Department of Translational Physiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Department of Intensive Care, Erasmus MC, University Medical Center, Rotterdam, The Netherlands.
Shock. 2018 Dec;50(6):655-663. doi: 10.1097/SHK.0000000000001096.
The pathogenesis of acute kidney injury (AKI) is characterized by the deterioration of tissue perfusion and oxygenation and enhanced inflammation. The purpose of this study was to investigate whether or not the hemodynamic and inflammatory effects of hypertonic saline (HS) protect the kidney by promoting renal microcirculatory oxygenation and possible deleterious effects of HS due to its high sodium content on renal functional and structural injury following ischemia/reperfusion. Mechanically ventilated and anesthetized rats were randomly divided into four groups (n = 6 per group): a sham-operated control group; a group subjected to renal ischemia for 45 min by supra-aortic occlusion followed by 2 h of reperfusion (I/R); and I/R group treated with a continuous i.v. infusion (5 mL/kg/h) of either % 0.9 NaCl (IR+NS) or %10 NaCl (I/R+HS) after releasing the clamp. Systemic and renal hemodynamic, renal cortical (CμPO2), and medullar microcirculatory pO2 (MμPO2) are measured by the oxygen-dependent quenching of the phosphorescence lifetime technique. Renal functional, inflammatory, and tissues damage parameters were also assessed. HS, but not NS, treatment restored I/R-induced reduced mean arterial pressure, CμPO2, renal oxygen deliver (DO2ren), and consumption (VO2ren). HS caused a decrease in tubular sodium reabsorption (TNa) that correlated with an elevation of fractional sodium excretion (EFNa) and urine output. HS had an anti-inflammatory effect by reducing the levels TNF-α, IL-6, and hyaluronic acid in the renal tissue samples as compared with the I/R and I/R+NS groups (P < 0.05). HS treatment was also associated with mild acidosis and an increased renal tubular damage. Despite HS resuscitation improving the systemic hemodynamics, microcirculatory oxygenation, and renal oxygen consumption as well as inflammation, it should be limited or strictly controlled for long-term use because of provoking widespread renal structural damage.
急性肾损伤 (AKI) 的发病机制以组织灌注和氧合恶化以及炎症增强为特征。本研究旨在探讨高渗盐水 (HS) 是否通过促进肾微循环氧合以及由于其高钠含量对肾缺血/再灌注后肾功能和结构损伤的潜在有害作用，通过改善血流动力学和炎症反应来保护肾脏。机械通气和麻醉大鼠随机分为四组（每组 6 只）：假手术对照组；主动脉夹闭 45min 后再灌注 2h 的肾缺血组 (I/R)；以及夹闭后连续静脉输注 5ml/kg/h%0.9 NaCl (I/R+NS)或%10 NaCl (I/R+HS)的 I/R 组。采用磷光寿命技术测量依赖氧的猝灭来测量系统和肾血流动力学、肾皮质 (CμPO2) 和髓质微循环 pO2 (MμPO2)。还评估了肾功能、炎症和组织损伤参数。HS 治疗，而不是 NS 治疗，恢复了 I/R 引起的平均动脉压、CμPO2、肾氧输送 (DO2ren) 和消耗 (VO2ren) 降低。HS 导致肾小管钠重吸收 (TNa) 减少，与 Fractional Sodium Excretion (EFNa) 和尿量升高相关。与 I/R 和 I/R+NS 组相比，HS 治疗具有抗炎作用，降低了肾组织样本中 TNF-α、IL-6 和透明质酸的水平 (P<0.05)。HS 治疗还与轻度酸中毒和肾小管损伤增加有关。尽管 HS 复苏改善了全身血流动力学、微循环氧合和肾氧消耗以及炎症，但由于引起广泛的肾结构损伤，应限制或严格控制其长期使用。
