Journal ArticleDOI
Gastric mucosal ulceration following vasoactive agents. A new experimental model.
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In this paper, the influence of vasoactive catecholamines, epinephrine and norepinephrine, has been investigated in regard to the comparative ulcerogenicity on the gastric glandular mucosa of the rat.Abstract:
The influence of the vasoactive catecholamines, epinephrine and norepinephrine, has been investigated in regard to the comparative ulcerogenicity on the gastric glandular mucosa of the rat. The unique extensive, hemorrhagic necrosis, and ulcerations which appear in the fundus—but not the antrum—following single injections of these drugs are readily quantified because of the continuous nature of the lesion. A standard assay has been developed with this new ulcer model, which results in extensive mucosal ulceration (43% of fundus with lesions) in 100% of treated animals after only 5 hr. The optimal procedure requires the single intraperitoneal epinephrine injection of 0.4 mg/kg to young adult Sprague-Dawley rats 4 hr after pylorus occlusion, and the sacrifice of animals 1 hr after injection. This experimental gastric lesion is dependent upon the presence of gastric acid, and is completely inhibited by bilateral vagotomy, and almost completely inhibited by the presence of a magnesium-aluminum hydroxide gel-type antacid.read more
Citations
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Effects of coping behavior in different warning signal conditions on stress pathology in rats.
TL;DR: Rats received electric shock that was preceded by either a warning signal, a series of signals forming an "external clock," or no signal at all, and subjects which could avoid and/or escape shock developed less ulceration than yoked "helpless" animals which received exactly the same shock but had no control over shock.
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The pathophysiological response to spinal cord injury. The current status of related research.
TL;DR: This review of spinal cord injury research has placed special emphasis on the controversial issues appropriate to a new, stimulating, and competitive area of research.
Journal ArticleDOI
Altered norepinephrine metabolism following experimental spinal cord injury. 1. Relationship to hemorrhagic necrosis and post-wounding neurological deficits.
TL;DR: It is hypothesized that toxic quantities of tissue NE induce intense vasospasm which impedes or arrests cord perfusion and causes the neuronal necrosis, vascular rupture, and parenchymal self-destruction manifest as central hemorrhagic necrosis.
Journal ArticleDOI
Pathogenesis, diagnosis and treatment of acute gastric mucosal lesions.
G. Marrone,William Silen +1 more
TL;DR: Endoscopic findings in conjunction with the history usually differentiates stress ulcer from other bleeding lesions, and antacids appear to be superior to cimetidine in preventing bleeding from stress ulcers.
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The pathophysiology of stress ulcer disease
TL;DR: A differential energy deficit in fundic mucosa as a result of ischemia probably contributes to mucosa damage by interfering with anion exchange (HCO3− for Cl−) and the exact role of steroids and prostaglandins is controversial.
References
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Journal ArticleDOI
Gastric secretion in relation to mucosal blood flow studied by a clearance technic.
Journal Article
Pharmacological properties of a new adrenergic blocking agent: N,N-dibenzyl-beta-chloroethylamine (dibenamine).
Mark Nickerson,Louis S. Goodman +1 more
TL;DR: Results are viewed as indicating that Dibenamine probably acts directly upon effector cells to prevent excitatory responses to epinephrine or sympathin E, and may be effective in lowering the blood pressure of rats with experimental renal hypertension.
Journal ArticleDOI
Relationship of stress-induced histidine decarboxylase to circulatory homeostasis and shock.
TL;DR: Histidine decarboxylase activity of mouse tissues is increased by stress and by injection of epinephrine and norepinephrine, suggesting a balance between histamine and catechol amines producing a component of circulatory homeostasis.