细胞因子和水钠通道蛋白在急性肾损伤致肺损伤中的作用(1)
【摘要】目的 通过双肾动静脉夹闭建立急性缺血性肾损伤大鼠模型，观察大鼠肺病理生理的变化，观察上皮细胞钠通道蛋白(α-ENaC)和水通道蛋白1(AQP1)在急性肾损伤所致肺损伤中的作用。方法 健康雄性Wistar大鼠60只。体质量300～320 g，随机(随机数字法)分成健康对照组(A组)，急性肾损伤组(B组)，每组30只。造模后，处死大鼠，苏木素伊红(HE)染色检查肺组织病理变化，计算肺W/D 比值，支气管肺泡灌洗液(BALF)中蛋白质量浓度。检测肺组织中水通道蛋白1、肺上皮钠通道蛋白的质量浓度。测定血清及 BALF 中IL-6与 TNF-α的质量浓度。结果 B组大鼠在实验后6 h动脉血pH值开始下降，酸中毒逐渐加重，与A组比较差异具有统计学意义(P<0.05)。B组与A组的氧分压各时间点之间相比差异无统计学意义(P>0.05)。与A组相比， B组在实验后2 h肺泡灌洗液中蛋白水平、肺W/D值开始明显增加，差异具有统计学意义(P<0.05)。B组实验后8 h肺泡上皮肿胀，肺泡壁增宽，肺泡间质水肿明显，肺泡内可见炎症细胞、红细胞和蛋白渗出，表现出急性肺损伤的病理改变。B组在实验后2 h血清及肺泡灌洗液中TNF-α、IL-6的质量浓度开始增加，肺组织中AQP1、α-ENaC表达开始逐渐减少，与A组比较，差异具有统计学意义(P<0.05)。结论 急性肾损伤早期肺泡上皮-内皮屏障功能已经受到了影响，急性肺损伤已经发生。急性肾损伤后早期体内TNF-α、IL-6 含量明显增加，肺表达AQP1及α-ENaC的减少，可能是急性肾损伤早期引起肺损伤的原因之一。
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【关键词】急性肾损伤；急性肺损伤；细胞因子；水通道蛋白1；肺上皮钠通道蛋白
The roles of cytokines and water sodium channel proteins in acute kidney injury-induced acute lung injury rats MA Tao， LIU Zhi.Department of Emergency Medicne， The First Hospital of China Medical University，Shenyang 110001，China
Corresponding author： LIU Zhi， Email： liuzhicmu2004@yahoo.com.cn
【Abstract】Objective To observe the physiopathologic changes of lung in rats with acute ischemic kidney injury， and to study the roles of cytokine，epithelial sodium channel protein (ENaC) and aquaporin 1 (AQP1) in acute lung injury brought on by acute ischemic kidney injury in rats.Methods A total of 60 healthy male Wistar rats (300-320 g) were randomly(random number) divided into control groups(group A， n=30)and acute kidney injury group(group B， n=30). The model of acute ischemic kidney injury in rats was made by bilateral renal arteiovenous blockage with clamps. Six rats of each group were sacrificed at 0， 2， 4， 6 and 8 hours after modeling. Lung tissue of rats was harvested and stained with hematoxylin-eosin (HE) staining method， and the pathological changes of lung were observed under microscope. The ratio of wet and dry weight (W/D) of lung was calculated. The levels of protein in bronchoalveolar lavage fluid (BALF) were measured. The levels of IL-6 and TNF-α both in serum and BALF were tested. The concentrations of AQP1 and α-ENaC in lung were measured. Results At six hours after modeling， the pH value of arterial blood of rats in group B began to get lowered compared to group A. There was no difference in partial pressure of oxygen in arterial blood between two groups during entire period of experiment(P>0.05). Protein level in BALF and W/D of lung increased significantly two hours after modeling in rats of group B(P<0.05).The histopathological changes of acute lung injury including swollen aleolar epithelium， widened interalveolar septum， edema of alveoli and alveolar interstitium， alveolar neurophil sequestration， erythrocytes and protein in exudates were observed. The levels of TNF-α and IL-6 in serum and in BALF began to increase at two hours after modeling. The levels of AQP1 and α-ENaC of lung in rats with acute kidney injury decreased gradually and were lower than those in rats of group A (P< 0.05). Conclusions Aleolar epithelial-endothelial barrier function was already compromised at the beginning of AKI， suggesting the acute lung injury was already brought on. The levels of TNF-α， IL-6 in serum and in BALF increased after the occurrence of acute kidney injury. The decreases in lung AQP1 and α-ENaC might contribute to the lung injury caused by early acute kidney injury.
, 百拇医药(马涛 刘志)
, http://www.100md.com
【关键词】急性肾损伤；急性肺损伤；细胞因子；水通道蛋白1；肺上皮钠通道蛋白
The roles of cytokines and water sodium channel proteins in acute kidney injury-induced acute lung injury rats MA Tao， LIU Zhi.Department of Emergency Medicne， The First Hospital of China Medical University，Shenyang 110001，China
Corresponding author： LIU Zhi， Email： liuzhicmu2004@yahoo.com.cn
【Abstract】Objective To observe the physiopathologic changes of lung in rats with acute ischemic kidney injury， and to study the roles of cytokine，epithelial sodium channel protein (ENaC) and aquaporin 1 (AQP1) in acute lung injury brought on by acute ischemic kidney injury in rats.Methods A total of 60 healthy male Wistar rats (300-320 g) were randomly(random number) divided into control groups(group A， n=30)and acute kidney injury group(group B， n=30). The model of acute ischemic kidney injury in rats was made by bilateral renal arteiovenous blockage with clamps. Six rats of each group were sacrificed at 0， 2， 4， 6 and 8 hours after modeling. Lung tissue of rats was harvested and stained with hematoxylin-eosin (HE) staining method， and the pathological changes of lung were observed under microscope. The ratio of wet and dry weight (W/D) of lung was calculated. The levels of protein in bronchoalveolar lavage fluid (BALF) were measured. The levels of IL-6 and TNF-α both in serum and BALF were tested. The concentrations of AQP1 and α-ENaC in lung were measured. Results At six hours after modeling， the pH value of arterial blood of rats in group B began to get lowered compared to group A. There was no difference in partial pressure of oxygen in arterial blood between two groups during entire period of experiment(P>0.05). Protein level in BALF and W/D of lung increased significantly two hours after modeling in rats of group B(P<0.05).The histopathological changes of acute lung injury including swollen aleolar epithelium， widened interalveolar septum， edema of alveoli and alveolar interstitium， alveolar neurophil sequestration， erythrocytes and protein in exudates were observed. The levels of TNF-α and IL-6 in serum and in BALF began to increase at two hours after modeling. The levels of AQP1 and α-ENaC of lung in rats with acute kidney injury decreased gradually and were lower than those in rats of group A (P< 0.05). Conclusions Aleolar epithelial-endothelial barrier function was already compromised at the beginning of AKI， suggesting the acute lung injury was already brought on. The levels of TNF-α， IL-6 in serum and in BALF increased after the occurrence of acute kidney injury. The decreases in lung AQP1 and α-ENaC might contribute to the lung injury caused by early acute kidney injury.
, 百拇医药(马涛 刘志)
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