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Enteral tranexamic acid attenuates vasopressor resistance and changes in alpha(1)-adrenergic receptor expression in hemorrhagic shock

机译:肠道促进酸衰减出血休克中α(1) - 肾上腺素能受体表达的血管加压率抗性和变化

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BACKGROUND: Irreversible 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 alpha(1) 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:不可逆的出血性休克的特点是对血管加压器和液体治疗的低反向性。 然而,众所周知,关于有助于这种现象的机制。 以前的研究表明,出血休克的肠道灌注降低导致蛋白水解介导的肠道渗透性增加,随后的血管活性物质系统性地出现。 血压维持部分由α(1)受体调节部分实现,可能受血管活性因子的影响; 因此,我们假设肠内蛋白酶抑制可以防止血流动力学稳定性和血管加压率反应的降低。

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