Batista Mariana B, Bravin Augusto C, Lopes Lais M, Gerenuti Elisa, Elias Lucila L K, Antunes-Rodrigues Jose, Giusti-Paiva Alexandre
Department of Biomedical Science, Federal University of Alfenas, Alfenas, Minas Gerais, Brazil.
Crit Care Med. 2009 Nov;37(11):2968-72. doi: 10.1097/CCM.0b013e3181b02e3b.
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.
探讨在血管升压素分泌异常低下的时期，液体复苏给药对内毒素休克中血管升压素分泌的影响及其与升压反应的关系。
前瞻性对照实验。
动物基础科学实验室。
体重250至300克的雄性Wistar大鼠。
大鼠接受脂多糖（2毫克/千克，静脉注射），并在接下来的4小时内监测其平均动脉压。随后，将动物随机分为七组之一（每组n = 6），这些组在给予的复苏液的成分或体积上有所不同：对照组（未给予液体）；等渗盐溶液（0.9%氯化钠；4毫升/千克）；高渗盐溶液（7.5%氯化钠；4毫升/千克）；6%羟乙基淀粉450/0.7中的0.9%氯化钠（4、8或16毫升/千克）；或6%羟乙基淀粉450/0.7中的7.5%氯化钠（4毫升/千克）。
脂多糖治疗组的血压较低。6%羟乙基淀粉450/0.7中给予0.9%氯化钠不会改变平均动脉压，但在剂量为16毫升/千克时会降低血管升压素血浆水平。与等渗盐溶液相比，给予高渗盐溶液或6%羟乙基淀粉450/0.7中的7.5%氯化钠后，血压立即恢复，血浆血管升压素水平也会升高。血管升压素V1受体拮抗剂（10微克/千克，静脉注射，输注前5分钟）完全消除了高渗盐溶液或6%羟乙基淀粉450/0.7中的7.5%氯化钠在内毒素血症大鼠中引起的平均动脉压升高。
等渗血容量扩充降低了血管升压素血浆水平。此外，内毒素休克期间高渗液体输注引起的升压反应中，随后血管升压素的释放至关重要。
