Intensive care medicine experimental · 2026
Hepatic and intestinal microcirculation and pulmonary inflammation in a model of veno-arterial extracorporeal membrane oxygenation in the rat.
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Edinger Fabian, Zajonz Thomas, Mayer Nico, Schmidt Götz, Schneck Emmanuel, Sander Michael, Koch Christian
Аннотация
BACKGROUND: Due to peripheral cannulation, veno-arterial (V-A) extracorporeal membrane oxygenation (ECMO) therapy is increasingly used outside the cardiac operation room. Despite significant efforts toward improving therapy for septic shock, mortality remains high. In this context, V-A ECMO therapy remains controversial and has been associated with reduced intestinal microcirculation in a septic rat model. In addition to ECMO-induced inflammation, peripheral V-A ECMO therapy is associated with lower-body hyperoxia. Therefore, this study investigated the impact of V-A ECMO therapy on intestinal microcirculation and systemic and pulmonary inflammation in healthy rats without septic shock.
METHODS: Thirty male Lewis rats were randomly assigned to three groups: sham, low-flow (60 mL/kg/min) and high-flow (90 mL/kg/min). V-A ECMO was established by jugular venous drainage and femoral arterial return. Intestinal and hepatic microcirculation were assessed by micro-light guide spectrophotometry after median laparotomy. Systemic and pulmonary inflammation were evaluated by measuring plasma and bronchoalveolar lavage (BAL) levels of tumour necrosis factor (TNF-α), interleukins 6 (IL-6) and 10 (IL-10), and C-X-C motif chemokine ligands 2 (CXCL-2) and 5 (CXCL-5). Hemodynamic data were captured using a left ventricular pressure-volume catheter.
RESULTS: Intestinal oxygenation did not differ significantly among groups (sham: 76%, low-flow: 77%, high-flow: 74%; all p > 0.05). In contrast, hepatic oxygenation was significantly lower during V-A ECMO therapy (sham: 43%, low-flow: 23%, high-flow: 27%; all p ≤ 0.001). TNF-α levels were significantly elevated during both low-flow (p = 0.027) and high-flow (p = 0.015) V-A ECMO therapy. In contrast, IL-10 levels were significantly reduced during low-flow (p = 0.009) but not high-flow (p = 1.000) V-A ECMO therapy, whereas IL-6 levels were not significantly affected (low-flow: p = 0.764, high-flow: p = 0.104). BAL analysis revealed significantly reduced IL-6 levels during high-flow (p = 0.010) but not low-flow (p = 0.288) V-A ECMO therapy, whereas CXCL-2 (low-flow: p = 1.000, high-flow: p = 0.634) and CXCL-5 (low-flow: p = 1.000, high-flow: p = 0.224) levels were not significantly affected.
CONCLUSIONS: In healthy rats, V-A ECMO therapy did not impair intestinal microcirculation and was associated with reduced pulmonary inflammation at the high flow rate, likely due to decreased pulmonary blood flow.
METHODS: Thirty male Lewis rats were randomly assigned to three groups: sham, low-flow (60 mL/kg/min) and high-flow (90 mL/kg/min). V-A ECMO was established by jugular venous drainage and femoral arterial return. Intestinal and hepatic microcirculation were assessed by micro-light guide spectrophotometry after median laparotomy. Systemic and pulmonary inflammation were evaluated by measuring plasma and bronchoalveolar lavage (BAL) levels of tumour necrosis factor (TNF-α), interleukins 6 (IL-6) and 10 (IL-10), and C-X-C motif chemokine ligands 2 (CXCL-2) and 5 (CXCL-5). Hemodynamic data were captured using a left ventricular pressure-volume catheter.
RESULTS: Intestinal oxygenation did not differ significantly among groups (sham: 76%, low-flow: 77%, high-flow: 74%; all p > 0.05). In contrast, hepatic oxygenation was significantly lower during V-A ECMO therapy (sham: 43%, low-flow: 23%, high-flow: 27%; all p ≤ 0.001). TNF-α levels were significantly elevated during both low-flow (p = 0.027) and high-flow (p = 0.015) V-A ECMO therapy. In contrast, IL-10 levels were significantly reduced during low-flow (p = 0.009) but not high-flow (p = 1.000) V-A ECMO therapy, whereas IL-6 levels were not significantly affected (low-flow: p = 0.764, high-flow: p = 0.104). BAL analysis revealed significantly reduced IL-6 levels during high-flow (p = 0.010) but not low-flow (p = 0.288) V-A ECMO therapy, whereas CXCL-2 (low-flow: p = 1.000, high-flow: p = 0.634) and CXCL-5 (low-flow: p = 1.000, high-flow: p = 0.224) levels were not significantly affected.
CONCLUSIONS: In healthy rats, V-A ECMO therapy did not impair intestinal microcirculation and was associated with reduced pulmonary inflammation at the high flow rate, likely due to decreased pulmonary blood flow.