The role of inflammation in oxygen-induced lung injury in the preterm guinea pig
The role of inflammation in oxygen-induced lung injury in the preterm guinea pig
This thesis describes the development and validation of the preterm guinea pig as a small animal model of respiratory distress syndrome and bronchopulmonary dysplasia. Guinea pig pups, delivered by Caesarian section up to 5 days before normal term at 68 days gestation, were used to study the pulmonary sequelae of prematurity and oxygen exposure. The essential hypothesis was that oxygen exposure is the primary pathogenetic factor in the evolution of acute and chronic neonatal lung disease and that the inflammatory process contributes to the evolution of chronic lung disease. Guinea pigs delivered at 63 days gestation (n= 60) had a 40% mortality in the first 12h of life. Respiratory distress occurred in all animals and respiratory insufficiency wsa the cause of all deaths in the first 24h. Pulmonary histology in animals dying in the first 12h experienced initial, transient respiratory distress and histologically there was evidence of acute lung injury including pulmonary atelectasis, vascular congestion, neutrophil infiltration and protein and fibrin exudation into the airspaces. Preterm animals exposed to 95% oxygen developed more extensive lung injury including the development of hyaline membranes, comprising cellular debris and fibrin. The term animal was less susceptible to oxygen-induced lung damage. The final section of the work comprised several pilot studies aimed at developing a model of longer term, sublethal oxygen toxicity in which to study the contribution of the inflammatory process to the evolution of chronic lung disease. Several protocols were studied by means of BAL and histology. A period of 95% oxygen for 3 days followed by 85% oxygen for 4 days appeared to produce evidence of sustained pulmonary inflammation, however when studied histologically at day 28 there was no evidence of chronic lung disease. The guinea pig model of oxygen-induced pulmonary inflammation has provided considerable insight into the pathogenesis of neonatal acute and chronic lung disease.
University of Southampton
1991
Town, George Ian
(1991)
The role of inflammation in oxygen-induced lung injury in the preterm guinea pig.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
This thesis describes the development and validation of the preterm guinea pig as a small animal model of respiratory distress syndrome and bronchopulmonary dysplasia. Guinea pig pups, delivered by Caesarian section up to 5 days before normal term at 68 days gestation, were used to study the pulmonary sequelae of prematurity and oxygen exposure. The essential hypothesis was that oxygen exposure is the primary pathogenetic factor in the evolution of acute and chronic neonatal lung disease and that the inflammatory process contributes to the evolution of chronic lung disease. Guinea pigs delivered at 63 days gestation (n= 60) had a 40% mortality in the first 12h of life. Respiratory distress occurred in all animals and respiratory insufficiency wsa the cause of all deaths in the first 24h. Pulmonary histology in animals dying in the first 12h experienced initial, transient respiratory distress and histologically there was evidence of acute lung injury including pulmonary atelectasis, vascular congestion, neutrophil infiltration and protein and fibrin exudation into the airspaces. Preterm animals exposed to 95% oxygen developed more extensive lung injury including the development of hyaline membranes, comprising cellular debris and fibrin. The term animal was less susceptible to oxygen-induced lung damage. The final section of the work comprised several pilot studies aimed at developing a model of longer term, sublethal oxygen toxicity in which to study the contribution of the inflammatory process to the evolution of chronic lung disease. Several protocols were studied by means of BAL and histology. A period of 95% oxygen for 3 days followed by 85% oxygen for 4 days appeared to produce evidence of sustained pulmonary inflammation, however when studied histologically at day 28 there was no evidence of chronic lung disease. The guinea pig model of oxygen-induced pulmonary inflammation has provided considerable insight into the pathogenesis of neonatal acute and chronic lung disease.
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Published date: 1991
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Local EPrints ID: 460571
URI: http://eprints.soton.ac.uk/id/eprint/460571
PURE UUID: 0562f8df-ec23-475b-8517-57674eebd941
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Date deposited: 04 Jul 2022 18:24
Last modified: 04 Jul 2022 18:24
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Author:
George Ian Town
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