title: Deleted form of hepatocyte growth factor ameliorates the mortality rate of severe thermal injury in rats.
abstract: The modulating effects of the deleted form of hepatocyte growth factor (dHGF) on burn-induced mortality rates and hepatic protein synthesis were studied in rats.
  
  
  
  Rats were anesthetized, subjected to a 40% full-thickness scald burn, and divided into 2 groups receiving dHGF and vehicle.
  
  
  
  In normal rats, dHGF-treatment (1 mg/kg intravenously, twice daily) for 5 days increased the circulating plasma volume. In burned rats that were receiving vehicle, the survival rate on day 23 after the burn was 27%. The serum albumin levels were decreased and did not reverse to the normal levels until day 23 after the burn. Serum alpha 2-concentration in the injured rats was increased, whereas serum levels of transferrin, total protein, and high-density lipoprotein-cholesterol were decreased. The treatment of animals with dHGF (1 mg/kg intravenously, 3 times daily) for 3 days increased the survival rate on day 23 by 64%. In the animals treated with dHGF for 3 or 6 days, serum alpha 1-, alpha 2-, and beta-globulin concentrations were increased by the dHGF treatment. The serum levels of albumin, transferrin, total protein, and high-density lipoprotein-cholesterol reversed to normal levels or higher.
  
  
  
  Our data show that dHGF treatment may attenuate the decrease of the circulating plasma volume after burn and reduce a high risk of burn shock. It is also indicated that dHGF accelerates synthesis of not only acute-phase reactants but also other hepatic proteins such as albumin and transferrin on severe burn injury. These findings suggest that the appropriate upregulation of hepatic protein synthesis induced by dHGF may accelerate the physiologic recovery process after thermal injury and contribute to ameliorating the burn-induced death.
authors.affiliation: Research Institute of Life Science, Snow Brand Milk Products Co, Ltd, Tochigi, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Arisawa
authors.forename: Y
authors.initials: Y
authors.lastname: Yamashita
authors.forename: H
authors.initials: H
authors.lastname: Ogawa
authors.forename: H
authors.initials: H
authors.lastname: Masunaga
authors.forename: K
authors.initials: K
authors.lastname: Higashio
mesh_terms: D000510:Alpha-Globulins / Q000032:analysis; D000818:Animals; D001609:Beta-Globulins / Q000032:analysis; D001798:Blood Proteins / Q000032:analysis; D001810:Blood Volume / Q000187:drug effects; D002056:Burns / Q000378:metabolism / Q000401:mortality* / Q000503:physiopathology*; D008076:Cholesterol, HDL / Q000097:blood; D017353:Gene Deletion; D014644:Genetic Variation; D017228:Hepatocyte Growth Factor / Q000235:genetics* / Q000494:pharmacology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D012709:Serum Albumin / Q000032:analysis; D014168:Transferrin / Q000032:analysis
chemical_list: D000510:Alpha-Globulins; D001609:Beta-Globulins; D001798:Blood Proteins; D008076:Cholesterol, HDL; D012709:Serum Albumin; D014168:Transferrin; D017228:Hepatocyte Growth Factor