title: Impaired pressor sensitivity to noradrenaline in septic shock patients with and without impaired adrenal function reserve.
abstract: OBJECTIVE
  To investigate the relationship between adrenal gland function and pressor response to noradrenaline in septic shock.
  
  
  METHODS
  Basal cortisol level, noradrenaline--mean arterial pressure dose-response curve and cortisol response to intravenous corticotrophin bolus were obtained in nine patients fulfilling usual criteria for septic shock and in six normal volunteers. In patients with septic shock, dose-response curve to noradrenaline was determined a second time 60 min after a 50 mg intravenous hydrocortisone bolus.
  
  
  RESULTS
  As compared with controls, patients with septic shock had increased basal cortisol levels (mean+/-s.d.: 1564+/-818 vs 378+/-104 nmol l(-1) , P=0.002, 95% confidence interval for difference in means: [452, 1920]) and a blunted cortisol response to corticotrophin (403+/-461 vs 1132+/-195 nmol l(-1), P=0.008, [-1163, -2951). Five patients had impaired adrenal function reserve. As compared with controls, septic patients displayed a moderate and non significant decrease in pressor sensitivity to noradrenaline (P=0.112). As compared with patients with adequate adrenal response, patients with impaired adrenal function reserve showed a significant decrease in pressor sensitivity to noradrenaline (P=0.038). In septic patients, hydrocortisone improved pressor response to noradrenaline (P=0.032). This effect was more marked in patients with impaired adrenal function reserve so that, as compared with patients with adequate response, the difference was no longer significant (P=0.123).
  
  
  CONCLUSIONS
  In septic shock, impaired adrenal function reserve may partly be accounted for by the depressed pressor sensitivity to noradrenaline. The latter may be substantially improved by physiological doses of hydrocortisone.
authors.affiliation: Service de Réanimation Médicale, Hôpital R. Poincaré, Garches, Université Paris V, France.
authors.forename: D
authors.initials: D
authors.lastname: Annane
authors.forename: E
authors.initials: E
authors.lastname: Bellissant
authors.forename: V
authors.initials: V
authors.lastname: Sebille
authors.forename: O
authors.initials: O
authors.lastname: Lesieur
authors.forename: B
authors.initials: B
authors.lastname: Mathieu
authors.forename: J C
authors.initials: JC
authors.lastname: Raphael
authors.forename: P
authors.initials: P
authors.lastname: Gajdos
mesh_terms: D000307:Adrenal Gland Diseases / Q000503:physiopathology; D000311:Adrenal Glands / Q000187:drug effects / Q000503:physiopathology*; D000328:Adult; D000368:Aged; D017704:Baroreflex / Q000187:drug effects*; D001794:Blood Pressure / Q000187:drug effects; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000494:pharmacology*; D012772:Shock, Septic / Q000188:drug therapy / Q000503:physiopathology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D014662:Vasoconstrictor Agents; D006854:Hydrocortisone; D009638:Norepinephrine