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Paul H. Guth

Researcher at Veterans Health Administration

Publications -  217
Citations -  8058

Paul H. Guth is an academic researcher from Veterans Health Administration. The author has contributed to research in topics: Gastric mucosa & Gastric acid. The author has an hindex of 48, co-authored 217 publications receiving 7929 citations. Previous affiliations of Paul H. Guth include West Los Angeles College & University of California.

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Journal ArticleDOI

Role of Oxygen-Derived Free Radicals in Hemorrhagic Shock-Induced Gastric Lesions in the Rat

Makoto Itoh, +1 more
- 01 May 1985 - 
TL;DR: It is suggested that oxygen-derived free radicals, particularly O2-, play an important role in the formation of gastric lesions produced by ischemia plus HCl, and both allopurinol and superoxide dismutase, but not dimethyl sulfoxide, significantly protected against hemorrhagic shock-induced Gastric lesions.
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Histologic and microcirculatory changes in alcohol-induced gastric lesions in the rat: effect of prostaglandin cytoprotection

Paul H. Guth, +2 more
- 01 Nov 1984 - 
TL;DR: Alcohol-induced stasis of flow in injured areas may be of pathogenetic significance and prostaglandin protection might involve prevention of this microcirculatory change.
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Topical Aspirin Plus HCl Gastric Lesions in the Rat: Cytoprotective Effect of Prostaglandin, Cimetidine, and Probanthine

Paul H. Guth, +2 more
- 01 Jan 1979 - 
TL;DR: All three classes of antisecretory agents studied are also cytoprotective, i.e., they can protect against gastric mucosal injury by topical aspirin plus HCl by some mechanism other than inhibition of acid and pepsin secretion.
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Contribution of no-reflow phenomenon to hepatic injury after ischemia-reperfusion: evidence for a role for superoxide anion.

Anthony Koo, +5 more
- 01 Mar 1992 - 
TL;DR: Intravenous administration of a longacting form of superoxide dismutase significantly decreased the hepatocellular necrosis and reduced the microcirculatory stasis in the liver sinusoids and established the important contribution of the no‐reflow phenomenon in ischemia‐reperfusion injury to the liver.
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Sensory neurons signal for an increase in rat gastric mucosal blood flow in the face of pending acid injury.

Peter Holzer, +5 more
- 01 Aug 1991 - 
TL;DR: The current findings show that the increase in gastric mucosal blood flow that follows disruption of the gastrics mucosal barrier in the presence of acid is mediated by sensory neurons that seem to monitor acid back-diffusion and in turn signal for a protective increase in blood flow.