Experimental Studies on Developmental Mechanism of Histamine Induced Ulcers and Ulcer Inhibitory Effects of Histamine Receptor Antagonists
Hiroshima Journal of Medical Sciences Volume 32 Issue 3
Page 311-318
published_at 1983-09
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Title ( eng ) |
Experimental Studies on Developmental Mechanism of Histamine Induced Ulcers and Ulcer Inhibitory Effects of Histamine Receptor Antagonists
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Title ( jpn ) |
ヒスタミン潰瘍発生機序ならびにヒスタミン受容体拮抗剤の潰瘍抑制効果
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Creator |
Kodama Motomu
Ogawa Yoshiteru
Ito Nobuaki
Takeuchi Hitoshi
Seikoh Rokuro
Tanaka Tsuneo
Harada Mitsuo
Kodama Osamu
Ezaki Haruo
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Source Title |
Hiroshima Journal of Medical Sciences
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Volume | 32 |
Issue | 3 |
Start Page | 311 |
End Page | 318 |
Journal Identifire |
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
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Abstract |
Study was made of the developmental mechanism of histamine induced ulcers and inhibitory effects of receptor antagonists from the view point of gastric acidity and microvasculature of the gastric mucosa, and the following results were obtained.
1. In histamine induced ulcers, hypersecretion of gastric acid caused by histamine is not the primary developmental mechanism of the lesion. The main cause is considered to be disturbance of microcirculation in the gastric mucosa attributable to the effects of histamine on the microvasculature of the mucosa. 2. Of the histamine receptor antagonists, diphenhydramine, an Hi-antagonist, was unable to inhibit hypersecretion of gastric acid and disturbance of microcirculation of the gastric mucosa caused by histamine, and thus could not suppress the development of histamine induced ulcers, but cimetidine, an H2-antagonist, inhibited not only hypersecretion of gastric acid, but also prevent disturbance of microcirculation in the mucosa, and consequently suppressed histamine induced ulcers. |
Keywords |
Histamine induced ulcer
Histamine receptor antagonists
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NDC |
Medical sciences [ 490 ]
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Language |
eng
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Resource Type | departmental bulletin paper |
Publisher |
Hiroshima University School of Medicine
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Date of Issued | 1983-09 |
Publish Type | Version of Record |
Access Rights | open access |
Source Identifier |
[ISSN] 0018-2052
[NCID] AA00664312
[PMID] 6643109
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