title: Corticosteroid effect on early beta-adrenergic down-regulation during circulatory shock: hemodynamic study and beta-adrenergic receptor assay.
abstract: OBJECTIVE
  The steroid effect on critically ill patients remains controversial. The aim of this study is to characterize the effect of methylprednisolone on the heart in a beta-adrenergically down-regulated condition.
  
  
  METHODS
  A prospective hemodynamic study and retrospective receptor assay.
  
  
  METHODS
  Multidisciplinary ICU in a university hospital.
  
  
  METHODS
  42 patients who required pulmonary arterial catheters and an additional 4 corpses who were available for study within 3 h of their deaths.
  
  
  METHODS
  Intravenous methylprednisolone (10 mg/kg).
  
  
  RESULTS
  We pursued a hemodynamic study following a glucocorticoid administration. In patients who had undergone a long term (> 72 h) catecholamine treatment, the cardiac index increased. In patients who had undergone a short term (1-72 h) catecholamine treatment and in patients with no record of catecholamine administration, the cardiac index showed no remarkable change. Among the corpses, who died soon after their arrival, and the patients, who later died in the ward and were available for further study, we measured beta-adrenergic receptor density in the left ventricular myocardium. It was found that receptor density was decreased after long term catecholamine treatment. Methylprednisolone, on the other hand increased the receptor density.
  
  
  CONCLUSIONS
  Methylprednisolone improved the cardiac index, intriguingly, in patients with long term catecholamine treatment in circulatory shock. Myocardial beta-adrenergic receptor also increased in number after the administration of methylprednisolone. However, the hemodynamic improvement caused by methylprednisolone was not observed in patients without beta-adrenergic down-regulation.
authors.affiliation: Department of Anesthesiology, Nippon Medical School, Tama-Nagayama Hospital, Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Saito
authors.forename: M
authors.initials: M
authors.lastname: Takanashi
authors.forename: E
authors.initials: E
authors.lastname: Gallagher
authors.forename: A
authors.initials: A
authors.lastname: Fuse
authors.forename: S
authors.initials: S
authors.lastname: Suzaki
authors.forename: O
authors.initials: O
authors.lastname: Inagaki
authors.forename: K
authors.initials: K
authors.lastname: Yamada
authors.forename: R
authors.initials: R
authors.lastname: Ogawa
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000378:metabolism; D000328:Adult; D000368:Aged; D001665:Binding Sites; D002102:Cadaver; D016022:Case-Control Studies; D015536:Down-Regulation / Q000187:drug effects; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007275:Injections, Intravenous; D008297:Male; D008775:Methylprednisolone / Q000494:pharmacology / Q000627:therapeutic use*; D008875:Middle Aged; D011412:Propanolamines / Q000378:metabolism; D011446:Prospective Studies; D011943:Receptors, Adrenergic, beta / Q000187:drug effects*; D012189:Retrospective Studies; D012769:Shock / Q000188:drug therapy* / Q000503:physiopathology
chemical_list: D000319:Adrenergic beta-Antagonists; D011412:Propanolamines; D011943:Receptors, Adrenergic, beta; C033394:CGP 12177; D008775:Methylprednisolone