Gastric blood flow in ethanol injury and prostaglandin cytoprotection.
Studies performed in the author's laboratory concerning the role of gastric mucosal blood flow in ethanol-induced gastric mucosal injury and prostaglandin cytoprotection are reviewed. Fluorescent in vivo microscopic and hydrogen gas clearance studies revealed total absence of blood flow in the gross ethanol-induced lesions. Prostaglandin pretreatment not only prevented gross lesion formation but flow was present throughout the mucosa. A cytoprotective dose of the prostaglandin analogue did not increase blood flow. Transmitted light in vivo microscopy revealed rapid cessation of blood flow through mucosal microvessels within 1 min of ethanol application. The microvessels remained filled with red blood cells, suggesting an intravascular coagulation phenomenon. Histologic studies revealed no necrotic lesion formation 1 min after ethanol, but increasing necrosis from 10 to 60 min. These findings suggest that the rapid ethanol-induced cessation of blood flow renders the gastric mucosa more susceptible to ethanol injury and prostaglandin acts by preventing this blood flow change.
Guth
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D015064:16,16-Dimethylprostaglandin E2 / Q000494:pharmacology*; D000818:Animals; D000431:Ethanol / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D005753:Gastric Mucosa / Q000098:blood supply* / Q000187:drug effects / Q000473:pathology; D008297:Male; D009336:Necrosis; D011459:Prostaglandins E, Synthetic / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012039:Regional Blood Flow / Q000187:drug effects; D014743:Videotape Recording
D011459:Prostaglandins E, Synthetic; D000431:Ethanol; D015064:16,16-Dimethylprostaglandin E2