The mechanism of acute gastric ulcer after induced hemorrhagic shock.

Abstract

Changes in gastric mucosal blood flow were investigated for their relationship to gastric mucosal prostaglandin E2 (PGE2) and noradrenaline (NA) in rats with hemorrhagic shock. The results were as follows: 1) Gastric mucosal blood flow and NA decreased after hemorrhage. Gastric mucosal PGE2 initially increased after exsanguination and then markedly decreased. 2) Administration of NA before hemorrhage resulted in an increase of PGE2. However, the PGE2 value for animals receiving NA after hemorrhage was not different from that of non-NA-treated group. 3) Pre-treatment with PGE2 suppressed the reduction in both gastric mucosal blood flow and NA and the development of ulcer. These results suggest that the increase in gastric mucosal PGE2 in the early stage of shock might represent a phenomenon of adaptation by the adrenergic activation, and the decrease in PGE2 in the late stage might result from impaired synthesis of PGE2 due to persistent hypoxia and might be one of the possible factors in ulcer formation.

• Authors: T Urakawa, Y Nagahata, Y Azumi, A Itoh, I Sano, K Takeda, Y Hashimoto, T Ichihara, H Moritomo, Y Saitoh
• Journal: Scandinavian journal of gastroenterology (Scand J Gastroenterol) Vol. 24 Issue 2 Pg. 193-201 (Mar 1989) ISSN: 0036-5521 [Print] England
• PMID: 2928735 (Publication Type: Journal Article)

Chemical References

• Dinoprostone
• Norepinephrine
• Indomethacin

Topics

• Acute Disease
• Animals
• Blood Pressure
• Dinoprostone (metabolism)
• Gastric Mucosa (blood supply, metabolism)
• Indomethacin (pharmacology)
• Male
• Norepinephrine (metabolism, pharmacology)
• Rats
• Rats, Inbred Strains
• Shock, Hemorrhagic (physiopathology)
• Stomach Ulcer (etiology, metabolism, physiopathology)