Enteric vascular endothelial response to bacterial endotoxin

• Published in: International journal of experimental pathology Vol. 74; no. 6; pp. 593 - 601
• Main Authors: KOSHI, R, MATHAN, V. I, DAVID, S, MATHAN, M. M
• Format: Journal Article
• Language: English
• Published: Oxford Blackwell Science 01.12.1993
• Subjects: Acute Disease; Animals; Arterioles - ultrastructure; Bacterial diseases; Bacterial diseases of the digestive system and abdomen; Biological and medical sciences; Diarrhea - etiology; Diarrhea - pathology; Endothelium, Vascular - drug effects; Endothelium, Vascular - ultrastructure; Endotoxins - pharmacology; Human bacterial diseases; Infectious diseases; Intestinal Mucosa - blood supply; Lipopolysaccharides - pharmacology; Medical sciences; Mice; Mice, Inbred Strains; Microscopy, Electron; Venules - ultrastructure; Human; Animal model; Immune response; Rodentia; Etiopathogenesis; Diarrhea; Electron microscopy; Endotoxin; Endothelium; Infection; Pathology; Microcirculation; Vertebrata; Experimental disease; Mammalia; Mouse; Bacteriosis; Digestive diseases; Intestinal disease; Vascular wall
• ISSN: 0959-9673; 1365-2613

The response of enteric vasculature to endotoxin was examined at the ultrastructural level using a murine model of endotoxin-induced acute diarrhoea. Morphological changes indicative of endothelial damage were evident as early as 15 minutes following endotoxin challenge. These changes, characterized by widening of intercellular spaces, increased microvillous projections and the appearance of stress fibres, preceded the leucocytic response. Endothelial damage increased with time, being associated with progressive degenerative changes in the plasma membrane, cytoplasm and organelles, ultimately leading to desquamation. These latter changes were temporally associated with margination of neutrophils and platelet adhesion to the denuded subendothelium. The venules were the primary site of these changes while the capillaries were the least affected. The arterioles were markedly constricted with minimal endothelial damage. These changes suggest that the enteric vascular endothelium may be an important target organ, and the resultant endothelial injury may have implications in host responses to endotoxin.