Pressor response to fluid resuscitation in endotoxic shock: Involvement of vasopressin*

Abstract

To investigate the effects of fluid resuscitation administration on vasopressin secretion and its association with pressor response in endotoxic shock during a period of inappropriately low vasopressin secretion. Prospective, controlled experiment. Animal basic science laboratory. Male Wistar rats, weighing 250 to 300 grams. Rats received lipopolysaccharide (2 mg/kg, intravenous) and had their mean arterial pressure monitored during the next 4 hrs. Subsequently, the animals were assigned randomly to one of seven groups (n = 6 per group) that differed in the composition or volume of the resuscitation fluid administered: control group (no fluid administered); isotonic saline solution (0.9% NaCl; 4 mL/kg); hypertonic saline solution (7.5% NaCl; 4 mL/kg); 0.9% NaCl in 6% hydroxyethyl starch 450/0.7 (4, 8, or 16 mL/kg); or 7.5% NaCl in 6% hydroxyethyl starch 450/0.7 (4 mL/kg). Blood pressure was lower in the lipopolysaccharide-treated group. Administration of 0.9% NaCl in 6% hydroxyethyl starch 450/0.7 did not change mean arterial pressure, but reduced vasopressin plasma levels at a dose of 16 mL/kg. Hypertonic saline solution or 7.5% NaCl in 6% hydroxyethyl starch 450/0.7 administration was followed by an immediate recovery of blood pressure and also by an increase in plasma vasopressin levels when compared to isotonic saline solution. The vasopressin V1 receptor antagonist (10 microg/kg, intravenous, 5 min before infusion) completely blunted the increase in mean arterial pressure induced by hypertonic saline solution or 7.5% NaCl in 6% hydroxyethyl starch 450/0.7 in endotoxemic rats. Isotonic blood volume expansion reduced vasopressin plasma levels. Furthermore, the subsequent release of vasopressin is essential for the pressor response caused by hypertonic fluid infusion during endotoxic shock.