title: Vasopressin deficiency contributes to the vasodilation of septic shock.
abstract: BACKGROUND
  The hypotension of septic shock is due to systemic vasodilation. On the basis of a clinical observation, we investigated the possibility that a deficiency in vasopressin contributes to the vasodilation of septic shock.
  
  
  RESULTS
  In 19 patients with vasodilatory septic shock (systolic arterial pressure [SAP] of 92 +/- 2 mm Hg [mean +/- SE], cardiac output [CO] of 6.8 +/- 0.7 L/min) who were receiving catecholamines, plasma vasopressin averaged 3.1 +/- 1.0 pg/mL. In 12 patients with cardiogenic shock (SAP, 99 +/- 7 mm Hg; CO, 3.5 +/- 0.9 L/min) who were also receiving catecholamines, it averaged 22.7 +/- 2.2 pg/mL (P < .001). A constant infusion of exogenous vasopressin to 2 patients with septic shock resulted in the expected plasma concentration, indicating that catabolism of vasopressin is not increased in this condition. Although vasopressin is a weak pressor in normal subjects, its administration at 0.04 U/min to 10 patients with septic shock who were receiving catecholamines increased arterial pressure (systolic/diastolic) from 92/52 to 146/66 mm Hg (P < .001/P < .05) due to peripheral vasoconstriction (systemic vascular resistance increased from 644 to 1187 dyne.s/cm5; P < .001). Furthermore, in 6 patients with septic shock who were receiving vasopressin as the sole pressor, vasopressin withdrawal resulted in hypotension (SAP, 83 +/- 3 mm Hg), and vasopressin administration at 0.01 U/min, which resulted in a plasma concentration (approximately 30 pg/mL) expected for the level of hypotension, increased SAP from 83 to 115 mm Hg (P < .01).
  
  
  CONCLUSIONS
  Vasopressin plasma levels are inappropriately low in vasodilatory shock, most likely because of impaired baroreflex-mediated secretion. The deficiency in vasopressin contributes to the hypotension of vasodilatory septic shock.
authors.affiliation: Department of Medicine, Columbia University, College of Physicians & Surgeons, New York, NY 10032, USA.
authors.forename: D W
authors.initials: DW
authors.lastname: Landry
authors.forename: H R
authors.initials: HR
authors.lastname: Levin
authors.forename: E M
authors.initials: EM
authors.lastname: Gallant
authors.forename: R C
authors.initials: RC
authors.lastname: Ashton
authors.forename: S
authors.initials: S
authors.lastname: Seo
authors.forename: D
authors.initials: D
authors.lastname: D'Alessandro
authors.forename: M C
authors.initials: MC
authors.lastname: Oz
authors.forename: J A
authors.initials: JA
authors.lastname: Oliver
mesh_terms: D000328:Adult; D001794:Blood Pressure; D002302:Cardiac Output; D004298:Dopamine / Q000097:blood; D004837:Epinephrine / Q000097:blood; D006339:Heart Rate; D006439:Hemodynamics; D006801:Humans; D009638:Norepinephrine / Q000097:blood; D012770:Shock, Cardiogenic / Q000097:blood / Q000503:physiopathology*; D012772:Shock, Septic / Q000097:blood / Q000503:physiopathology*; D012964:Sodium / Q000097:blood; D014655:Vascular Resistance; D014664:Vasodilation; D014667:Vasopressins / Q000097:blood / Q000172:deficiency*
chemical_list: D014667:Vasopressins; D012964:Sodium; D004298:Dopamine; D009638:Norepinephrine; D004837:Epinephrine