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首页> 外文期刊>American Journal of Physiology >Uncovering the pathway of sepsis-induced renal tubular dysfunction. Focus on Basolateral LPS inhibits NHE3 and HCOFormula absorption through TLR4/MyD88-dependent ERK activation in medullary thick ascending limb'.
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Uncovering the pathway of sepsis-induced renal tubular dysfunction. Focus on Basolateral LPS inhibits NHE3 and HCOFormula absorption through TLR4/MyD88-dependent ERK activation in medullary thick ascending limb'.

机译:揭示败血症诱导的肾小管功能障碍的途径。 通过TLR4 / MYD88依赖性ERK活化在髓质厚的上升肢体中抑制NHE3和HCOFORMULA吸收的关注抑制NHE3和HCOFORMULA吸收“。

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摘要

sepsis is the body's systemic response to severe infection, and it is associated with multiple organ dysfunction (e.g., neurological, pulmonary and renal). Indeed, severe sepsis affects millions of patients each year with a mortality rate'between 30% and 40% (2). During sepsis, arterial blood pressure drops significantly leading to sepsis-induced hypotension in septic shock. This drop in blood pressure is due to the activation of a complex hemodynamic response, which, in the kidney, leads to vaso-constriction and low renal blood flow followed by renal tissue hypoxia, ischemia, and rapid loss of kidney function (10).
机译:败血症是身体对严重感染的全身反应,它与多器官功能障碍有关(例如神经系统,肺和肾)。 实际上,严重的败血症每年都会影响数百万患者,其中死亡率为30%和40%(2)。 在败血症期间,动脉血压显着导致脓毒症诱导的脓毒症休克中的低血压。 这种血压下降是由于肾脏中的复杂血液动力学反应的激活,导致血管收缩和低肾血流,然后是肾组织缺氧,缺血和肾功能的快速丧失(10)。

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