The Mechanism of Acute Gastric Ulcer after Induced Hemorrhagic Shock

T. Urakawa The First Dept. of Surgery, Kobe University School of Medicine, Kobe, Japan

Y. Nagahata The First Dept. of Surgery, Kobe University School of Medicine, Kobe, Japan

Y. Azumi The First Dept. of Surgery, Kobe University School of Medicine, Kobe, Japan

A. Itoh The First Dept. of Surgery, Kobe University School of Medicine, Kobe, Japan

I. Sano The First Dept. of Surgery, Kobe University School of Medicine, Kobe, Japan

K. Takeda The First Dept. of Surgery, Kobe University School of Medicine, Kobe, Japan

Y. Hashimoto The First Dept. of Surgery, Kobe University School of Medicine, Kobe, Japan

T. Ichihara The First Dept. of Surgery, Kobe University School of Medicine, Kobe, Japan

H. Moritomo The First Dept. of Surgery, Kobe University School of Medicine, Kobe, Japan

Y. Saitoh The First Dept. of Surgery, Kobe University School of Medicine, Kobe, Japan

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Abstract

Changes in gastric mucosal blood flow were investigated for their relationship to gastric mucosal prostaglandin E, (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 PGE_z value for animals receiving NA after hemorrhage was not different from that of non-NA-treated group. 3) Pre-treatment with PGE, 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 PGE, due to persistent hypoxia and might be one of the possible factors in ulcer formation.

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The Mechanism of Acute Gastric Ulcer after Induced Hemorrhagic Shock

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