title: [The protective effect of intensive insulin treatment on the myocardium in severely scalded rats].
abstract: OBJECTIVE
  To study the protective effect of intensive insulin treatment on the myocardium of severely scalded rats, and to primarily explore its mechanism.
  
  
  METHODS
  Eighteen SD rats were divided into three groups, with 6 rats in each group. The rats in burn and intensive insulin group were inflicted with 30% TBSA full-thickness injury on the back. Isotonic saline containing 0.12 U/ml insulin solution, and 100 g/L glucose solution were infused into the rats in the intensive insulin group to keep plasma glucose at the level of 4.0 - 6.6 mmol/L (the total fluid amount was 2 ml x kg(-1) x 8h(-1)). In sham burn group,fluid was given according to physiological demand. The same amount of isotonic saline was infused into the rats in burn group. The venous blood was obtained for the detection of plasma glucose contents, and the left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVEDP) were recorded via aortic ventricle cannula before scald and at 1, 2, 3, 4, 5, 6 post-scald hours (PSH). The tissue of the left ventricle was harvested at 6 PSH for the detection of troponin T expression in myocardiocytes.
  
  
  RESULTS
  Plasma glucose level was increased to (7.6 +/- 1.7) mmol/L - (8.4 +/- 4.7) mmol/L in burn group during 1-6 PSH, which was significantly higher than that in intensive insulin group (4.5 +/- 0.9) mmol/L - (5.2 +/- 1.3) mmol/L, P < 0.01). Compared with the intensive insulin group, LVSP was markedly decreased in the burn group (60 +/- 11 mm Hg vs 72 +/- 8 mm Hg, P < 0.05) at 1 PSH,whereas LVEDP was increased significantly (21.3 +/- 11.3 mmHg vs 11.7 +/- 5.2 mmHg, P < 0.05). Intensive insulin treatment could significantly inhibit the loss of troponin T protein in myofilaments of myocardium.
  
  
  CONCLUSIONS
  Intensive insulin treatment possesses a protective effect on myocardia function after severe burns, and it may be related to its preventive effect on the loss of contractile protein in cardiocytes.
authors.affiliation: Center of Burn Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, PR China.
authors.forename: Gen-Fa
authors.initials: GF
authors.lastname: Lv
authors.forename: Bi
authors.initials: B
authors.lastname: Chen
authors.forename: Wan-Fu
authors.initials: WF
authors.lastname: Zhang
authors.forename: Yun-Chuan
authors.initials: YC
authors.lastname: Wang
authors.forename: Wei-Xia
authors.initials: WX
authors.lastname: Cai
authors.forename: Chao-Wu
authors.initials: CW
authors.lastname: Tang
authors.forename: Xiong-Xiang
authors.initials: XX
authors.lastname: Zhu
authors.forename: Mao-Long
authors.initials: ML
authors.lastname: Dong
authors.forename: Da-Hai
authors.initials: DH
authors.lastname: Hu
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002056:Burns / Q000188:drug therapy* / Q000378:metabolism; D007328:Insulin / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020107:Troponin T / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D007328:Insulin; D020107:Troponin T