PDF(Pubmed)
Abstract：
Despite significant efforts toward improving therapy for septic shock, mortality remains high. Applying veno-arterial (V-A) extracorporeal membrane oxygenation (ECMO) in this context remains controversial. Since the cannulation of the femoral artery for V-A ECMO return leads to lower body hyperoxia, this study investigated the impact of V-A ECMO therapy on the intestinal and hepatic microcirculation during septic shock in a rodent model. Thirty male Lewis rats were randomly assigned to receive V-A ECMO therapy with low (60 mL/kg/min) or high (90 mL/kg/min) blood flow or a sham procedure. Hemodynamic data were collected through a pressure-volume catheter in the left ventricle and a catheter in the lateral tail artery. Septic shock was induced by intravenous administration of lipopolysaccharide (1 mg/kg). The rats received lung-protective ventilation during V-A ECMO therapy. The hepatic and intestinal microcirculation was measured by micro-lightguide spectrophotometry after median laparotomy for two hours. Systemic and pulmonary inflammation was detected via enzyme-linked immunosorbent assays (ELISA) of the plasma and bronchoalveolar lavage (BAL), respectively, measuring tumor necrosis factor-alpha (TNF-α), interleukins 6 (IL-6) and 10 (IL-10), and C-X-C motif ligands 2 (CXCL2) and 5 (CXCL5). Oxygen saturation and relative hemoglobin concentration were reduced in the hepatic and intestinal microcirculation during V-A ECMO therapy, independent of the blood flow rate. Further, rats treated with V-A ECMO therapy also presented elevated systolic, diastolic, and mean arterial blood pressure and increased stroke volume, cardiac output, and left ventricular end-diastolic volume. However, left ventricular end-diastolic pressure was only elevated during high-flow V-A ECMO therapy. Blood gas analysis revealed a dilutional anemia during V-A ECMO therapy. ELISA analysis showed an elevated plasma CXCL2 concentration only during high-flow V-A ECMO therapy and elevated BAL CXCL2 and CXCL5 concentrations only during low-flow V-A ECMO therapy. Rats undergoing V-A ECMO therapy exhibited impaired microcirculation of the intestine and liver during septic shock despite increased blood pressure and cardiac output. Increased pulmonary inflammation was detected only during low-flow V-A ECMO therapy in septic shock.
摘要：
尽管在改善感染性休克的治疗方面做出了重大努力，死亡率仍然很高。在这种情况下应用静脉动脉（V-A）体外膜氧合（ECMO）仍然存在争议。由于股动脉插管用于V-AECMO返回会导致下体高氧，这项研究调查了V-AECMO治疗对啮齿动物模型感染性休克期间肠和肝微循环的影响.30只雄性Lewis大鼠被随机分配接受低（60mL/kg/min）或高（90mL/kg/min）血流量或假手术的V-AECMO治疗。通过左心室中的压力容积导管和尾外侧动脉中的导管收集血液动力学数据。通过静脉内施用脂多糖(lmg/kg)诱导感染性休克。大鼠在V-AECMO治疗期间接受肺保护性通气。中位剖腹手术2小时后，通过微光导分光光度法测量肝脏和肠道微循环。通过血浆和支气管肺泡灌洗（BAL）的酶联免疫吸附测定（ELISA）检测全身和肺部炎症，分别,测量肿瘤坏死因子-α（TNF-α），白细胞介素6（IL-6）和10（IL-10），和C-X-C基序配体2(CXCL2)和5(CXCL5)。在V-AECMO治疗期间，肝脏和肠道微循环中的氧饱和度和相对血红蛋白浓度降低，与血液流速无关。Further,用V-AECMO治疗的大鼠也表现出收缩压升高，舒张压,平均动脉血压和每搏输出量增加,心输出量,和左心室舒张末期容积。然而,左心室舒张末期压仅在高流量V-AECMO治疗期间升高.血气分析显示在V-AECMO治疗期间存在稀释性贫血。ELISA分析显示，仅在高流量V-AECMO治疗期间血浆CXCL2浓度升高，仅在低流量V-AECMO治疗期间BALCXCL2和CXCL5浓度升高。尽管血压和心输出量增加，但接受V-AECMO治疗的大鼠在感染性休克期间肠和肝的微循环受损。仅在感染性休克的低流量V-AECMO治疗期间检测到肺部炎症增加。
