Ilyina Yana, Fot Eugenia, Kuzkov Vsevolod, Kirov Mikhail
Department of Anaesthesiology and Intensive Care, Northern State Medical University, Arkhangelsk, Russian Federation; Department of Anesthesiology and Intensive Care, City Hospital # 1, Arkhangelsk, Russian Federation.
Turk J Anaesthesiol Reanim. 2022 Apr;50(2):94-100. doi: 10.5152/TJAR.2021.21224.
Sepsis-associated endothelial dysfunction and degradation result in release of inflammatory mediators, compromise endothelial permeability, and impair alveolar fluid clearance leading to pulmonary edema. Excessive fluid therapy in septic shock damage the endothelial glycocalyx which will increase capillary leakage. The aim of our study was to assess the relationship of endothelial glycocalyx shedding with hemodynamic and metabolic response to fluid load in patients with septic shock.
Eighteen adult patients were included in prospective observational study. To predict the response to infusion, we performed fluid load test by using crystalloids 7 mL kg-1 for 10 minutes. The plasma concentrations of endothelial glycocalyx components including heparan sulfate proteoglycan and syndecan 1 were measured at baseline, 2, 24 hours after fluid load test.
We observed associations of syndecan 1 with extravascular lung water index (rho = 0.48, P =.04) at baseline and of heparan sulfate proteoglycan with extravascular lung water index (rho= -0.56, P = .03) and pulse pressure variation (rho = 0.53, P = .04) at 24 hours after fluid load test. The plasma concentration of syndecan 1 correlated with lactate at baseline (rho = 0.51, P = .02) and at 24 hours after fluid load test (rho = 0.76, P = .009). At 2 hours after fluid load test, the concentration of syndecan 1 correlated with global end-diastolic volume index (rho= 0.93, P = .001) in normovolemic patients.
The shedding of endothelial glycocalyx after fluid load test in septic shock is associated with hemodynamic and metabolic responses and related with the severity of pulmonary edema.
脓毒症相关的内皮功能障碍和降解导致炎症介质释放，破坏内皮通透性，并损害肺泡液体清除，从而导致肺水肿。脓毒性休克中过度的液体治疗会损害内皮糖萼，这会增加毛细血管渗漏。我们研究的目的是评估脓毒性休克患者内皮糖萼脱落与液体负荷的血流动力学和代谢反应之间的关系。
18名成年患者纳入前瞻性观察研究。为预测输液反应，我们使用晶体液按7 mL/kg输注10分钟进行液体负荷试验。在基线、液体负荷试验后2小时和24小时测量内皮糖萼成分（包括硫酸乙酰肝素蛋白聚糖和多配体蛋白聚糖1）的血浆浓度。
我们观察到，基线时多配体蛋白聚糖1与血管外肺水指数相关（rho = 0.48，P = 0.04），液体负荷试验后24小时硫酸乙酰肝素蛋白聚糖与血管外肺水指数相关（rho = -0.56，P = 0.03）以及与脉压变异相关（rho = 0.53，P = 0.04）。多配体蛋白聚糖1的血浆浓度在基线时（rho = 0.51，P = 0.02）以及液体负荷试验后24小时（rho = 0.76，P = 0.009）与乳酸相关。在液体负荷试验后2小时，正常血容量患者中多配体蛋白聚糖1的浓度与全心舒张末期容积指数相关（rho = 0.93，P = 0.001）。
脓毒性休克患者液体负荷试验后内皮糖萼的脱落与血流动力学和代谢反应相关，并与肺水肿的严重程度有关。
