Communications medicine · 2026
Venular-centered thrombo-inflammation drives microvascular failure after arterial recanalization in acute mesenteric ischemia.
СтатьяНазвание и аннотация: Перевод в очереди
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François Déborah, Kernanet Lambert, Bajul Melinda, Brami Abigail, Arocas Véronique, Bouton Marie-Christine, Cazals-Hatem Dominique, Guedj Kevin, Ho-Tin-Noé Benoit, Corcos Olivier, Boulaftali Yacine, Nuzzo Alexandre
Аннотация
BACKGROUND: Acute mesenteric ischemia (AMI) remains associated with high mortality despite prompt revascularization, suggesting that downstream ischemia-reperfusion injury contributes to poor outcomes. However, the microvascular mechanisms underlying this process are not entirely defined.
METHODS: We analyzed admission blood samples from patients with arterial AMI and non-ischemic controls enrolled in the SURVIBIO diagnostic study (NCT03518099). We also investigated thrombo-inflammatory responses in a murine superior mesenteric artery occlusion (SMAO) model. In mice, intravital microscopy was used to directly visualize mesenteric microcirculatory flow and thrombo-inflammatory events during ischemia-reperfusion.
RESULTS: Patients with AMI display a marked systemic thrombo-inflammatory profile, characterized by elevated inflammatory markers, neutrophil activation, platelet activation, and alterations in coagulation-related proteins, which are closely mirrored in the SMAO model. Intravital microscopy reveals a dissociation between arterial and microvascular reperfusion: while arteriolar flow partially recovers after recanalization, venular perfusion remains severely impaired and is associated with early blood cell stasis and stable venular thrombus formation. Thrombi develop through a sequential process initiated during ischemia and amplified during reperfusion.
CONCLUSION: Together, these findings suggest that venular-centered thrombo-inflammation is closely associated with microvascular dysfunction and intestinal injury in arterial AMI. This work provides a framework for targeting thrombo-inflammatory pathways beyond arterial reperfusion that may extend to other clinical forms of AMI, including non-occlusive mesenteric ischemia (NOMI).
METHODS: We analyzed admission blood samples from patients with arterial AMI and non-ischemic controls enrolled in the SURVIBIO diagnostic study (NCT03518099). We also investigated thrombo-inflammatory responses in a murine superior mesenteric artery occlusion (SMAO) model. In mice, intravital microscopy was used to directly visualize mesenteric microcirculatory flow and thrombo-inflammatory events during ischemia-reperfusion.
RESULTS: Patients with AMI display a marked systemic thrombo-inflammatory profile, characterized by elevated inflammatory markers, neutrophil activation, platelet activation, and alterations in coagulation-related proteins, which are closely mirrored in the SMAO model. Intravital microscopy reveals a dissociation between arterial and microvascular reperfusion: while arteriolar flow partially recovers after recanalization, venular perfusion remains severely impaired and is associated with early blood cell stasis and stable venular thrombus formation. Thrombi develop through a sequential process initiated during ischemia and amplified during reperfusion.
CONCLUSION: Together, these findings suggest that venular-centered thrombo-inflammation is closely associated with microvascular dysfunction and intestinal injury in arterial AMI. This work provides a framework for targeting thrombo-inflammatory pathways beyond arterial reperfusion that may extend to other clinical forms of AMI, including non-occlusive mesenteric ischemia (NOMI).