Sequential changes in small intestinal structure and function during rotavirus infection in neonatal rats.

摘要: Rotavirus infection is the most common cause of acute diarrhoea in children worldwide. The structural and functional consequences mammalian rotavirus small intestine have been incompletely studied mechanism enterocyte damage poorly defined. This study used a neonatal rat model group B to natural history, clinical features, intestine. Group eight day old rats produced by 24-36 hours, which was accompanied weight loss during early stages infection. By seven days had ceased body similar noninfected controls. could be recovered faeces from 24-72 hours. Light microscopy morphometry confirmed reduction villous height both jejunum ileum, with total mucosal thickness indicating true flat mucosa. Increase crypt depth followed shortening continued as progressively increased between 96-168 Steady state perfusion entire plasma electrolyte solution presence net secretory for water 12-48 parallel sodium absorption. produces self limiting diarrhoeal illness human Infection causes reversible mucosa resulting associated impaired absorption correlate. These findings may relevance pathogenesis