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:揭示败血症诱发的肾小管功能障碍的途径。专注于基底外侧脂多糖通过髓样厚上升肢中的TLR4 / MyD88依赖性ERK活化抑制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:败血症是人体对严重感染的全身反应,并与多器官功能障碍(例如神经,肺和肾)有关。实际上,严重的败血症每年影响数百万患者,死亡率在30%至40%之间(2)。在败血症期间,动脉血压显着下降,导致败血症诱发的败血性休克低血压。血压下降是由于复杂的血液动力学反应的激活,在肾脏中导致血管收缩和低肾血流量,继而导致肾组织缺氧,局部缺血和肾功能迅速丧失(10)。

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