Numerous premature infants subjected to oxidant stress are afflicted with retinopathy of prematurity (ROP). Reactive oxygen species (ROS) and increased products of peroxidation with vasoconstrictor and cytotoxic properties ultimately lead to the degeneration of retinal microvessels. However, synthesis and activity of the vasodilator, nitric oxide (NO), are increased in the newborn. Furthermore, NO has been reported to protect cells, including endothelial cells, against injury associated with excess production of ROS. We thus postulated that NO plays a protective role in the development of oxygen-induced retinopathy by limiting the extent of microvascular obliteration and tested this hypothesis in a rat model of ROP. / Rat pups receiving inhibitors with differential selectivity for the NO synthase (NOS) isoforms were exposed to 80% O2 from postnatal days 6 to 12 and retinas were compared for extent of capillary obliteration. Endothelial cells being particularly susceptible to oxidative injury, we tested the effect of NO directly on microvascular endothelial cell cultures under oxidant stress. (Abstract shortened by UMI.)
Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.33846 |
Date | January 2001 |
Creators | Speranza, Giovanna. |
Contributors | Chemtob, Sylvain (advisor) |
Publisher | McGill University |
Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
Language | English |
Detected Language | English |
Type | Electronic Thesis or Dissertation |
Format | application/pdf |
Coverage | Master of Science (Department of Pharmacology & Therapeutics.) |
Rights | All items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated. |
Relation | alephsysno: 001862482, proquestno: MQ78963, Theses scanned by UMI/ProQuest. |
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