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Vascular hyporeactivity to vasoconstrictors happens throughout sepsis and trauma. Hemorrhage would be the big underlying mechanism of microcirculation failure, refractory hypotension, no-reflow phenomenon and vital-organ hypoperfusion. It is also viewed as to become a significant reason for a persistent severe shock condition (1). Numerous studies showed that receptor desensitization (two,three), hyperpolarization of membrane potential (4-6) and decreased + sensitivity of contractile components to Ca2+ in vascular smooth muscle cells (VSMCs) (7-10) all contribute for the improvement of vascular hyporeactivity. Research in recent years have shown that post-shock mesenteric lymph (PSML) features a pivotal function in endothelial cell injury and multiple organ dysfunction induced by gut-derived infections (11-14). Findings from our laboratory suggested that mesenteric duct ligation and PSML drainage each improved the reactivity and calcium sensitivity of vascular r.
