Uhlich Rindi M, Richter Robert P, Hu Parker J, Kirkman Alyssa A, Ashtekar Amit R, Zheng Lei, Walker Shannon C, Reynolds Lindy M, Griffin Russell L, Jansen Jan O, Kerby Jeffrey D, Richter Jillian R
Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama.
Division of Critical Care Medicine, Department of Pediatrics, University of Alabama at Birmingham, Birmingham, Alabama.
Shock. 2020 Dec;54(6):703-709. doi: 10.1097/SHK.0000000000001597.
Traumatic injury and hemorrhagic shock result in endothelial cell activation and vascular dysfunction that, if not corrected, can propagate multiorgan failure. Angiopoietin-1 and angiopoietin-2 are important regulators of endothelial cell function, and the ratio of plasma angiopoietin-2-to-1 is a useful indicator of overall vascular health. We therefore characterized plasma angiopoietin-2/-1 ratios over time after trauma in adults in an effort to gain insight into the pathophysiology that may drive post-traumatic vasculopathy and organ injury. We performed a single-center prospective observational study to measure plasma angiopoietin-1 and -2 levels and determine angiopoietin-2/-1 ratios in adult trauma patients upon hospital arrival and after 12, 24, and 48 h. Compared with levels in healthy adults, angiopoietin-1 levels were significantly elevated at hospital arrival, and angiopoietin-2 levels were significantly elevated at 12, 24, and 48 h. These kinetics translated in angiopoietin-2/-1 ratios that were significantly greater than controls at 24 and 48 h. After regression analysis, elevated angiopoietin-2 levels were independently associated with blunt injuries at admission, with coagulopathy at admission and 12 h, and with hemorrhagic shock at 24 and 48 h. Significant correlations were observed between both angiopoietins and 24-h transfusion requirements. Angiopoietin-2/-1 ratios correlated with mechanical ventilation duration and intensive care unit and hospital lengths of stay. In this study, we demonstrate novel temporal associations between angiopoietin dysregulation and blunt injuries, acute coagulopathy, and hemorrhagic shock. Moreover, our findings highlight the presence of endothelial activation following traumatic insults in adults that may contribute to worse clinical outcomes.
创伤性损伤和失血性休克会导致内皮细胞活化和血管功能障碍，若不纠正，可能会引发多器官功能衰竭。血管生成素-1和血管生成素-2是内皮细胞功能的重要调节因子，血浆血管生成素-2与1的比值是整体血管健康的有用指标。因此，我们对成人创伤后不同时间点的血浆血管生成素-2/-1比值进行了特征分析，以期深入了解可能导致创伤后血管病变和器官损伤的病理生理学机制。我们进行了一项单中心前瞻性观察研究，以测量成年创伤患者入院时以及入院后12、24和48小时的血浆血管生成素-1和-2水平，并确定血管生成素-2/-1比值。与健康成年人的水平相比，入院时血管生成素-1水平显著升高，而在12、24和48小时时血管生成素-2水平显著升高。这些动力学变化导致血管生成素-2/-1比值在24和48小时时显著高于对照组。经过回归分析，血管生成素-2水平升高与入院时的钝性损伤、入院时和12小时时的凝血病以及24和48小时时的失血性休克独立相关。两种血管生成素与24小时输血需求量之间均观察到显著相关性。血管生成素-2/-1比值与机械通气时间、重症监护病房住院时间和住院总时长相关。在本研究中，我们证明了血管生成素失调与钝性损伤、急性凝血病和失血性休克之间存在新的时间关联。此外，我们的研究结果突出了成人创伤性损伤后内皮细胞活化的存在，这可能导致更差的临床结局。
