and lysosomal stability in acute canine gastric erosions

Prostaglandin cytoprotection may be related to lysosomal stability. In six mongrel dogs, bacterial peritonitis was created by the intraperitoneal instillation of Bacteroides fragilis, Pseudomonas aeruginosa, Streptococcus faecalis and Klebsiella pneumoniae in addition to canine gallbladder bile. In three dogs, gallbladder bile alone was instilled. Three of the six dogs with bacterial peritonitis also received 16,16-dimethyl prostaglandin E2 (PGE2) (0.2 micrograms/kg intramuscularly q6h) 24 hours before and for 3 days after the induction of peritonitis. In the dogs with bacterial peritonitis not receiving PGE2, gastroscopic examination demonstrated acute fundic erosions. None of the other dogs developed acute gastric erosions. In the dogs with bacterial peritonitis not receiving PGE2, fundic mucosal biopsy specimens demonstrated decreased lysosomal stability. In the dogs receiving PGE2, lysosomal stability was similar to that in the animals with bile peritonitis. These experiments demonstrate that PGE2 prevents the development of acute gastric erosions by stabilizing lysosomal membranes.