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Journal Article
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[Indications of vasopressin in the management of septic shock].
OBJECTIVE: Vasopressin (antidiuretic hormone) is emerging as a potentially major advancement in the treatment of septic shock. Vasopressin is both a vasopressor and an antidiuretic hormone. It also has haemostatic, gastrointestinal, and thermoregulatory effects. This article reviews the physiology of vasopressin and all the relevant clinical literature on its use in the treatment of septic shock.
DATA SOURCES AND EXTRACTION: Extraction from Pubmed database of French and English articles on the physiology and clinical use of vasopressin. The following key words were selected: vasodilatory shock, vasopressin, septic shock, catecholamines, norepinephrine, renal function, diuresis, mesenteric haemodynamic. The collected articles were reviewed and selected according to their quality and originality.
DATA SYNTHESIS: Vasopressin mediates vasoconstriction via V1-receptor activation on vascular smooth muscle. Septic shock causes first a transient early increase in blood vasopressin concentrations that decreases later to very low concentrations compared to other causes of hypotension. Vasopressin infusion of 0.01-0.04 U min(-1) in septic shock patients increases plasma vasopressin concentrations. This increase is associated with a lesser need for other vasopressors. Vasopressin has been shown to produce greater blood flow diversion from non-vital to vital organ beds than does adrenaline. A large randomized clinical trial should be performed to assess its place as a therapeutic agent of septic shock patient.
DATA SOURCES AND EXTRACTION: Extraction from Pubmed database of French and English articles on the physiology and clinical use of vasopressin. The following key words were selected: vasodilatory shock, vasopressin, septic shock, catecholamines, norepinephrine, renal function, diuresis, mesenteric haemodynamic. The collected articles were reviewed and selected according to their quality and originality.
DATA SYNTHESIS: Vasopressin mediates vasoconstriction via V1-receptor activation on vascular smooth muscle. Septic shock causes first a transient early increase in blood vasopressin concentrations that decreases later to very low concentrations compared to other causes of hypotension. Vasopressin infusion of 0.01-0.04 U min(-1) in septic shock patients increases plasma vasopressin concentrations. This increase is associated with a lesser need for other vasopressors. Vasopressin has been shown to produce greater blood flow diversion from non-vital to vital organ beds than does adrenaline. A large randomized clinical trial should be performed to assess its place as a therapeutic agent of septic shock patient.
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