title: Effects of glycine supplementation on myocardial damage and cardiac function after severe burn.
abstract: BACKGROUND
  Glycine has been shown to participate in protection from hypoxia/reoxygenation injury. However, the cardioprotective effect of glycine after burn remains unclear. This study aimed to explore the protective effect of glycine on myocardial damage in severely burned rats.
  
  
  METHODS
  Seventy-two Wistar rats were randomly divided into three groups: normal controls (C), burned controls (B), and glycine-treated (G). Groups B and G were given a 30% total body surface area full-thickness burn. Group G was administered 1.5 g/(kg d) glycine and group B was given the same dose of alanine via intragastric administration for 3d. Serum creatine kinase (CK), lactate dehydrogenase (LDH), aspartate transaminase (AST), and blood lactate, as well as myocardial ATP and glutathione (GSH) content, were measured. Cardiac contractile function and histopathological changes were analyzed at 12, 24, 48, and 72 hours.
  
  
  RESULTS
  Serum CK, LDH, AST, and blood lactate increased, while myocardial ATP and GSH content decreased in both burned groups. Compared with group B, the levels of CK, LDH, and AST significantly decreased, whereas blood lactate as well as myocardial ATP and GSH content increased in group G. Moreover, cardiac contractile function inhibition and myocardial histopathological damage in group G significantly decreased compared with group B.
  
  
  CONCLUSIONS
  Myocardial histological structure and function were damaged significantly after burn. Glycine is beneficial to myocardial preservation by improving cardiomyocyte energy metabolism and increasing ATP and GSH abundance.
authors.affiliation: State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Burns of PLA, Southwest Hospital, Third Military Medical University, Chongqing 400038, PR China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Zhang
authors.forename: Shang-jun
authors.initials: SJ
authors.lastname: Lv
authors.forename: Hong
authors.initials: H
authors.lastname: Yan
authors.forename: Lin
authors.initials: L
authors.lastname: Wang
authors.forename: Guang-ping
authors.initials: GP
authors.lastname: Liang
authors.forename: Qian-xue
authors.initials: QX
authors.lastname: Wan
authors.forename: Xi
authors.initials: X
authors.lastname: Peng
mesh_terms: D000255:Adenosine Triphosphate / Q000032:analysis; D000409:Alanine / Q000008:administration & dosage; D000704:Analysis of Variance; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D015415:Biomarkers / Q000032:analysis; D002056:Burns / Q000150:complications* / Q000628:therapy; D009202:Cardiomyopathies / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D003402:Creatine Kinase / Q000097:blood; D019587:Dietary Supplements; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000502:physiology; D005978:Glutathione / Q000032:analysis; D005998:Glycine / Q000008:administration & dosage*; D007770:L-Lactate Dehydrogenase / Q000097:blood; D019344:Lactic Acid / Q000097:blood; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar
chemical_list: D015415:Biomarkers; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D003402:Creatine Kinase; D005978:Glutathione; D000409:Alanine; D005998:Glycine