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Enteral tranexamic acid attenuates vasopressor resistance and changes in α1-adrenergic receptor expression in hemorrhagic shock

机译:失血性休克肠内氨甲环酸削弱血管升压药耐药性和α1-肾上腺素能受体表达的变化

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摘要

BACKGROUNDIrreversible hemorrhagic shock is characterized by hyporesponsiveness to vasopressor and fluid therapy. Little is known, however, about the mechanisms that contribute to this phenomenon. Previous studies have shown that decreased intestinal perfusion in hemorrhagic shock leads to proteolytically-mediated increases in gut permeability, with subsequent egress of vasoactive substances systemically. Maintenance of blood pressure is achieved in part by α1 receptor modulation, which may be affected by vasoactive factors; we thus hypothesized that decreases in hemodynamic stability and vasopressor response in shock can be prevented by enteral protease inhibition.
机译:背景技术不可治愈的失血性休克的特征在于对血管加压药和液体疗法的反应不足。但是,对于导致这种现象的机理知之甚少。先前的研究表明,失血性休克的肠道灌注减少会导致蛋白水解介导的肠道通透性增加,随后系统性释放血管活性物质。血压的维持部分通过α1受体调节来实现,该调节可能受血管活性因子的影响。因此,我们假设可以通过肠内蛋白酶抑制作用来预防休克时血液动力学稳定性和升压反应的降低。

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