RESUMO
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(-1) i.v.) or isotonic saline (IS; 0.9% NaCl, 4 ml kg(-1) i.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 V(1) receptor.
Assuntos
Pressão Arterial , Hidratação/métodos , Neuro-Hipófise/fisiopatologia , Solução Salina Hipertônica/administração & dosagem , Choque Séptico/terapia , Animais , Antagonistas dos Receptores de Hormônios Antidiuréticos , Pressão Arterial/efeitos dos fármacos , Modelos Animais de Doenças , Frequência Cardíaca , Homeostase , Antagonistas de Hormônios/farmacologia , Infusões Intravenosas , Masculino , Concentração Osmolar , Ocitocina/sangue , Neuro-Hipófise/efeitos dos fármacos , Neuro-Hipófise/metabolismo , Ratos , Ratos Wistar , Receptores de Ocitocina/antagonistas & inibidores , Receptores de Ocitocina/metabolismo , Receptores de Vasopressinas/metabolismo , Choque Séptico/sangue , Choque Séptico/fisiopatologia , Sódio/sangue , Fatores de Tempo , Vasopressinas/sangue , Equilíbrio HidroeletrolíticoRESUMO
Septic shock is characterized by vasodilation and hypotension despite increased vasoconstrictors. While nitric oxide is known to be responsible for vasodilation, failure of vascular smooth muscle to constrict may be due in part to low plasma levels of vasopressin, a neurohypophyseal hormone. In the initial phase of septic shock, vasopressin concentration usually increases but then decreases to a significantly lower concentration after onset of septic shock. In this review, we discuss the neural mechanisms for the regulation of vasopressin secretion during septic shock.