Faculty Collaboration Database

Oxidative stress and adaptation of the infant heart to hypoxia and ischemia. Antioxid Redox Signal 2004 Apr;6(2):423-9

Date

03/18/2004

Pubmed ID

15025944

DOI

10.1089/152308604322899495

Scopus ID

2-s2.0-1542619247 (requires institutional sign-in at Scopus site)   37 Citations

Abstract

The potential contribution of oxidative stress to cardioprotection in infants induced by adaptation to chronic hypoxia and by ischemic preconditioning is poorly understood. Under conditions of oxidative stress, reactive oxygen species and reactive nitrogen species may contribute to phenotypic changes in hearts adapted to chronic hypoxia and to the pathogenesis of myocardial injury during both ischemia/reperfusion and hypoxia/reoxygenation. Hearts from infant rabbits normoxic from birth can be preconditioned by brief periods of ischemia. In contrast, hearts from infant rabbits adapted to hypoxia from birth appear resistant to ischemic preconditioning. Chronically hypoxic infant rabbit hearts are already resistant to ischemia compared with age-matched normoxic controls, and thus additional cardioprotection by ischemic preconditioning may not be possible. Endothelial nitric oxide synthase (NOS3) protein and its product nitric oxide are increased, but not NOS3 message, in chronically hypoxic infant hearts to protect against ischemia. Chronic hypoxia from birth also increases cardioprotection of infant hearts by increasing association of heat shock protein 90 with NOS3. Normoxic infant hearts also generate more superoxide by an N(omega)-nitro-L-arginine methyl ester-inhibitable mechanism than chronically hypoxic hearts. Thus, NOS3 appears to be critically important in adaptation of infant hearts to chronic hypoxia and in resistance to subsequent ischemia by regulating the production of reactive oxygen and nitrogen species.

Author List

Baker JE

Author

John E. Baker PhD Professor in the Surgery department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Adaptation, Physiological
Animals
Animals, Newborn
Heart
Heart Defects, Congenital
Humans
Hypoxia
Infant
Ischemic Preconditioning, Myocardial
Myocardial Ischemia
Myocardial Reperfusion Injury
Nitric Oxide Synthase
Nitric Oxide Synthase Type III
Oxidation-Reduction
Oxidative Stress
Potassium Channels, Inwardly Rectifying
Protein Kinases
Signal Transduction