title: Changes in Energy Levels by Dexamethasone in Ischemic Hearts and Brains in Male Mice.
abstract: BACKGROUND
  Glucocorticoids have been shown to alleviate ischemia-induced myocardial injury, while aggravating neuronal damage caused by ischemia. As energy failure is a predominant factor in cellular viability, we examined the effects of glucocorticoids on energy utilization in the mouse heart and brain.
  
  
  METHODS
  Seventy-two male ddY mice were assigned to 1 of 3 groups: saline (S), dexamethasone (a glucocorticoid without mineralocorticoid activity, 5 mg/kg) (D), and metyrapone (a potent inhibitor of the synthesis of glucocorticoids, 100 mg/kg) (M) groups (n=24 in each). Three hours after intraperitoneal administration, all animals were decapitated, and the heads were frozen in liquid nitrogen after 0, 0.5, 1, or 2 minutes (n=6 in each). The hearts were immediately removed and frozen in liquid nitrogen after 0, 5, 10, or 20 minutes of incubation at 37°C (n=6 in each). The concentrations of adenylates and monoamines were determined by high-performance liquid chromatography.
  
  
  RESULTS
  In the heart, the adenosine 5'-triphosphate (ATP) concentration did not differ among the 3 groups at 0 minute of ischemia (3 h of S, D, or M treatment). Ischemia for 5 minutes decreased the ATP content to 21% of the basal level in the S group. The ATP decrease was suppressed by either the D or M treatment, such that after 5 minutes ATP levels were 63% and 64% of each basal level, respectively. In the brain, the ATP level in the M group was 62% of that in the S group at 0 minute of ischemia, and the 5'-monophosphate (AMP) level was 276% of that in the S group. Brain dopamine metabolism was facilitated by dexamethasone, and suppressed by metyrapone.
  
  
  CONCLUSIONS
  The relationship between effects of glucocorticoids on ischemia-induced changes in energy levels and cellular viability was not clearly elucidated.
authors.affiliation: Department of Anesthesia and Perioperative Medicine, Ehime University Graduate School of Medicine, Ehime, Japan.
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Yorozuya
authors.forename: Chikara
authors.initials: C
authors.lastname: Namba
authors.forename: Naoto
authors.initials: N
authors.lastname: Adachi
authors.forename: Kazuo
authors.initials: K
authors.lastname: Nakanishi
authors.forename: Kentaro
authors.initials: K
authors.lastname: Dote
authors.forename: Takumi
authors.initials: T
authors.lastname: Nagaro
mesh_terms: D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D015306:Biogenic Monoamines / Q000378:metabolism; D001831:Body Temperature / Q000187:drug effects; D001923:Brain Chemistry / Q000187:drug effects*; D002316:Cardiotonic Agents / Q000494:pharmacology*; D003907:Dexamethasone / Q000494:pharmacology*; D004734:Energy Metabolism / Q000187:drug effects*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007274:Injections, Intraperitoneal; D008297:Male; D008797:Metyrapone / Q000494:pharmacology; D051379:Mice; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism; D017202:Myocardial Ischemia / Q000378:metabolism*
chemical_list: D015306:Biogenic Monoamines; D002316:Cardiotonic Agents; D004791:Enzyme Inhibitors; D000249:Adenosine Monophosphate; D000244:Adenosine Diphosphate; D003907:Dexamethasone; D000255:Adenosine Triphosphate; D008797:Metyrapone