Document Detail


Animal experiment studies on the role of inflammation mediators in corneal neovascularization
MedLine Citation:
PMID:  6205837     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Natural and synthetic inflammatory compounds were implanted in the corneas of rabbits to clarify the question whether corneal neovascularization is induced by stromal edema alone, or by neovascular mediators. It could be demonstrated that prostaglandin E1 and E2 have an angiogenetic capacity, whereas their precursor (arachidonic acid) as well as PGA1, A2, B2, I2 and Thromboxan A2 were inactive in this regard. Histology showed that corneal neovascularization is always accompanied by the invasion of polymorphonuclear leukocytes. Corneal edema in the beginning of vascularization can be explained by the activities of PGE (vasodilation, increase of vascular permeability, liberation of histamine). The implantation of lipoxygenase-dependent arachidonic acid compounds (5-HETE, Leukotriene B4) demonstrated that these mediators share in the process of neovascularization by inducing the chemotaxis. The above mentioned activities of prostaglandins and leukotrienes could also be demonstrated following penetrating keratoplasty and alkali burns of the anterior segment inducing extensive corneal neovascularization. An analysis of the prostaglandin- and leukotriene-dependent mechanisms could be achieved by selective PG- and LT-inhibitors. Radioimmunoassays showed a definite correlation between the concentrations of PGE and the amount of neovascularization following alkali burns. The results of our research lead to the following scheme of pathophysiology of corneal neovascularization: hypoxic, chemical, thermic and mechanical alterations of the cornea induce an activation of corneal cytomembranes, thus initiating the cyclooxygenase-dependent synthesis of prostaglandins with consecutive vasodilation and increase of vascular permeability as well as histamine liberation resulting in corneal edema; on the other hand, prostaglandins proved to have a minimal chemotactic activity; the lipoxygenase-dependent synthesis of leukotrienes inducing chemotaxis and diapedesis of polymorphonuclear leukocytes into the corneal stroma. These inflammatory cells are then the main source of newly synthesized leukotrienes maintaining the chemotaxis, and prostaglandins with angiogenetic activity. Cyclooxygenase- and lipoxygenase-inhibitors can inhibit these activities at two different levels, leading to an approach of successful therapy of corneal diseases inducing neovascularization.
Authors:
R Rochels
Publication Detail:
Type:  English Abstract; Journal Article    
Journal Detail:
Title:  Documenta ophthalmologica. Advances in ophthalmology     Volume:  57     ISSN:  0012-4486     ISO Abbreviation:  Doc Ophthalmol     Publication Date:  1984 May 
Date Detail:
Created Date:  1984-10-22     Completed Date:  1984-10-22     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0370667     Medline TA:  Doc Ophthalmol     Country:  NETHERLANDS    
Other Details:
Languages:  ger     Pagination:  215-62     Citation Subset:  IM    
Vernacular Title:
Tierexperimentelle Untersuchungen zur Rolle von Entzündungsmediatoren bei der Hornhautneovaskularisation.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arachidonic Acid
Arachidonic Acids / physiology
Burns, Chemical / physiopathology
Cornea / blood supply*,  injuries
Corneal Transplantation
Eye Burns / chemically induced
Female
Keratitis / physiopathology*
Leukotriene B4 / physiology
Lipoxygenase / physiology
Male
Neovascularization, Pathologic / physiopathology*
Prostaglandin-Endoperoxide Synthases / physiology
Prostaglandins / physiology*
Rabbits
Thromboxane A2 / physiology
Chemical
Reg. No./Substance:
0/Arachidonic Acids; 0/Prostaglandins; 506-32-1/Arachidonic Acid; 57576-52-0/Thromboxane A2; 71160-24-2/Leukotriene B4; EC 1.13.11.12/Lipoxygenase; EC 1.14.99.1/Prostaglandin-Endoperoxide Synthases

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