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KMID : 0371319960500060921
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Journal of the Korean Surgical Society
1996 Volume.50 No. 6 p.921 ~ p.929
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Effect of Hypoxia/reoxygenation on Acid Secretion and Nitric Oxide Synthase in the Isolated Rabbit Gastric Glands
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Abstract
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Hypoxia causes gastric mucosal damage, which is caused by releasing chemical mediators such as oxygen derived free radicals, leukotrienes and platelet activating factor etc. It is further aggravated by reoxygenation. NO suppresses the stimulated
acid
secretion in vivo. Increasing evidence suggests that endogenous NO plays a role in maintaining gastric mucosal integrity and in protecting the mucosa against hypoxic injury. However the reported results about NO function after
hypoxia/reoxygenation
were
not always consistent. This study was conducted using isolated rabbit gastric glands to investigate the effect of hypoxia/reoxygenation on acid secretion and NO synthase.
@ES The results were as follows;
@EN 1) Basal and stimulated acid secretion after hypoxia/reoxygenation were decreased and hypoxia did not influenced the viability of the gastric glands.
2) Nitric oxide synthase activity after hypoxia/reoxygenation was significantly decreased.
3) Dibutyryl cAMP stimulation did not influence NO synthase activity.
4) Nitric oxide did not influence basal acid secretion, but it did suppress the stimulated acid secretion. Nitric oxide synthase inhibitor increased acid secretion in the stimulated gastric glands.
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KEYWORD
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