title: Effects of neonatal dexamethasone administration on cardiac recovery ability under ischemia-reperfusion in 24-wk-old rats.
abstract: Evaluations of stress-induced cardiac functional alterations in adults after neonatal glucocorticoid (GC) treatment have been limited. In the present study, we evaluated adult cardiac functional recovery during postischemic reperfusion and measured cardiac gene expression involved energy metabolism in rats neonatally treated with dexamethasone (DEX).
  
  
  
  Male Wistar rats were injected DEX in first 3 d after birth and controls were received saline (SAL). At 24 wk of age, insulin tolerance tests were performed, plasma lipid levels were measured, and left ventricular function and myocardial infarct size were evaluated. Expressions of genes involved in cardiac energy metabolism were measured by quantitative real-time polymerase chain reaction (PCR) and western blot.
  
  
  
  In 24-wk-old rats, neonatal DEX administration caused dyslipidemia, impaired cardiac recovery function and increased size of infarction, decreased cardiac expression of glucose transporter 4(GLUT4), peroxisome proliferative-activated receptor gamma coactivator 1α (PGC-1α) and ratios of phospho-forkhead box O1/forkhead box O1 (p-FoxO1/FoxO1) and phospho AMP-activated protein kinase/AMP-activated protein kinase (p-AMPK/AMPK) but increased pyruvate dehydrogenase kinase isoenzyme 4 (PDK4) expression compared with controls.
  
  
  
  Neonatal DEX administration impairs cardiac functional recovery during reperfusion following ischemia in 24-wk-old rats. Reduced cardiac glucose utilization may contribute to the long-term detrimental effects caused by neonatal DEX treatment.
authors.affiliation: Department of Ophthalmology, the Third Hospital of Hebei Medical University, Shijiazhuang, China.
authors.forename: Xinli
authors.initials: X
authors.lastname: Jiang
authors.affiliation: Department of Physiology, Hebei Medical University, Shijiazhuang, China.
authors.forename: Huijie
authors.initials: H
authors.lastname: Ma
authors.affiliation: Department of Endocrinology, the Third Hospital of Hebei Medical University, Shijiazhuang, China.
authors.forename: Chunguang
authors.initials: C
authors.lastname: Li
authors.affiliation: Department of Endocrinology, the Third Hospital of Hebei Medical University, Shijiazhuang, China.
authors.forename: Yue
authors.initials: Y
authors.lastname: Cao
authors.affiliation: Department of Endocrinology, the Third Hospital of Hebei Medical University, Shijiazhuang, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Physiology, Hebei Medical University, Shijiazhuang, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Endocrinology, the Third Hospital of Hebei Medical University, Shijiazhuang, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Liu
mesh_terms: D000091162:AMP-Activated Protein Kinase Kinases; D000818:Animals; D003907:Dexamethasone / Q000627:therapeutic use*; D004734:Energy Metabolism / Q000187:drug effects; D005938:Glucocorticoids / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism; D006321:Heart / Q000187:drug effects*; D008297:Male; D008928:Mitochondria / Q000378:metabolism; D009203:Myocardial Infarction / Q000503:physiopathology; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism; D011494:Protein Kinases / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000188:drug therapy*; D013997:Time Factors
chemical_list: D005938:Glucocorticoids; D003907:Dexamethasone; D011494:Protein Kinases; D000091162:AMP-Activated Protein Kinase Kinases; D005947:Glucose