title: Effects of glutamine treatment on myocardial damage and cardiac function in rats after severe burn injury.
abstract: Treatment with glutamine has been shown to reduce myocardial damage associated with ischemia/reperfusion injury. However, the cardioprotective effect of glutamine specifically after burn injury remains unclear. The present study explores the ability of glutamine to protect against myocardial damage in rats that have been severely burned. Seventy-two Wistar rats were randomly divided into three groups: normal controls (C), burned controls (B) and a glutamine-treated group (G). Groups B and G were subjected to full thickness burns comprising 30% of total body surface area. Group G was administered 1.5 g/ (kg•d) glutamine and group B was given the same dose of alanine via intragastric administration for 3 days. Levels of serum creatine kinase (CK), lactate dehydrogenase (LDH), aspartate transaminase (AST) and blood lactic acid were measured, as well as myocardial ATP and glutathione (GSH) contents. Cardiac function indices and histopathological changes were analyzed at 12, 24, 48 and 72 post-burn hours. In both burned groups, levels of serum CK, LDH, AST and blood lactic acid increased significantly, while myocardial ATP and GSH contents decreased. Compared with group B, CK, LDH, and AST levels were lower and blood lactic acid, myocardial ATP and GSH levels were higher in group G. Moreover, cardiac contractile function inhibition and myocardial histopathological damage were significantly reduced in group G compared to B. Taken together, these results show that glutamine supplementation protects myocardial structure and function after burn injury by improving energy metabolism and by promoted the synthesis of ATP and GSH in cardiac myocytes.
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: Hong
authors.initials: H
authors.lastname: Yan
authors.forename: Yong
authors.initials: Y
authors.lastname: Zhang
authors.forename: Shang-jun
authors.initials: SJ
authors.lastname: Lv
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 / Q000096:biosynthesis; D000284:Administration, Oral; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D015415:Biomarkers / Q000378:metabolism; D002056:Burns / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D052279:Creatine Kinase, MB Form / Q000097:blood; D004195:Disease Models, Animal; D004489:Edema, Cardiac / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D005973:Glutamine / Q000008:administration & dosage / Q000494:pharmacology*; D005978:Glutathione / Q000096:biosynthesis; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006331:Heart Diseases / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D006334:Heart Function Tests; D007770:L-Lactate Dehydrogenase / Q000097:blood; D019344:Lactic Acid / Q000097:blood; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000737:chemistry / Q000201:enzymology / Q000473:pathology; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism; D020011:Protective Agents / Q000008:administration & dosage / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D014867:Water / Q000032:analysis / Q000378:metabolism
chemical_list: D015415:Biomarkers; D020011:Protective Agents; D014867:Water; D005973:Glutamine; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D052279:Creatine Kinase, MB Form; D005978:Glutathione