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1
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Role of leukotrienes and platelet activating factor in gastric mucosal damage and repair

100%
Konturek S. J., Brzozowski T.
Journal of Physiology and Pharmacology
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1991
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tom 42
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nr 2
Gastric mucosal integrity depends upon the balance between „aggressive” factors and „defensive” mechanisms. The formation of mucosal lesions results from the disruption of defense lines, including the breaking of unstirred mucus layer, the reduction of surface hydrophobicity, extensive exfoliation of surface epithelium, penetration of offending agents deeply into the mucosa and damage to the microvessels. The release of proinflam- matory and vasoactive mediators such as leukotrienes (LT), thromboxanes, platelet activating factor (PAP), endothelins and others has been thought to be involved in the pathomechanism of mucosal injury, especially damage to the micro vascular endothelium, increased vascular permeability, reduction in mucosal blood flow, vascular stasis, tissue ischemia and glandular cell necrosis. This paper reviews the mechanisms and possible pathogenetic implication of two related compounds, LT and PAP in acute mucosal injury by topical irritants such as ethanol, aspirin, bile salts and by stress. LT and PAP arise from similar membrane phospholipids and may regulate the biosynthesis of one another in the damaged mucosa. Although pharmacological studies have clearly demonstrated the noxious effects of cysteinyl LT and PAP on the mucosa, especially when exposed to topical irritants, recent publications have challenged the primary role of these mediators in the pathogenesis of mucosal lesions and ulcerations because the treatment with agents that selectively antagonize their biosynthesis or the receptor sites at the target cells did not always interrupt the chain of events leading to mucosal injury. The role of these mediators in the mucosal repair processes has been little studied but both cysteinyl LT and PAP seem to delay the restitution and healing of the mucosa. Further studies are necessary to clarify to what extent the biosynthesis of LT and PAP and the pharmacological inhibition of their action on the target tissues is related to noxious, protective and reparative events in the mucosa exposed to mild irritants and ulcerogens.
2
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ATP-induced Ca2plus-signalling enhances rat gastric microvascular endothelial cell migration

100%
Ehring G. R., Szabo I. L., Jones M. K., Sarfeh I. J., Tarnawski A. S.
Journal of Physiology and Pharmacology
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2000
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tom 51
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nr 4,2
3

Microvasculature of the human fetal laryngeal anterior commissure

84%
Strek P., Nowogrodzka-Zagorska M., Miodonski A. J., Olszewski E.
Folia Morphologica
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1997
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tom 56
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nr 4
4
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Evidence for an infarctive pathogenesis of acute and chronic gastroduodenal ulceration

84%
Piasecki C.
Journal of Physiology and Pharmacology
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1992
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tom 43
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nr 2
It is clear that all mucosal defensive mechanisms acting against aggressive ulcerogenic factors depend on adequate blood flow. When defence is active, ulcers tend to heal and do so faster when luminal aggression is prevented by reduction of acidity or eradication of H. pylori. Such successful treatment is so profitable that pharmaceutical companies invest vast fortunes on research into every aspect of therapy. This may explain why research on basic aetiology has been slower. Nevertheless there have been recent advances which increasingly point towards an ischaemic pathogenesis of both acute and chronic ulcers. We have been studying those ischaemic mechanisms that may be triggered by alteration of normal physiological processes, and we now have a body of evidence supporting an infarction-like mechanism induced by abnormal motility which might explain the initiation of both acute and chronic human ulceration. In this article we review the evidence for this and show that such a pathogenesis is compatible with the features and current concepts of gastro-duodenal ulceration. Perhaps the most striking feature of chronic ulcers is their singularity, and localisation to the lesser curvature and first part of the duodenum. Within the lesser curvature there is an increasing incidence from the oesophageal end towards pylorus, with maximal incidence in the incisural area (1). Duodenal ulcers occur on the anterior or posterior walls of the first 4 cm. uncommonly on the superior “cap” and rarely on the inferior wall. Such localisation points to a primary cause which, by analogy with other localised necroses eg coronary or stroke, is usually an infarction of an end-artery system.
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Regional hypoxia correlates with the uptake of a radiolabeled targeted marker of angiogenesis in rat model of myocardial hypertrophy and ischemic injury

67%
Dobrucki L. W., Meoli D. F., Hu J., Sadeghi M. M., Sinusas A. J.
Journal of Physiology and Pharmacology. Supplement
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2009
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tom 60
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nr 4
6
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Isolation and characterization of rat gastric microvascular endothelial cells as a model for studying gastric angiogenesis in vitro

67%
Jones M. K., Wang H., Tomikawa M., Szabo I. L., Kawanaka H., Sarfeh I. J., Tarnawski A. S.
Journal of Physiology and Pharmacology
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2000
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tom 51
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nr 4,2
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