The Effect of Liposome-Encapsulated Hemoglobin on Mediators in the Mesenteric Lymph Following Hemorrhagic Shock
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Hemorrhagic shock-induced mesenteric hypoperfusion causes gut injury, leading to production of inflammatory mediators that activate neutrophils (PMNs) and damage endothelial cells. Previous studies have shown that the ligation of the mesenteric lymph duct prevents hemorrhagic shock-induced lung injury. Mesenteric lymph is thought to be crucial in the pathogenesis of multiple organ dysfunction syndrome (MODS). Our previous data have shown that liposome-encapsulated hemoglobin (LEH) reduces lung permeability in the rat hemorrhagic shock model. We therefore hypothesize that LEH attenuates mesenteric lymph induced PMN activation. Male Sprague-Dawley rats were exposed to hemorrhagic shock (40mmHg, 30min) and resuscitated over 2 hours with shed blood+normal saline (NS) (shed blood×2) (whole blood group) or LEH (=shed blood)+NS (shed blood×2) (LEH group). A sham group underwent identical procedures without hemorrhage and resuscitation. We use dmesenteric lymph collected between 1 and 2 hours in the resuscitation phase and examined rat PMN activation. Superoxide anion production was measured with the superoxide dismutase inhibitable cytochrome c reduction method. In addition, adhesion was measured by the radioactivity of adherent PMNs labeled with 51Cr to fibrinogen, and CD11b surface expression was determined with flow cytometry. Mesenteric lymph in the whole blood group significantly increased superoxide production compared with the LEH and sham groups. Mesenteric lymph in whole blood group, but not the LEH group, significantly increased rat PMN adherence. Mesenteric lymph in whole blood group significantly up-regulated CD11b surface expression compared with the LEH and sham groups. LEH attenuates mesenteric lymph induced PMN activation following hemorrhagic shock, and may therefore be one of strategies to prevent MODS.
- 一般社団法人 日本救急医学会の論文
一般社団法人 日本救急医学会 | 論文
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