Department of Adult Intensive Care, Erasmus MC, University Medical Center Rotterdam, Erasmus University, Doctor Molewaterplein 40, 3015 GD, Rotterdam, The Netherlands.
Department of Biomedical Engineering, Thorax Center, Erasmus MC, Rotterdam, The Netherlands.
J Clin Monit Comput. 2023 Oct;37(5):1193-1205. doi: 10.1007/s10877-023-00978-7. Epub 2023 Feb 6.
Acute kidney injury (AKI) is frequently seen in patients with hemorrhagic shock due to hypotension, tissue hypoxia, and inflammation despite adequate resuscitation. There is a lack of information concerning the alteration of renal microcirculation and perfusion during shock and resuscitation. The aim of this study was to investigate the possible role of renal microcirculatory alterations on development of renal dysfunction in a pig model of non-traumatic hemorrhagic shock (HS) induced AKI.Fully instrumented female pigs were divided into the two groups as Control (n = 6) and HS (n = 11). HS was achieved by withdrawing blood until mean arterial pressure (MAP) reached around 50 mmHg. After an hour cessation period, fluid resuscitation with balanced crystalloid was started for the duration of 1 h. The systemic and renal hemodynamics, renal microcirculatory perfusion (contrast-enhanced ultrasound (CEUS)) and the sublingual microcirculation were measured.CEUS peak enhancement was significantly increased in HS during shock, early-, and late resuscitation indicating perfusion defects in the renal cortex (p < 0.05 vs. baseline, BL) despite a stable renal blood flow (RBF) and urine output. Following normalization of systemic hemodynamics, we observed persistent hypoxia (high lactate) and high red blood cell (RBC) velocity just after initiation of resuscitation resulting in further endothelial and renal damage as shown by increased plasma sialic acid (p < 0.05 vs. BL) and NGAL levels. We also showed that total vessel density (TVD) and functional capillary density (FCD) were depleted during resuscitation (p < 0.05).In this study, we showed that the correction of systemic hemodynamic variables may not be accompanied with the improvement of renal cortical perfusion, intra-renal blood volume and renal damage following fluid resuscitation. We suggest that the measurement of renal injury biomarkers, systemic and renal microcirculation can be used for guiding to the optimization of fluid therapies.
急性肾损伤（AKI）在低血压、组织缺氧和炎症导致的出血性休克患者中很常见，尽管进行了充分的复苏。关于休克和复苏期间肾微循环和灌注的变化，目前还缺乏信息。本研究旨在探讨非创伤性出血性休克（HS）诱导 AKI 猪模型中肾微循环改变在肾功能障碍发展中的可能作用。
对照组（n=6）和 HS 组（n=11）。HS 通过抽血使平均动脉压（MAP）降至约 50mmHg 来实现。停止 1 小时后，开始用平衡晶体液进行液体复苏 1 小时。测量全身和肾脏血流动力学、肾脏微循环灌注（对比增强超声（CEUS））和舌下微循环。
尽管肾血流量（RBF）和尿量稳定，但在休克、早期和晚期复苏期间，HS 中的 CEUS 峰值增强显著增加，表明肾皮质灌注缺陷（与基线相比，p<0.05）。在全身血流动力学正常化后，我们观察到在复苏开始后仍存在持续缺氧（高乳酸）和高红细胞（RBC）速度，这导致内皮和肾损伤进一步增加，表现为血浆唾液酸（p<0.05）和 NGAL 水平升高。我们还表明，在复苏期间总血管密度（TVD）和功能性毛细血管密度（FCD）减少（p<0.05）。
在这项研究中，我们表明，在液体复苏后，纠正全身血流动力学变量可能不会伴有肾皮质灌注、肾内血容量和肾损伤的改善。我们建议，测量肾损伤生物标志物、全身和肾脏微循环可以用于指导液体治疗的优化。
