Vasopressin deficiency contributes to the vasodilation of septic shock

Donald W. Landry, Howard R. Levin, Ellen M. Gallant, Robert C. Ashton, Susan Seo, David D'Alessandro, Mehmet C. Oz, Juan A. Oliver

Research output: Contribution to journalArticle

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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. Methods and 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 catecbolamines 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 (≃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.

Original languageEnglish (US)
Pages (from-to)1122-1125
Number of pages4
JournalCirculation
Volume95
Issue number5
StatePublished - 1997
Externally publishedYes

Fingerprint

Neurogenic Diabetes Insipidus
Septic Shock
Vasopressins
Vasodilation
Arterial Pressure
Hypotension
Blood Pressure
Cardiac Output
Catecholamines
Cardiogenic Shock
Baroreflex
Vasoconstriction
Vascular Resistance
Shock
Observation

Keywords

  • hypotension
  • shock
  • vasodilation

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Landry, D. W., Levin, H. R., Gallant, E. M., Ashton, R. C., Seo, S., D'Alessandro, D., ... Oliver, J. A. (1997). Vasopressin deficiency contributes to the vasodilation of septic shock. Circulation, 95(5), 1122-1125.

Vasopressin deficiency contributes to the vasodilation of septic shock. / Landry, Donald W.; Levin, Howard R.; Gallant, Ellen M.; Ashton, Robert C.; Seo, Susan; D'Alessandro, David; Oz, Mehmet C.; Oliver, Juan A.

In: Circulation, Vol. 95, No. 5, 1997, p. 1122-1125.

Research output: Contribution to journalArticle

Landry, DW, Levin, HR, Gallant, EM, Ashton, RC, Seo, S, D'Alessandro, D, Oz, MC & Oliver, JA 1997, 'Vasopressin deficiency contributes to the vasodilation of septic shock', Circulation, vol. 95, no. 5, pp. 1122-1125.
Landry DW, Levin HR, Gallant EM, Ashton RC, Seo S, D'Alessandro D et al. Vasopressin deficiency contributes to the vasodilation of septic shock. Circulation. 1997;95(5):1122-1125.
Landry, Donald W. ; Levin, Howard R. ; Gallant, Ellen M. ; Ashton, Robert C. ; Seo, Susan ; D'Alessandro, David ; Oz, Mehmet C. ; Oliver, Juan A. / Vasopressin deficiency contributes to the vasodilation of septic shock. In: Circulation. 1997 ; Vol. 95, No. 5. pp. 1122-1125.
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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. Methods and 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 catecbolamines 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 (≃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.",
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T1 - Vasopressin deficiency contributes to the vasodilation of septic shock

AU - Landry, Donald W.

AU - Levin, Howard R.

AU - Gallant, Ellen M.

AU - Ashton, Robert C.

AU - Seo, Susan

AU - D'Alessandro, David

AU - Oz, Mehmet C.

AU - Oliver, Juan A.

PY - 1997

Y1 - 1997

N2 - 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. Methods and 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 catecbolamines 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 (≃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.

AB - 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. Methods and 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 catecbolamines 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 (≃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.

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KW - shock

KW - vasodilation

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