兔急性百草枯中毒后血小板内皮细胞黏附分子-1水平对肺损伤的影响

目的 观察急性百草枯(PQ)中毒致肺损伤后血小板内皮细胞黏附分子-1(PECAM-1)水平的变化.方法 36只成年新西兰大白兔按随机数字表法分为PQ 8、16和32 mg/kg 3组,每组12只.胃管灌入20%PQ制模,7d后处死动物取肺组织行苏木素-伊红(HE)染色,观察肺组织病理改变,进行肺损伤评分,Masson染色鉴定肺纤维化程度,免疫组化半定量分析PECAM-1表达;将PECAM-1表达与肺损伤评分、肺纤维化程度进行相关分析.结果 随PQ中毒剂量增加,肺损伤评分、肺纤维化程度逐渐加重,肺PECAM-1表达逐渐下降;8、16、32 mg/kg PQ中毒组肺损伤评分(分)分别为8.33±1.03、9.83±1.17、11.50土1.38;肺纤维化程度分别为(31.09±2.05)%、(34.37±1.62)%、(36.54±0.44)%;PECAM-1表达分别为(20.31±0.70)%、(19.34±0.68)%、(18.37±0.46)%,组间两两比较差异均有统计学意义(P＜0.05或P＜0.01).Pearson相关分析显示,PECAM-1表达与肺损伤评分(r=-0.732,P=0.001)、肺纤维化程度(r=-0.779,P＜0.001)均呈明显负相关.结论 PQ中毒后,兔肺组织内PECAM-1表达明显下降,呈剂量依赖性,其与肺损伤程度、肺纤维化程度密切相关;PQ对PECAM-1的抑制是肺损伤发生发展的重要因素之一.     

血小板内皮细胞黏附分子-1基因多态性与急性心肌梗死的相关性研究

目的 研究血小板内皮细胞黏附分子-1(PECAM-1)基因单核昔酸多态性及其单倍型与急性心肌梗死(AMI)易感性之间的关系;同时分析PECAM-1基因型及血清水平与AMI的相关性.方法 以180例AMI患者和200例健康对照者为研究对象,应用聚合酶链反应一限制性片段长度多态性(PCR-RFLP)和DNA测序的方法 对PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单苷酸多态性进行基因分型,同时采用酶联免疫吸附法检测血清PECAM-1水平.用SHEsis软件分析PECAM-1基因的连锁不平衡及单倍型频率.结果 PECAM-1基因Asn563Ser和Gly670Arg多态性在AMI患者和正常人群中分布差异无统计学意义(P>0.05),而PECAM-1基因Leu125Val多态性在两组人群中的分布差异存在统计学意义(P<0.05).等位基因频率的相对风险分析发现,Val等位基因携带者患AMI的风险是Leu等位基因的1.480倍[比值比(OR)=1.480,95%可信区间(CI)为1.111～1.972,P=0.007];携带Val等位基因的AMI患者血清PECAM-1水平显著高于不携带者(P<0.01).联合基因型分析发现,PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单核苷酸多态性存在着强烈的连锁不平衡,与对照组比较,Val-Ser-Arg基因单倍型携带者显著增加了AMI的发病风险(OR=1.489,95%CI为1.118～1.984,P=0.006).结论 PECAM-1基因Leu125Val多态性和Val-Ser-Arg单倍型与AMI的发病具有相关性,其中Val等位基因可能足AMI的遗传易感基因,携带Val等位基因的个体可能通过促进PECAM-1的高度表达进而增加了AMI的发病风险.     

血小板内皮细胞黏附分子-1基因多态性与急性心肌梗死的相关性研究

目的 研究血小板内皮细胞黏附分子-1(PECAM-1)基因单核昔酸多态性及其单倍型与急性心肌梗死(AMI)易感性之间的关系;同时分析PECAM-1基因型及血清水平与AMI的相关性.方法 以180例AMI患者和200例健康对照者为研究对象,应用聚合酶链反应一限制性片段长度多态性(PCR-RFLP)和DNA测序的方法 对PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单苷酸多态性进行基因分型,同时采用酶联免疫吸附法检测血清PECAM-1水平.用SHEsis软件分析PECAM-1基因的连锁不平衡及单倍型频率.结果 PECAM-1基因Asn563Ser和Gly670Arg多态性在AMI患者和正常人群中分布差异无统计学意义(P>0.05),而PECAM-1基因Leu125Val多态性在两组人群中的分布差异存在统计学意义(P<0.05).等位基因频率的相对风险分析发现,Val等位基因携带者患AMI的风险是Leu等位基因的1.480倍[比值比(OR)=1.480,95%可信区间(CI)为1.111～1.972,P=0.007];携带Val等位基因的AMI患者血清PECAM-1水平显著高于不携带者(P<0.01).联合基因型分析发现,PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单核苷酸多态性存在着强烈的连锁不平衡,与对照组比较,Val-Ser-Arg基因单倍型携带者显著增加了AMI的发病风险(OR=1.489,95%CI为1.118～1.984,P=0.006).结论 PECAM-1基因Leu125Val多态性和Val-Ser-Arg单倍型与AMI的发病具有相关性,其中Val等位基因可能足AMI的遗传易感基因,携带Val等位基因的个体可能通过促进PECAM-1的高度表达进而增加了AMI的发病风险.     

血小板内皮细胞黏附分子-1基因多态性与急性心肌梗死的相关性研究

目的 研究血小板内皮细胞黏附分子-1(PECAM-1)基因单核昔酸多态性及其单倍型与急性心肌梗死(AMI)易感性之间的关系;同时分析PECAM-1基因型及血清水平与AMI的相关性.方法 以180例AMI患者和200例健康对照者为研究对象,应用聚合酶链反应一限制性片段长度多态性(PCR-RFLP)和DNA测序的方法 对PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单苷酸多态性进行基因分型,同时采用酶联免疫吸附法检测血清PECAM-1水平.用SHEsis软件分析PECAM-1基因的连锁不平衡及单倍型频率.结果 PECAM-1基因Asn563Ser和Gly670Arg多态性在AMI患者和正常人群中分布差异无统计学意义(P>0.05),而PECAM-1基因Leu125Val多态性在两组人群中的分布差异存在统计学意义(P<0.05).等位基因频率的相对风险分析发现,Val等位基因携带者患AMI的风险是Leu等位基因的1.480倍[比值比(OR)=1.480,95%可信区间(CI)为1.111～1.972,P=0.007];携带Val等位基因的AMI患者血清PECAM-1水平显著高于不携带者(P<0.01).联合基因型分析发现,PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单核苷酸多态性存在着强烈的连锁不平衡,与对照组比较,Val-Ser-Arg基因单倍型携带者显著增加了AMI的发病风险(OR=1.489,95%CI为1.118～1.984,P=0.006).结论 PECAM-1基因Leu125Val多态性和Val-Ser-Arg单倍型与AMI的发病具有相关性,其中Val等位基因可能足AMI的遗传易感基因,携带Val等位基因的个体可能通过促进PECAM-1的高度表达进而增加了AMI的发病风险.     

血小板内皮细胞黏附分子-1基因多态性与急性心肌梗死的相关性研究

目的 研究血小板内皮细胞黏附分子-1(PECAM-1)基因单核昔酸多态性及其单倍型与急性心肌梗死(AMI)易感性之间的关系;同时分析PECAM-1基因型及血清水平与AMI的相关性.方法 以180例AMI患者和200例健康对照者为研究对象,应用聚合酶链反应一限制性片段长度多态性(PCR-RFLP)和DNA测序的方法 对PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单苷酸多态性进行基因分型,同时采用酶联免疫吸附法检测血清PECAM-1水平.用SHEsis软件分析PECAM-1基因的连锁不平衡及单倍型频率.结果 PECAM-1基因Asn563Ser和Gly670Arg多态性在AMI患者和正常人群中分布差异无统计学意义(P>0.05),而PECAM-1基因Leu125Val多态性在两组人群中的分布差异存在统计学意义(P<0.05).等位基因频率的相对风险分析发现,Val等位基因携带者患AMI的风险是Leu等位基因的1.480倍[比值比(OR)=1.480,95%可信区间(CI)为1.111～1.972,P=0.007];携带Val等位基因的AMI患者血清PECAM-1水平显著高于不携带者(P<0.01).联合基因型分析发现,PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单核苷酸多态性存在着强烈的连锁不平衡,与对照组比较,Val-Ser-Arg基因单倍型携带者显著增加了AMI的发病风险(OR=1.489,95%CI为1.118～1.984,P=0.006).结论 PECAM-1基因Leu125Val多态性和Val-Ser-Arg单倍型与AMI的发病具有相关性,其中Val等位基因可能足AMI的遗传易感基因,携带Val等位基因的个体可能通过促进PECAM-1的高度表达进而增加了AMI的发病风险.     

血小板内皮细胞黏附分子-1基因多态性与急性心肌梗死的相关性研究

目的 研究血小板内皮细胞黏附分子-1(PECAM-1)基因单核昔酸多态性及其单倍型与急性心肌梗死(AMI)易感性之间的关系;同时分析PECAM-1基因型及血清水平与AMI的相关性.方法 以180例AMI患者和200例健康对照者为研究对象,应用聚合酶链反应一限制性片段长度多态性(PCR-RFLP)和DNA测序的方法 对PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单苷酸多态性进行基因分型,同时采用酶联免疫吸附法检测血清PECAM-1水平.用SHEsis软件分析PECAM-1基因的连锁不平衡及单倍型频率.结果 PECAM-1基因Asn563Ser和Gly670Arg多态性在AMI患者和正常人群中分布差异无统计学意义(P>0.05),而PECAM-1基因Leu125Val多态性在两组人群中的分布差异存在统计学意义(P<0.05).等位基因频率的相对风险分析发现,Val等位基因携带者患AMI的风险是Leu等位基因的1.480倍[比值比(OR)=1.480,95%可信区间(CI)为1.111～1.972,P=0.007];携带Val等位基因的AMI患者血清PECAM-1水平显著高于不携带者(P<0.01).联合基因型分析发现,PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单核苷酸多态性存在着强烈的连锁不平衡,与对照组比较,Val-Ser-Arg基因单倍型携带者显著增加了AMI的发病风险(OR=1.489,95%CI为1.118～1.984,P=0.006).结论 PECAM-1基因Leu125Val多态性和Val-Ser-Arg单倍型与AMI的发病具有相关性,其中Val等位基因可能足AMI的遗传易感基因,携带Val等位基因的个体可能通过促进PECAM-1的高度表达进而增加了AMI的发病风险.     

血小板内皮细胞黏附分子-1基因多态性与急性心肌梗死的相关性研究

目的 研究血小板内皮细胞黏附分子-1(PECAM-1)基因单核昔酸多态性及其单倍型与急性心肌梗死(AMI)易感性之间的关系;同时分析PECAM-1基因型及血清水平与AMI的相关性.方法 以180例AMI患者和200例健康对照者为研究对象,应用聚合酶链反应一限制性片段长度多态性(PCR-RFLP)和DNA测序的方法 对PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单苷酸多态性进行基因分型,同时采用酶联免疫吸附法检测血清PECAM-1水平.用SHEsis软件分析PECAM-1基因的连锁不平衡及单倍型频率.结果 PECAM-1基因Asn563Ser和Gly670Arg多态性在AMI患者和正常人群中分布差异无统计学意义(P>0.05),而PECAM-1基因Leu125Val多态性在两组人群中的分布差异存在统计学意义(P<0.05).等位基因频率的相对风险分析发现,Val等位基因携带者患AMI的风险是Leu等位基因的1.480倍[比值比(OR)=1.480,95%可信区间(CI)为1.111～1.972,P=0.007];携带Val等位基因的AMI患者血清PECAM-1水平显著高于不携带者(P<0.01).联合基因型分析发现,PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单核苷酸多态性存在着强烈的连锁不平衡,与对照组比较,Val-Ser-Arg基因单倍型携带者显著增加了AMI的发病风险(OR=1.489,95%CI为1.118～1.984,P=0.006).结论 PECAM-1基因Leu125Val多态性和Val-Ser-Arg单倍型与AMI的发病具有相关性,其中Val等位基因可能足AMI的遗传易感基因,携带Val等位基因的个体可能通过促进PECAM-1的高度表达进而增加了AMI的发病风险.     

血小板内皮细胞黏附分子-1基因多态性与急性心肌梗死的相关性研究

目的 研究血小板内皮细胞黏附分子-1(PECAM-1)基因单核昔酸多态性及其单倍型与急性心肌梗死(AMI)易感性之间的关系;同时分析PECAM-1基因型及血清水平与AMI的相关性.方法 以180例AMI患者和200例健康对照者为研究对象,应用聚合酶链反应一限制性片段长度多态性(PCR-RFLP)和DNA测序的方法 对PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单苷酸多态性进行基因分型,同时采用酶联免疫吸附法检测血清PECAM-1水平.用SHEsis软件分析PECAM-1基因的连锁不平衡及单倍型频率.结果 PECAM-1基因Asn563Ser和Gly670Arg多态性在AMI患者和正常人群中分布差异无统计学意义(P>0.05),而PECAM-1基因Leu125Val多态性在两组人群中的分布差异存在统计学意义(P<0.05).等位基因频率的相对风险分析发现,Val等位基因携带者患AMI的风险是Leu等位基因的1.480倍[比值比(OR)=1.480,95%可信区间(CI)为1.111～1.972,P=0.007];携带Val等位基因的AMI患者血清PECAM-1水平显著高于不携带者(P<0.01).联合基因型分析发现,PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单核苷酸多态性存在着强烈的连锁不平衡,与对照组比较,Val-Ser-Arg基因单倍型携带者显著增加了AMI的发病风险(OR=1.489,95%CI为1.118～1.984,P=0.006).结论 PECAM-1基因Leu125Val多态性和Val-Ser-Arg单倍型与AMI的发病具有相关性,其中Val等位基因可能足AMI的遗传易感基因,携带Val等位基因的个体可能通过促进PECAM-1的高度表达进而增加了AMI的发病风险.     

血小板内皮细胞黏附分子-1基因多态性与急性心肌梗死的相关性研究

目的 研究血小板内皮细胞黏附分子-1(PECAM-1)基因单核昔酸多态性及其单倍型与急性心肌梗死(AMI)易感性之间的关系;同时分析PECAM-1基因型及血清水平与AMI的相关性.方法 以180例AMI患者和200例健康对照者为研究对象,应用聚合酶链反应一限制性片段长度多态性(PCR-RFLP)和DNA测序的方法 对PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单苷酸多态性进行基因分型,同时采用酶联免疫吸附法检测血清PECAM-1水平.用SHEsis软件分析PECAM-1基因的连锁不平衡及单倍型频率.结果 PECAM-1基因Asn563Ser和Gly670Arg多态性在AMI患者和正常人群中分布差异无统计学意义(P>0.05),而PECAM-1基因Leu125Val多态性在两组人群中的分布差异存在统计学意义(P<0.05).等位基因频率的相对风险分析发现,Val等位基因携带者患AMI的风险是Leu等位基因的1.480倍[比值比(OR)=1.480,95%可信区间(CI)为1.111～1.972,P=0.007];携带Val等位基因的AMI患者血清PECAM-1水平显著高于不携带者(P<0.01).联合基因型分析发现,PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单核苷酸多态性存在着强烈的连锁不平衡,与对照组比较,Val-Ser-Arg基因单倍型携带者显著增加了AMI的发病风险(OR=1.489,95%CI为1.118～1.984,P=0.006).结论 PECAM-1基因Leu125Val多态性和Val-Ser-Arg单倍型与AMI的发病具有相关性,其中Val等位基因可能足AMI的遗传易感基因,携带Val等位基因的个体可能通过促进PECAM-1的高度表达进而增加了AMI的发病风险.     

血小板内皮细胞黏附分子-1基因多态性与急性心肌梗死的相关性研究

目的 研究血小板内皮细胞黏附分子-1(PECAM-1)基因单核昔酸多态性及其单倍型与急性心肌梗死(AMI)易感性之间的关系;同时分析PECAM-1基因型及血清水平与AMI的相关性.方法 以180例AMI患者和200例健康对照者为研究对象,应用聚合酶链反应一限制性片段长度多态性(PCR-RFLP)和DNA测序的方法 对PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单苷酸多态性进行基因分型,同时采用酶联免疫吸附法检测血清PECAM-1水平.用SHEsis软件分析PECAM-1基因的连锁不平衡及单倍型频率.结果 PECAM-1基因Asn563Ser和Gly670Arg多态性在AMI患者和正常人群中分布差异无统计学意义(P>0.05),而PECAM-1基因Leu125Val多态性在两组人群中的分布差异存在统计学意义(P<0.05).等位基因频率的相对风险分析发现,Val等位基因携带者患AMI的风险是Leu等位基因的1.480倍[比值比(OR)=1.480,95%可信区间(CI)为1.111～1.972,P=0.007];携带Val等位基因的AMI患者血清PECAM-1水平显著高于不携带者(P<0.01).联合基因型分析发现,PECAM-1基因Leu125Val、Asn563Ser和Gly670Arg单核苷酸多态性存在着强烈的连锁不平衡,与对照组比较,Val-Ser-Arg基因单倍型携带者显著增加了AMI的发病风险(OR=1.489,95%CI为1.118～1.984,P=0.006).结论 PECAM-1基因Leu125Val多态性和Val-Ser-Arg单倍型与AMI的发病具有相关性,其中Val等位基因可能足AMI的遗传易感基因,携带Val等位基因的个体可能通过促进PECAM-1的高度表达进而增加了AMI的发病风险.     

The relationship between platelet endothelial cell adhesion molecule-1 and paraquat-induced lung injury in rabbits

BACKGROUND:

Platelet endothelial cell adhesion molecule-1 (PECAM-1), also known as CD31, is mainly distributed in vascular endothelial cells. Studies have shown that PECAM-1 is a very significant indicator of angiogenesis, and has been used as an indicator for vascular endothelial cells. The present study aimed to explore the relationship between the expression of PECAM-1 and the degree of acute lung injury (ALI) and fibrosis in paraquat (PQ) induced lung injury in rabbits.

METHODS:

Thirty-six adult New Zealand rabbits were randomly divided into three groups (12 rabbits in each group) according to PQ dosage: 8 mg/kg (group A), 16 mg/kg (group B), and 32 mg/kg (group C). After PQ infusion, the rabbits were monitored for 7 days and then euthanized. The lungs were removed for histological evaluation. Masson staining was used to determine the degree of lung fibrosis (LF), and semi-quantitative immune-histochemistry analysis to determine the expression of PECAM-1. Pearson’s product-moment correlation analysis was performed to evaluate the relationship between the expression of PECAM-1 and the extent of lung injuries expressed by ALI score and degree of LF.

RESULTS:

Rabbits in the three groups showed apparent poisoning. The rabbits survived longer in group A than in groups B and C (6.47±0.99 days vs. 6.09±1.04 days vs. 4.77±2.04 days) (P<0.05). ALI score was lower in group A than in groups B and C (8.33±1.03 vs. 9.83±1.17 vs. 11.50±1.38) (P<0.05), and there was statistically significant difference between group B and group C (P=0.03). LF was slighter in group A than in groups B and C (31.09%±2.05 % vs. 34.37%±1.62 % vs. 36.54%±0.44%) (P<0.05), and there was statistically significant difference between group B and group C (P=0.026). The PEACAM-1 expression was higher in group A than in groups B and C (20.31%±0.70% vs. 19.34%±0.68% vs. 18.37%±0.46%) (P<0.05), and there was statistically significant difference between group B and group C (P=0.017). Pearson’s correlation analysis showed that the expression of PECAM-1 was negatively correlated to both ALI score (Coe=–0.732, P=0.001) and degree of LF (Coe=–0.779, P<0.001).

CONCLUSIONS:

The PECAM-1 expression significantly decreases in New Zealand rabbits after PQ poisoning, and the decrease is dose-dependent. The PECAM-1 expression is negatively correlated with ALI score and LF, showing a significant role in the development of lung injuries induced by PQ.KEY WORDS: Platelet endothelial cell adhesion molecule-1, Paraquat, Acute lung injury, Lung fibrosis     

Cleavage of platelet endothelial cell adhesion molecule-1 (PECAM-1) in platelets exposed to high shear stress

Platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31) is a 130 kDa transmembrane glycoprotein that belongs to the immunoglobulin superfamily and is expressed on the surface of endothelial cells, platelets, and other blood cells. Although the importance of this adhesion molecule in various cell-cell interactions is established, its functional role in platelets remains to be elucidated. In this study, we examined whether PECAM-1 underwent changes in platelets exposed to high shear stress. Platelet PECAM-1 was cleaved under high shear stress and was released into the extracellular fluid as a fragment with an approximate molecular weight of 118 kDa. The cleavage was inhibited by an anti-VWF MoAb, but not by recombinant VWF A1 domains. These findings suggest that the GPIb-VWF interaction is involved in PECAM-1 cleavage under high shear stress, and that the cleavage is independent of GPIb clustering by VWF multimers. Furthermore, EGTA or calpeptin inhibited PECAM-1 cleavage. This finding provides evidence for the involvement of calpain in PECAM-1 cleavage. Flow-cytometric analysis revealed that PECAM-1 expression on the platelet surface was decreased under high shear stress. This reduction occurred exclusively in a specific population of platelets, which corresponded to platelet-derived microparticles (PMP). In conclusion, PECAM-1 cleavage under high shear stress is closely related to the activation of calpain and the process of PMP formation mediated by the GPIb-VWF interaction.     

急性肺损伤肺组织PECAM-1 mRNA的表达

目的探讨急性肺损伤（ＡＬＩ）肺组织血小板内皮细胞粘附分子－１（ＰＥＣＡＭ－１）ｍＲＮＡ表达的变化和可能作用。方法在脂多糖（ＬＰＳ）诱发的大鼠ＡＬＩ模型,使用斑点杂交观察肺组织ＰＥＣＡＭ－１ｍＲＮＡ表达的变化。结果正常肺组织表达较高水平的ＰＥＣＡＭ－１ｍＲＮＡ;在ＡＬＩ大鼠肺组织,ＰＥＣＡＭ－１ｍＲＮＡ表达早期下调,但致伤６ｈ时,又基本恢复至正常水平。结论正常肺组织表达较高水平的ＰＥＣＡＭ－１ｍＲＮＡ,ＰＥＣＡＭ－１可能参与ＡＬＩ的发病。     

46例百草枯中毒患者肺损害的护理

通过对46例百草枯中毒患者肺损害的护理，认为采取积极、合理的护理措施对预防或减轻肺损害．降低病死率有着重要意义。让患者取半坐卧位，改善呼吸困难，缩小肺纤维化的范围；创造良好的室内环境，加强口腔护理，有效地预防肺部感染；高度谨慎应用氧疗，正确掌握用氧指征及用氧方法，避免增强百草枯的毒性；加强肺纤维化的护理，提高患者的生存质量：严密观察病情变化，严格掌握输液量及速度，避免发生或加重肺水肿，是百草枯中毒患者肺护理的关键。     

Soluble intercellular adhesion molecule-1 and clinical outcomes in patients with acute lung injury

Objective  To determine if levels of soluble intercellular adhesion molecule-1 (sICAM-1), a marker of alveolar epithelial and endothelial injury, differ in patients with hydrostatic pulmonary edema and acute lung injury (ALI) and are associated with clinical outcomes in patients with ALI. Design, setting, and participants  Measurement of sICAM-1 levels in (1) plasma and edema fluid from 67 patients with either hydrostatic pulmonary edema or ALI enrolled in an observational, prospective single center study, and (2) in plasma from 778 patients with ALI enrolled in a large multi-center randomized controlled trial of ventilator strategy. Results  In the single-center study, levels of sICAM-1 were significantly higher in both edema fluid and plasma (median 938 and 545 ng/ml, respectively) from ALI patients compared to hydrostatic edema patients (median 384 and 177 ng/ml, P < 0.03 for both comparisons). In the multi-center study, higher plasma sICAM-1 levels were associated with poor clinical outcomes in both unadjusted and multivariable models. Subjects with ALI whose plasma sICAM-1 levels increased over the first 3 days of the study had a higher risk of death, after adjusting for other important predictors of outcome (odds ratio 1.48; 95% CI 1.03–2.12, P = 0.03). Conclusions  Both plasma and edema fluid levels of sICAM-1 are higher in patients with ALI than in patients with hydrostatic pulmonary edema. Higher plasma sICAM-1 levels and increasing sICAM-1 levels over time are associated with poor clinical outcomes in ALI. Measurement of sICAM-1 levels may be useful for identifying patients at highest risk of poor outcomes from ALI. The members of the NHLBI ARDS Clinical Trials Network are listed in the Appendix.     

不同百草枯中毒剂量对兔肺损伤程度的影响

目的研究不同百草枯(PQ)中毒剂量对兔中毒性急性肺损伤(ALI)及肺纤维化(PF)程度的影响。方法将36只成年新西兰大白兔随机分成3组(A、B、C组),每组12只,分别经胃管灌入8mg/kg(A组)、16mg/kg(B组)和32mg/kg(C组)不同剂量的PQ。7d后处死动物,取肺组织行HE染色、ALI评分并行Masson染色以鉴定PF程度。结果 A组ALI评分为(8.33±1.03)分,明显低于B组([9.83±1.17)分,P=0.047)]和C组([11.50±1.38)分,P0.01],B组较C组差异也有统计学意义(P=0.03);A组PF程度为(31.09±2.05)%,明显低于B组([34.37±1.62)%,P=0.002]和C组([36.54±0.44)%,P0.01],B组较C组差异也有统计学意义(P=0.026)。Pearson相关分析显示不同剂量的PQ与ALI、PF程度明显相关。结论随中毒剂量的增大,兔急性肺损伤及PF的病理改变越显著。PQ剂量与肺损伤程度及PF程度密切相关。     

糖皮质激素在百草枯致急性肺损伤中应用的研究进展

百草枯(PQ)中毒可以导致全身多器官损伤,以肺部受损最为严重,肾上腺皮质激素有稳定细胞膜、对抗脂质过氧化、抗炎和非特异性免疫抑制作用,能有效清除肺间质水肿和预防肺纤维化,已成为治疗百草枯致急性肺损伤患者的重要综合措施之一,但有关激素的给药时机、具体用量、给药途径及疗程等还需进一步研究.     

阿魏酸钠对百草枯中毒大鼠急性肺损伤的保护作用

目的探讨阿魏酸钠(sodium ferulate,SF)对百草枯(paraquat,PQ)中毒致大鼠急性肺损伤的治疗作用及其可能机制。方法大鼠一次性腹腔注射PQ 15 mg/kg,染毒同时及染毒后不同时间腹腔注射SF,分别测定染毒后8、24、48、72h时点的大鼠血浆和肺组织匀浆中的肿瘤坏死因子(TNF-α)及内皮素(ET)含量,并观察肺组织结构变化。结果与正常对照组相比,大鼠染毒后8h血浆TNF-α、ET含量及肺组织中的ET含量明显升高(P＜0．01),中毒后24h肺组织中的TNF-α含量开始显著升高(P＜0．01),并持续升高至染毒后72h,其中血浆TNF-α含量于染毒后48h达峰值。给予SF治疗后与相应的中毒组比较,SF治疗8h后血浆和肺组织中ET含量显著降低(P＜0．05),24h后血浆和肺组织中TNF-α含量开始明显降低(P＜0．05)。肺组织病理学检查可见PQ中毒后肺泡壁增厚、血管扩张、充血,巨噬细胞浸润,肺泡腔内有大量浆液渗出；SF治疗后肺泡壁毛细血管扩张、充血减轻,肺泡腔浆液性渗出明显减少。结论SF对急性PQ中毒有治疗作用,其作用机制与抑制介导PQ中毒后大鼠急性肺损伤的TNF-α因子及ET有关。     

保护性通气策略治疗海水淹溺急性肺损伤兔的实验研究

目的 观察保护性肺通气策略在海水淹溺急性肺损伤应用时的治疗作用和安全性.方法 应用保护性机械通气策略对SWD-ALI兔进行分组救治,在不同时间点观察血气分析、呼吸动力学、血液动力学、肺损伤指标,并进行肺组织学检查,以评价治疗效果和安全性.结果 采用6～8 mL/kg小潮气量机械通气不仅能改善SWD-ALI时的氧合(P＜0.05),而且能有效控制气道峰压和平台压,从而避免呼吸机相关肺损伤.结论 肺保护性通气策略联合应用治疗SWD-ALI,能够明显改善氧和,避免继发肺损伤,是一种安全有效的治疗SWD-ALI的机械通气手段.