目的探讨慢性阻塞性肺疾病(COPD)合并阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆内皮素-1(ET-1)、一氧化氮(NO)与肺动脉高压的关系。方法选择COPD患者53例,其中合并肺动脉高压患者18例;OSAHS患者50例,其中合并肺动脉高压患者14例...目的探讨慢性阻塞性肺疾病(COPD)合并阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆内皮素-1(ET-1)、一氧化氮(NO)与肺动脉高压的关系。方法选择COPD患者53例,其中合并肺动脉高压患者18例;OSAHS患者50例,其中合并肺动脉高压患者14例和重叠综合征(COPD合并OSAHS,即OS)患者25例,其中合并肺动脉高压患者12例,应用超声心动图评估肺动脉压,放射免疫法测定血浆ET-1水平,硝酸酶还原法测定NO水平,比较3组患者睡眠呼吸暂停严重程度及睡眠时缺氧程度。结果 3组患者睡眠呼吸暂停低通气指数(apneahypopnea index,AHI)、血氧饱和度(SaO2)<90%时间占总睡眠时间百分比(cumulative percentage of sleep time withSaO2below90%,TSaO2<90%)、最低血氧饱和度(MinSaO2)比较,差异均有统计学意义(P<0.01),OS组与COPD组、OSAHS组相比夜间MinSaO2降低(P<0.05)、TSaO2<90%增加,差异均有统计学意义(P<0.05);AHI升高亦有统计学意义(P<0.05)。3组合并肺动脉高压患者NO和ET-1水平比较,差异均有统计学意义(P<0.01)。OS合并肺动脉高压患者较未合并肺动脉高压患者ET-1水平升高,NO水平降低,差异均有统计学意义(P<0.05)。结论 OS患者较单纯的COPD和单纯OSAHS患者夜间缺氧更明显,更易形成肺动脉高压。血浆NO降低、ET-1升高与肺动脉压升高有一定关系。展开更多
The loss of endothelial connective integrity and endothelial barrier dysfunction can lead to increased vascular injury, which is related to the activation of endothelial inflammasomes. There are evidences that low con...The loss of endothelial connective integrity and endothelial barrier dysfunction can lead to increased vascular injury, which is related to the activation of endothelial inflammasomes. There are evidences that low concentrations of aspirin can effectively prevent cardiovascular diseases. We hypothesized that low-dose aspirin could ameliorate endothelial injury by inhibiting the activation of NLRP3 inflammasomes and ultimately prevent cardiovascular diseases. Microvascular endothelial cells were stimulated by lipopolysaccharide(2 μg/mL) and administrated by 0.1–2 mmol/L aspirin. The wild type mice were stimulated with LPS(100 μg/kg/day), and 1 h later treated with aspirin(12.5, 62.5, or125 mg/kg/day) and dexamethasone(0.0182 mg/kg/day) for 7 days. Plasma and heart were harvested for measurement of ELISA and immunofluorescence analyses. We found that aspirin could inhibit NLRP3 inflammasome formation and activation in vitro in dose-dependent manner and has correlation between the NLRP3 inflammasome and the ROS/TXNIP pathway. We also found that low-concentration aspirin could inhibit the formation and activation of NLRP3 inflammasome and restore the expression of theendothelial tight junction protein zonula occludens-1/2(ZO1/2). We assume that aspirin can ameliorate the endothelial layer dysfunction by suppressing the activation of NLRP3 inflammasome.展开更多
INTRODUCTIONMultiple organ dysfunction syndrome (MODS) isthought to be a frequent consequence of sepsis[1-3].Despite substantial advances in our knowledge and understanding of the basic pathophysiologic mechanisms[4-7...INTRODUCTIONMultiple organ dysfunction syndrome (MODS) isthought to be a frequent consequence of sepsis[1-3].Despite substantial advances in our knowledge and understanding of the basic pathophysiologic mechanisms[4-7], in critically ill patients infections and sepsis are still associated with a high mortality[8,9].展开更多
文摘目的探讨慢性阻塞性肺疾病(COPD)合并阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆内皮素-1(ET-1)、一氧化氮(NO)与肺动脉高压的关系。方法选择COPD患者53例,其中合并肺动脉高压患者18例;OSAHS患者50例,其中合并肺动脉高压患者14例和重叠综合征(COPD合并OSAHS,即OS)患者25例,其中合并肺动脉高压患者12例,应用超声心动图评估肺动脉压,放射免疫法测定血浆ET-1水平,硝酸酶还原法测定NO水平,比较3组患者睡眠呼吸暂停严重程度及睡眠时缺氧程度。结果 3组患者睡眠呼吸暂停低通气指数(apneahypopnea index,AHI)、血氧饱和度(SaO2)<90%时间占总睡眠时间百分比(cumulative percentage of sleep time withSaO2below90%,TSaO2<90%)、最低血氧饱和度(MinSaO2)比较,差异均有统计学意义(P<0.01),OS组与COPD组、OSAHS组相比夜间MinSaO2降低(P<0.05)、TSaO2<90%增加,差异均有统计学意义(P<0.05);AHI升高亦有统计学意义(P<0.05)。3组合并肺动脉高压患者NO和ET-1水平比较,差异均有统计学意义(P<0.01)。OS合并肺动脉高压患者较未合并肺动脉高压患者ET-1水平升高,NO水平降低,差异均有统计学意义(P<0.05)。结论 OS患者较单纯的COPD和单纯OSAHS患者夜间缺氧更明显,更易形成肺动脉高压。血浆NO降低、ET-1升高与肺动脉压升高有一定关系。
基金supported by the National Key Research and Development Program of China(No.2017YFC1700400)National Natural Science Foundation of China(Nos.81603587 and 81603668)+4 种基金Guangdong Natural Science Funds for Distinguished Young Scholar(No.2018B030306027,China)Science and Technology Development Plan of Guangdong Province(2017A020211016,China)Science&Technology Award for Young-Aged Talents of China Association of Traditional Chinese Medicine(No.CACM-2017-QNRC2-C12)the National Institutes of Health of USA(No.HL122769)Project of Guangzhou University of Chinese Medicine(No.A1-AFD018171Z11020,China)
文摘The loss of endothelial connective integrity and endothelial barrier dysfunction can lead to increased vascular injury, which is related to the activation of endothelial inflammasomes. There are evidences that low concentrations of aspirin can effectively prevent cardiovascular diseases. We hypothesized that low-dose aspirin could ameliorate endothelial injury by inhibiting the activation of NLRP3 inflammasomes and ultimately prevent cardiovascular diseases. Microvascular endothelial cells were stimulated by lipopolysaccharide(2 μg/mL) and administrated by 0.1–2 mmol/L aspirin. The wild type mice were stimulated with LPS(100 μg/kg/day), and 1 h later treated with aspirin(12.5, 62.5, or125 mg/kg/day) and dexamethasone(0.0182 mg/kg/day) for 7 days. Plasma and heart were harvested for measurement of ELISA and immunofluorescence analyses. We found that aspirin could inhibit NLRP3 inflammasome formation and activation in vitro in dose-dependent manner and has correlation between the NLRP3 inflammasome and the ROS/TXNIP pathway. We also found that low-concentration aspirin could inhibit the formation and activation of NLRP3 inflammasome and restore the expression of theendothelial tight junction protein zonula occludens-1/2(ZO1/2). We assume that aspirin can ameliorate the endothelial layer dysfunction by suppressing the activation of NLRP3 inflammasome.
基金Supported by the National Natural Science Foundation of China, No. 39870796
文摘INTRODUCTIONMultiple organ dysfunction syndrome (MODS) isthought to be a frequent consequence of sepsis[1-3].Despite substantial advances in our knowledge and understanding of the basic pathophysiologic mechanisms[4-7], in critically ill patients infections and sepsis are still associated with a high mortality[8,9].
