Moss M, Gillespie M K, Ackerson L, Moore F A, Moore E E, Parsons P E
Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO, USA.
Crit Care Med. 1996 Nov;24(11):1782-6. doi: 10.1097/00003246-199611000-00004.
The endothelial cell produces many bioactive compounds that are presumed to play important roles in the pathogenesis of the adult respiratory distress syndrome (ARDS). We postulated that individuals with sepsis and trauma-two at-risk diagnoses for the development of ARDS--might demonstrate differences in the degree of endothelial cell activity.
Prospective cohort study.
Intensive care unit patients in a tertiary, university-affiliated, city hospital.
Fifty-five intensive care unit patients (19 with sepsis and 36 trauma patients).
Plasma measurements of three endothelial cell products--von Willebrand factor antigen, soluble intercellular adhesion molecule-1 (ICAM-1), and soluble E-selectin-were performed within 8 hrs of patients meeting our inclusion criteria, and at the clinical onset of ARDS.
Twenty-six percent of the septic patients and 25% of the trauma patients developed ARDS. The median (and 25% to 75% quartiles) concentrations of all three mediators measured in the sepsis patients (von Willebrand factor antigen 399% [375% to 452%], ICAM-1 573 ng/mL [470 to 980], and soluble E-selectin 180 ng/mL [81 to 340]) were significantly higher (p < .001 for each individual analysis) than in the trauma patients (von Willebrand factor antigen 256% [217% to 310%], ICAM-1 148 ng/mL [113 to 210], and soluble E-selectin 42 ng/mL [31 to 65 ng/ mL]). In addition, neither the ICAM-1 nor soluble E-selectin concentrations measured in the trauma patients were different (p = .17 and p = .24, respectively) from normal controls. In those patients who developed ARDS, the differences in the concentrations of all three endothelial cell mediators between the sepsis and trauma patients persisted (p = .008 for von Willebrand factor antigen, p = .003 for ICAM-1, and p = .003 for E-selectin).
These findings suggest that differences in endothelial cell activity exist between sepsis and trauma patients who are at risk for the development of ARDS.
内皮细胞产生许多生物活性化合物，推测它们在成人呼吸窘迫综合征（ARDS）的发病机制中起重要作用。我们推测，患有脓毒症和创伤（这两种疾病是发生ARDS的高危诊断）的个体，其内皮细胞活性程度可能存在差异。
前瞻性队列研究。
一所大学附属的三级城市医院的重症监护病房。
55例重症监护病房患者（19例脓毒症患者和36例创伤患者）。
在患者符合纳入标准后8小时内以及ARDS临床发作时，对三种内皮细胞产物进行血浆检测，这三种产物分别是血管性血友病因子抗原、可溶性细胞间黏附分子-1（ICAM-1）和可溶性E-选择素。
26%的脓毒症患者和25%的创伤患者发生了ARDS。脓毒症患者中测量的所有三种介质的中位数（及25%至75%四分位数）浓度（血管性血友病因子抗原399%[375%至452%]，ICAM-1 573 ng/mL[470至980]，可溶性E-选择素180 ng/mL[81至340]）显著高于创伤患者（血管性血友病因子抗原256%[217%至310%]，ICAM-1 148 ng/mL[113至210]，可溶性E-选择素42 ng/mL[31至65 ng/mL]）（每项单独分析p<0.001）。此外，创伤患者中测量的ICAM-1和可溶性E-选择素浓度与正常对照组相比无差异（分别为p = 0.17和p = 0.24）。在发生ARDS的患者中，脓毒症患者和创伤患者之间所有三种内皮细胞介质浓度的差异仍然存在（血管性血友病因子抗原p = 0.008，ICAM-1 p = 0.003，E-选择素p = 0.003）。
这些发现表明，有发生ARDS风险的脓毒症患者和创伤患者之间存在内皮细胞活性差异。
