家兔动脉粥样硬化与血小板源内皮型氧化氮合酶表达的相关性

Objective To explore the correlation of atheroselerosis progression and the expression of platelet derived endothelial nitric oxide synthase (eNOS) in rabbits. Methods A total of 24 male New Zealand white rabbits were used in this study. Six of the animals were fed with normal food (control group). Eighteen rabbits were fed with cholesterol-rich food (1 g/d) for 12 weeks to establish the atherosclerosis model. Among 18 models, 6 rabbits were executed immediately and their aorta and platelet samples were collected for further analysis (model group), 6 rabbits were orally administered with pravastatin (10 rag/d) for additional 12 weeks (treated group), and the remaining 6 rabbits were left untreated until the end of the study (untreated group). The control, treated and untreated animals were then killed, and the aorta and platelet samples were collected for eNOS expression analysis (RT-PCR). Results The aorta samples in model and untreated group exhibited rough intima and a lot of longitudinal fatty streaks, which indicated that atherosclerosis models were established successfully. While in treated group, the degree of atherosclerosis was decreased. The average percent of thickness of fatty streaks or atheroselerotic plaques relative to the whole thickness of vessel walls was 0. 04±0. 02, 0. 82±0. 16, 0. 33±0. 18,0. 77±0. 14 in control, model, treated and untreated group, respectively. The thickness of fatty streaks or atherosclerotic plaques was significantly increased in the model and untreated groups and decreased in treated group compared with the control group (both P<0. 05). The expressions of platelet derived eNOS/mRNA were 1. 02± 0. 28, 0. 41± 0. 27, 1.00 ± 0. 77, 0. 40±0. 29 in control, model, treated and untreated group, respectively. The expression of eNOS/mRNA was markedly decreased in model group and untreated group compared with the control group, but was increased in treated group compared with untreated and model groups (F=3. 544, P = 0. 024). Conclusions There is a negative correlation between eNOS expression and atherosclerosis development, which suggests that the reversal effect of pravastatin on atheroselerosis progression and plaque formation may relate to the expression of platelet derived eNOS.     

家兔动脉粥样硬化与血小板源内皮型氧化氮合酶表达的相关性

Objective To explore the correlation of atheroselerosis progression and the expression of platelet derived endothelial nitric oxide synthase (eNOS) in rabbits. Methods A total of 24 male New Zealand white rabbits were used in this study. Six of the animals were fed with normal food (control group). Eighteen rabbits were fed with cholesterol-rich food (1 g/d) for 12 weeks to establish the atherosclerosis model. Among 18 models, 6 rabbits were executed immediately and their aorta and platelet samples were collected for further analysis (model group), 6 rabbits were orally administered with pravastatin (10 rag/d) for additional 12 weeks (treated group), and the remaining 6 rabbits were left untreated until the end of the study (untreated group). The control, treated and untreated animals were then killed, and the aorta and platelet samples were collected for eNOS expression analysis (RT-PCR). Results The aorta samples in model and untreated group exhibited rough intima and a lot of longitudinal fatty streaks, which indicated that atherosclerosis models were established successfully. While in treated group, the degree of atherosclerosis was decreased. The average percent of thickness of fatty streaks or atheroselerotic plaques relative to the whole thickness of vessel walls was 0. 04±0. 02, 0. 82±0. 16, 0. 33±0. 18,0. 77±0. 14 in control, model, treated and untreated group, respectively. The thickness of fatty streaks or atherosclerotic plaques was significantly increased in the model and untreated groups and decreased in treated group compared with the control group (both P<0. 05). The expressions of platelet derived eNOS/mRNA were 1. 02± 0. 28, 0. 41± 0. 27, 1.00 ± 0. 77, 0. 40±0. 29 in control, model, treated and untreated group, respectively. The expression of eNOS/mRNA was markedly decreased in model group and untreated group compared with the control group, but was increased in treated group compared with untreated and model groups (F=3. 544, P = 0. 024). Conclusions There is a negative correlation between eNOS expression and atherosclerosis development, which suggests that the reversal effect of pravastatin on atheroselerosis progression and plaque formation may relate to the expression of platelet derived eNOS.     

普伐他汀在体外对血小板聚集和血小板TXB_2、cAMP含量的影响

降低血胆固醇和血小板的高反应性是动脉粥样硬化和血栓住心脑血管疾病防治的主要措施。本文探讨了普伐他汀在体外对血小板聚集和血小板血栓烷素Ｂ２（ＴＸＤ２）及环磷酸腺苷（ｃＡＭＰ）含量的影响。血源标本来自２８例高胆固醇血症（ＨＣ）病人和１０例健康体检者。结果显示，ＨＣ病人的血小板功能增强。与加药前比较，不同浓度的普伐他汀（０．０３μｍｏｌ／Ｌ，０．３μｍｏｌ／Ｌ）均可降低ＨＣ组的血小板聚集反应，降低血小板ＴＸＢ２量，增加血小板ｃＡＭＰ量，提示普伐他汀具有抗血小板作用。     

普伐他汀在调脂治疗中对血小板功能的影响

高胆固醇血症 (ｈｙｐｅｒｃｈｏｌｅｓｔｅｒｏｌｅｍｉａ ,ＨＣ)是动脉粥样硬化(ａｔｈｅｒｏｓｃｌｅｃｒｏｓｉｓ,ＡＳ)和血栓形成的危险因素。在其病理过程中 ,血小板功能的异常受到普遍重视 ,ＨＣ患者血小板活性增高。我们观察了ＨＣ患者在普伐他汀降脂治疗过程中血小板胞浆游离Ｃａ2 (血小板 [Ｃａ2 ]ｉ)、血小板聚集功能 (ＰＡＧ)、粘附功能 (ＰＡＤ)及血小板血栓烷Ｂ2 (ＴＸＢ2 )的变化 ,探讨调脂药的非降脂作用。材料和方法1　对象与分组　ＨＣ组 2 4例 ,男 13例 ,女 11例 ,平均年龄5 4.7岁。ＨＣ患者入选标准 :血清总胆固醇 …     

高旦固醇血症患者血小板L-精氨酸/一氧化氮系统的改变

目的观察高胆固醇血症(HC)患者血小板L-精氨酸(L-Arg)/一氧化氮(NO)系统活性的变化。方法采用比色法检测21例HC患者和26名健康体检者血小板的NO水平,采用放射性核素(3H-L-精氨酸)标记法检测血小板一氧化氮合成酶(NOS)及L-Arg转运系统活性。结果HC患者血小板NO水平为(24.06±3.70)nmol/10     

家兔动脉粥样硬化与血小板源内皮型氧化氮合酶表达的相关性

Objective To explore the correlation of atheroselerosis progression and the expression of platelet derived endothelial nitric oxide synthase (eNOS) in rabbits. Methods A total of 24 male New Zealand white rabbits were used in this study. Six of the animals were fed with normal food (control group). Eighteen rabbits were fed with cholesterol-rich food (1 g/d) for 12 weeks to establish the atherosclerosis model. Among 18 models, 6 rabbits were executed immediately and their aorta and platelet samples were collected for further analysis (model group), 6 rabbits were orally administered with pravastatin (10 rag/d) for additional 12 weeks (treated group), and the remaining 6 rabbits were left untreated until the end of the study (untreated group). The control, treated and untreated animals were then killed, and the aorta and platelet samples were collected for eNOS expression analysis (RT-PCR). Results The aorta samples in model and untreated group exhibited rough intima and a lot of longitudinal fatty streaks, which indicated that atherosclerosis models were established successfully. While in treated group, the degree of atherosclerosis was decreased. The average percent of thickness of fatty streaks or atheroselerotic plaques relative to the whole thickness of vessel walls was 0. 04±0. 02, 0. 82±0. 16, 0. 33±0. 18,0. 77±0. 14 in control, model, treated and untreated group, respectively. The thickness of fatty streaks or atherosclerotic plaques was significantly increased in the model and untreated groups and decreased in treated group compared with the control group (both P<0. 05). The expressions of platelet derived eNOS/mRNA were 1. 02± 0. 28, 0. 41± 0. 27, 1.00 ± 0. 77, 0. 40±0. 29 in control, model, treated and untreated group, respectively. The expression of eNOS/mRNA was markedly decreased in model group and untreated group compared with the control group, but was increased in treated group compared with untreated and model groups (F=3. 544, P = 0. 024). Conclusions There is a negative correlation between eNOS expression and atherosclerosis development, which suggests that the reversal effect of pravastatin on atheroselerosis progression and plaque formation may relate to the expression of platelet derived eNOS.     

尼氟灭酸对糖尿病人血小板胞浆游离钙及聚集功能的影响

【目的】探讨糖尿病人血小板胞浆游离钙([Ca2+]i)、血小板聚集率变化及氯通道阻断剂尼氟灭酸对其的影响。【方法】用Fura-2荧光测钙技术检测血小板[Ca2+]i,血小板聚集仪检测血小板聚集率,观察氯通道阻断剂尼氟灭酸、钙通道阻断剂硝苯地平及两者联合对糖尿病人的血小板[Ca2+]i、血小板聚集率的作用。【结果】①糖尿病人血小板聚集率为(74.9±13.7)%,高于正常人(P<0.05);糖尿病人的静息血小板[Ca2+]i值、钙释放、钙內流分别为(124．5±38．1)nmol／L、(497．1±95．1)nmol/L、(354.3±75.0)nmol/L,均高于正常人(P均<0.05);②尼氟灭酸及硝苯地平抑制血小板钙内流呈浓度依赖性,半数抑制浓度(IC50)的尼氟灭酸(50μmol/L)对糖尿病人血小板钙内流的抑制率为(54.7±14.5)%,对血小板聚集率的抑制率为(32.3±21.4)%;IC50的硝苯地平(7.5μmol/L)对糖尿病人血小板钙内流的抑制率为(17.9±11.9)%,对血小板聚集率的抑制率为(32.3±20.4)%;③尼氟灭酸联合硝苯地平对糖尿病人血小板钙有抑制作用,联合作用时尼氟灭酸对钙内流抑制率为(51.9±12.8)%;硝苯地平对钙内流抑制率为(12.4±8.5)%(P均<0.05),两者间不存在交互效应。【结论】糖尿病人血小板聚集率、静息血小板[Ca2+]i及钙运动均高于正常人,血小板呈高反应状态。尼氟灭酸可抑制糖尿病人血小板聚集和钙内流,可能与血小板膜存在对尼氟灭酸敏感的氯通道有关。尼氟灭酸与硝苯地平联合对糖尿病患者的血小板钙运动无协同及遏制作用。     

高胆固醇血症患者血小板功能、血液流变学及纤维蛋白原的变化

目的：观察高胆固醇血症患者血小板功能、血液流变学及纤维蛋白原的变化。方法：选择28例高胆固醇血症患者和正常健康对照者25例,分别测定血小板聚集功能（PAG）、血小板粘附功能（PAD）、血流流变学[包括全血高切、低切粘度、血浆粘度、血沉（ESR）、红细胞压积（Hct)]及纤维蛋白原（FIB）。结果：高胆固醇血症患者PAG、PAD、全血高切粘度,全血低切粘度、血浆粘讴、ESR及FIB均明显高于正常人。结论：高胆固醇血症患者处于多种危险因素并存的状态,为避免血栓形成需要尽早进行多方面的综合治疗。     

妊娠期糖尿病患者血小板功能状态的研究

既往妊娠期糖尿病(GDM)患者的血液系统改变的研究报道很少。为此，我们检测了23例GDM患者血小板计数(PLT)、平均血小板容积(MPV)、血小板最大聚集率[PAG(M)]和血小板α-颗粒膜蛋白GMP-140(CD62P)的改变，探讨GDM妇女血小板的功能状态及其临床意义。     

ADP和CPA诱导的高血压病人血小板胞浆游离钙的变化

[目的]探讨高血压病人血小板胞浆游离钙浓度(cytoplasmicfreeCa2 concentration,[Ca2 ]i)的变化.[方法]采用Fura-2/Am荧光双波长测定[Ca2 ]i技术,动态观察激动剂二磷酸腺苷(adenosinediphosphate,ADP)和环匹阿尼酸(cyclopiazonicacid,CPA)对高血压病人血小板[Ca2 ]i的影响.[结果]高血压病人静息血小板[Ca2 ]i与正常人比较明显增高(P<0.05);ADP和CPA激动的高血压病人的血小板平台钙与静息钙比较有统计学意义(P<0.05);峰位钙-平台钙的差(既钙释放)与正常人比较明显增高(P分别<0.05和<0.01);平台钙-静息钙的差(既钙内流)与正常人比较无明显差异(P>0.05).[结论]高血压病人静息血小板[Ca2 ]i增高,平台钙水平明显增高,血小板呈高反应状态;高血压病人的血小板被ADP和CPA激活不能恢复至静息动状态;ADP和CPA激动的高血压病人的血小板钙释放增多,钙内流正常.