Neurohypophyseal response to fluid resuscitation with hypertonic saline during septic shock in rats

摘要

New findings: ? What is the central question of this study? Small-volume resuscitation with hypertonic saline (HS) has been proposed to restore physiological haemodynamics during haemorrhagic and endotoxic shock. Hypertonic solutions rapidly increase intravascular volume by generating an osmotic gradient that pulls water from the intracellular and interstitial space into the intravascular compartment. Infusion of HS increases plasma sodium levels and osmolality, which may stimulate hormone release from the neurohypophysis. In the present study, we sought to investigate the effects of HS administration during septic shock caused by caecal ligation and perforation. ? What is the main finding and its importance? The present study demonstrated that HS infusion into rats subjected to caecal ligation and perforation induced neurohypophyseal hormone secretion, as well as a transient increase in blood pressure that was mediated by the V1 receptor. Septic shock is a serious condition with a consequent drop in blood pressure and inadequate tissue perfusion. Small-volume resuscitation with hypertonic saline (HS) has been proposed to restore physiological haemodynamics during haemorrhagic and endotoxic shock. In the present study, we sought to determine the effects produced by an HS infusion in rats subjected to caecal ligation and perforation (CLP). Male Wistar rats were randomly grouped and submitted to either CLP or sham surgery. Either HS (7.5% NaCl, 4 ml kg-1i.v.) or isotonic saline (IS; 0.9% NaCl, 4 ml kg-1i.v.) was administered 6 h after CLP. Recordings of mean arterial pressure and heart rate were made during this protocol. Moreover, measurements of electrolyte, vasopressin and oxytocin secretion were analysed after either the HS or the IS treatment. Six hours after CLP, we observed a characteristic decrease in mean arterial pressure that occurs after CLP. The HS infusion in these rats produced a transient elevation of the plasma sodium concentration and osmolality and increased plasma vasopressin and oxytocin levels. Moreover, the HS infusion could restore the mean arterial pressure after CLP, which was completely blunted by the previous injection of the vasopressin but not the oxytocin antagonist. The present study demonstrated that rats subjected to CLP and an infusion of hypertonic saline respond with secretion of neurohypophyseal hormones and a transient increase in blood pressure mediated by the V1 receptor.