冠心病患者血管内皮细胞功能的变化

目的　探讨血管内皮细胞功能障碍与冠心病 (CHD)的关系。方法　采用二维超声检测 70例CHD患者肱动脉血管内径 (内皮依赖性和内皮非依赖性舒缩功能 ) ,同时采用生化比色法测定CHD患者血浆一氧化氮 (NO) ,用放射免疫法测定血浆内皮素 (ET)、前列腺素 (PGI2 )、血栓素A2 (TXA2 )、肿瘤坏死因子 (TNF)、心钠素 (ANP)及降钙素基因相关肽 (CGRP)浓度 ,并以 2 0例健康人为对照组。结果　CHD组内皮依赖性血管舒缩功能与对照组比较明显降低 ,内皮非依赖性血管舒缩功能与对照组比较差异无显著性意义 ;CHD组与对照组比较 ,血浆平均ET、TXA2 、TNF显著升高 ,而血浆NO、PGI2 、ANP、CGRP水平显著降低。结论　内皮细胞功能障碍及其内皮源性血管活性物质和影响内皮功能的血管活性物质的失衡 ,在CHD的发病机制中起重要作用     

非洛地平对高血压患者内皮功能的影响

目的　探讨高血压患者内皮血管活性物质的变化及非洛地平对其影响。方法　对 30例高血压患者和 2 4例正常对照组的血浆采用化学比色法测定 NO、NOS及采用射放免疫分析法测定 ET、Ang- 、TXA2 及 PGI2 ,并进行对照研究 ;对高血压组给予非洛地平治疗 ,并进行治疗前后的对照研究。结果　高血压组 ET、Ang- 及 TXA2 明显高于正常对照组 ,而 NO、NOS及 PGI2 明显低于正常对照组 ;非洛地平治疗组治疗后 ET、Ang- 及 TXA2 明显低于治疗前 ,NO、NOS及 PGI2 较治疗前无明显变化 ;非洛地平治疗高血压有效率 83.3%。结论　非洛地平抗高血压作用除主要通过拮抗钙通道以外 ,尚可通过降低 ET、Ang- 及 TXA2 起作用 ,而 NO通路不是其主要的作用机制。     

赖诺普利、氨氯地平和比索洛尔对高血压病患者血浆一氧化氮、前列环素与内皮素的影响

目的：探讨高血压病患者血浆一氧化氮（ Ｎ０）,前列环素（ Ｐ Ｇ Ｉ２ ）与内皮素（ Ｅ Ｔ）水平变化及赖诺普利、氨氯地平、比索洛尔对这些物质的影响。　方法：测定２０ 名正常人、８４ 名高血压病患者的血浆硝酸盐和亚硝酸盐（ Ｎ Ｏ 的代谢产物）、６┐酮┐前列腺素 Ｆ１α（ Ｐ Ｇ Ｉ２ 代谢产物）、 Ｅ Ｔ水平与血压,并进行治疗前后的对比分析。４６ 名患者用赖诺普利治疗,２０ 名用氨氯地平治疗,１８ 名用比索洛尔治疗,疗程均为８ 周。　结果：患者血浆 Ｎ Ｏ 和 Ｐ Ｇ Ｉ２ 水平明显低于正常人,而 Ｅ Ｔ水平显著高于正常人。这种变化与病情严重程度相平衡。赖诺普利组治疗后各期 Ｎ Ｏ、 Ｐ Ｇ Ｉ２ 水平提高, Ｅ Ｔ水平下降。氨氯地平组治疗后 Ｅ Ｔ水平下降,但 Ｎ Ｏ、 Ｐ Ｇ Ｉ２ 水平无改变。比索洛尔组治疗后 Ｎ Ｏ、 Ｐ Ｇ Ｉ２、 Ｅ Ｔ均无显著改变。　结论：高血压病与血浆 Ｎ Ｏ、 Ｐ Ｇ Ｉ２ 水平呈负相关,而与 Ｅ Ｔ水平呈正相关,此现象随着病情加重而更显著。赖诺普利组治疗后其疗效与 Ｎ Ｏ、 Ｐ Ｇ Ｉ２ 水平呈正相关,而与 Ｅ Ｔ水平呈负相关,这可能是 Ａ Ｃ Ｅ Ｉ赖诺普利的降压机理之一。     

The effects of a cyclooxygenase-2 inhibitor, FK3311, on total hepatic ischemia-reperfusion injury of the rat

BACKGROUND/AIMS: This study was designed to investigate the effects of a selective cyclooxygenase-2 inhibitor, FK3311, on warm ischemia-reperfusion injury of the rat liver. METHODOLOGY: Male Sprague-Dawley rats were used in this experimental study. Total hepatic ischemia was induced with a clamping portal triad. The animals were divided into two groups: the control group and the FK group, in which FK3311 (FK, 1.0 mg/kg) was administered via the penile vein. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) were measured 2 h after reperfusion, while those of thromboxane (Tx) B2 and 6-ketoprostaglandin (PG) F1alpha (stable metabolites of TxA2 and PGI2) were measured 30 min after reperfusion. The liver tissue blood flow was measured at preischemia, end-ischemia, and 30, 60, 90, and 120 min after reperfusion. The liver tissues obtained from animals at 2h after reperfusion were excised for histopathology. RESULTS: The serum levels of AST, ALT, and LDH were significantly lower in the FK group than in the control group. Similarly, in the FK group, the serum levels of TxB2 were significantly lower than in the control group. By contrast, the 6-keto-PG F1a levels were not significantly reduced. The liver tissue blood flow at 120 min after reperfusion was significantly higher in the FK group than in the control group. The histopathological study showed that hepatic tissue damage was milder in the FK group than in the control group. CONCLUSIONS: FK has protective effects on hepatic ischemia-reperfusion injury stemming from the marked inhibition of TxA2.     

螺内酯对冠心病患者内皮细胞功能的影响

目的　本实验旨在探讨螺内酯对冠心病患者内皮细胞功能的影响。方法　选择 5 0例冠心病患者作为实验组 ,5 0例健康者作为对照组 ,给药前先测定实验组和对照组的内皮素 (ET)、血栓素 A2 (TXA2 )、一氧化氮 (NO)、前列环素 (PGI2 ) ,再予以实验组螺内酯 2 0 m g/ d,3个月后再测定实验组的 ET、TXA2 、NO、PGI2 并进行比较。结果　给药前实验组的 ET、TXA2 水平较对照组高 ,NO、PGI2 水平较对照组低 ;给药后 NO、PGI2 水平较给药前高 ,ET、TXA2 较给药前低。结论　螺内酯可以有效地改善血管内皮细胞功能 ,对逆转冠心病患者内皮细胞功能紊乱起着重要的作用。     

葛根素对再灌注损伤肝能量代谢的保护作用及机制

[目的]研究葛根素对兔缺血再灌注损伤中肝脏能量代谢的改善作用及其机制。[方法]将30只家兔随机均分为对照组(C组)、缺血/再灌注组(IR组)和葛根素组(Pur组)。测定血浆中谷丙转氨酶(ALT)浓度和肝组织内一磷酸腺苷(AMP)、二磷酸腺苷(ADP)、三磷酸腺苷(ATP)、总腺苷酸量(TAN)、肝脏的细胞能荷(EC)、丙二醛(MDA)、超氧化物歧化酶(SOD)、一氧化氮(NO)、内皮素(ET)、NO/ET、血栓素B2(TXB2)、前列腺素F1α(PGF1α)、TXB2/PGF1α水平,并观察肝细胞形态学的改变。[结果]与C组比较,IR组血浆ALT浓度、肝组织AMP、ADP、MDA、ET含量显著升高(P0.01),TXB2、TXB2/PGF1α亦明显升高(P0.05),肝组织ATP、EC、SOD、NO/ET显著下降(P0.01),NO、PGF1α亦明显降低(P0.05),TAN差异无统计学意义(P0.05),肝细胞形态学异常改变;与IR组比较,Pur组血浆ALT浓度、肝组织AMP、MDA、ET含量显著降低(P0.01),肝组织ADP、TXB2/PGF1α亦明显减少(P0.05),TXB2略低于IR组(P0.05),肝组织ATP、EC、SOD、NO/ET显著升高(P0.01),肝组织NO、PGF1α亦明显增高(P0.05),TAN差异无统计学意义(P0.05),肝细胞形态学异常改变较大程度减轻。[结论]葛根素(60mg/kg)预处理可通过拮抗氧化损伤、调节NO/ET和前列腺素I2/血栓素A2(PGI2/TXA2)失衡而改善肝细胞的能量代谢,有效防治兔肝再灌注损伤。     

非酒精性脂肪性肝病大鼠血浆前列环素与血栓素的变化及其与肝脏损伤的关系

目的 探讨非酒精性脂肪性肝病(NAFLD)大鼠血浆前列环素(PG12)和血栓索(TX)A2的动念变化及其与肝组织学改变之间的关系。 方法 48只模型组SD大鼠给予高脂肪高胆固醇饮食饲养,分批于第8、12、16、24周处死,24只正常饮食大鼠作对照。放射免疫法检测血浆PGI 2和TXA 2的稳定代谢产物6酮-前列环素1α(PGF1 α)和TXB2含量,光镜观察肝组织切片病理学改变。 结果 模型组大鼠8周呈现单纯性脂肪肝,12～24周从脂肪性肝炎进展至脂肪性肝纤维化。模型组大鼠血浆TXB 2在造模第8、24周分别为(52.4±3.15)ng/L和(117.7±7.47)ng/L,对照组为(41.1±1.45)ng/L,t值为9.12和31.34,P<0.01和P<0.001。 血浆PGF1 α水平在造模8、24周分别为(31.1±1.6)ng/L和(3.4±2.4)ng/L,对照组为(36.5±1.7)ng/L,t值为6.27和34.62,P<0.01和,P<0.001。模型组大鼠血浆TXB2和PGF1 α水平分别与其肝组织损伤程度呈显著正相关(r=0.537,P<0.001)及负相关(r=-0.452,P<0.01)。 结论 持续24周的高脂饮食可以成功复制大鼠NAFLD模型,模型大鼠血浆TXA 2与PGI 2平衡失调,可能参与NAFLD的发病。     

Differential effects of oxidative stress on hepatic endothelial and Kupffer cell eicosanoid release in response to endothelin-1

OBJECTIVE: The vasoconstrictor endothelin-1 can induce vasomodulators release like nitric oxide in the liver. Here the authors explored whether endothelin-1 can stimulate endothelial and Kupffer cells release of other vasomodulators under normal and stress conditions. METHODS: Cells were cultured for 24 h and treated with H2O2 (25 microM) for 6 h and subsequently with endothelin-1 (10 nM) for 10 min. Eicosanoid release was assessed in the media by enzyme immunoassay. RESULTS: Endothelin-1 mediated cPLA2 phosphorylation and increased prostaglandin (PG) I2, PGE2 and thromboxane A2 (TXA2) release in endothelial cells while it only increased TXA2 in Kupffer cells. H2O2 significantly increased PGI2, PGE2 and TXA2 in endothelial cells through an upregulation of cyclooxygenase-2, thromboxane synthase A2, and phosphorylation of cPLA2. Endothelin-1-induced PGI2, PGE2, and TXA2 release in endothelial cells were inhibited by H2O2 correlating with the absence of further cPLA2 phosphorylation. In Kupffer cells, H2O2 only increased TXA2 synthesis and further endothelin-1 stimulation of TXA2 was possible through a higher increase in cPLA2. CONCLUSION: These results indicate that under normal conditions endothelial cells play a pivotal role in liver microcirculation regulation. Oxidative stress not only disrupts the basal balance of vasomodulators in the liver but also affects endothelin-1-induced effects in both Kupffer cells and endothelial cells.     

Effects of a selective thromboxane synthetase inhibitor (OKY-046) in patients with coronary artery disease during exercise

We studied the levels of thromboxane B2 (TXB2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), platelet aggregability, beta-thromboglobulin and platelet factor 4 in 30 coronary artery disease (CAD) patients and 21 normal subjects during exercise. During treadmill exercise, 13 of 30 CAD patients reported chest pain. We administered a selective thromboxane synthetase inhibitor (OKY-046) for 2 weeks to 10 CAD patients with exercise-induced chest pain and studied its effects. At rest, the plasma TXB2 levels and platelet aggregation were significantly lower in normal subjects than in CAD patients, and there was no difference between CAD patients with and without exercise-induced chest pain. On treadmill testing, plasma TXB2 levels and platelet aggregation increased significantly only in the CAD patients with exercise-induced chest pain. Plasma 6-keto-PGF1 alpha levels in normal subjects were significantly higher than those in CAD patients both at rest and during exercise. After administration of OKY-046, mean exercise time increased significantly from 7.5 to 8.6 min (p less than 0.001). Plasma TXB2 level and platelet aggregation decreased significantly after OKY-046 administration both at rest and during exercise. These results suggest that a marked increase in TXA2, with only a minimal change in PGI2, during exercise may contribute to exercise-induced myocardial ischemia, and that OKY-046 is useful in the treatment of CAD patients.     

Orchidectomy increases the formation of non-endothelial thromboxane A2 and modulates its role in the electrical field stimulation-induced response in rat mesenteric artery

The aim of this study was to analyze whether endogenous male sex hormones influence the release of thromboxane A2(TXA2) and its role in the electrical field stimulation (EFS)-induced response, as well as the mechanism involved. For this purpose, endothelium-denuded mesenteric arteries from control and orchidectomized male Sprague-Dawley rats were used to measure TXA2 release; EFS-induced response, nitric oxide (NO), norepinephrine (NA), and prostaglandin (PG) I2 release were also measured in the presence of the TXA2 synthesis inhibitor furegrelate. Orchidectomy increased basal and EFS-induced TXA2 release. Furegrelate decreased the EFS-induced contraction in arteries from control rats, but did not modify it in arteries from orchidectomized rats. The EFS-induced neuronal NO release and vasodilator response were increased by furegrelate in arteries from control rats, but were not modified in arteries from orchidectomized rats. Furegrelate did not modify the EFS-induced NA release or vasoconstrictor response in arteries from either control or orchidectomized rats. The EFS-induced PGI2 release was not modified by furegrelate in arteries from control rats, but was increased in arteries from orchidectomized rats. The results of the present study show that endogenous male sex hormone deprivation i) increases non-endothelial TXA2 release and ii) regulates the effect of endogenous TXA2 on the EFS-induced response through different mechanisms that, at the least, involve the NO and PGI2 systems. In arteries from control rats, inhibition of TXA2 formation decreases the EFS-induced response by increasing neuronal NO release. In arteries from orchidectomized rats, the EFS-induced response is unaltered after the inhibition of TXA2 formation, by increasing PGI2 release.     

Intestinal prostacyclin and thromboxane production in irreversible hemorrhagic shock

Arterial and intestinal venous blood were sampled every hour for measurement of thromboxane B2 (TXB2) and 6-keto-PGF1 alpha, stable metabolites of thromboxane A2 and prostacyclin, respectively, in dogs subjected to hemorrhagic hypotension at 32.8 +/- 1.4 mm Hg for 3 h, followed by reinfusion of the remaining shed blood. Control dogs were treated alike without hypotension. Arterial and intestinal venous TXB2 significantly increased during hypotensive and post-transfusion periods, the venous concentration being significantly higher than the corresponding arterial. The arterial and venous 6-keto-PGF1 alpha increased during hypotension but decreased during post-transfusion periods. Furthermore, arterial and venous TXB2 to 6-keto-PGF1 alpha concentration ratio increased. Intestinal TXB2 release (blood flow X arteriovenous concentration difference) increased progressively, whereas 6-keto-PGF1 alpha release decreased. No significant changes occurred in the control dogs. This study shows an imbalance in intestinal production and release of TXA2 and PGI2, in favor of TXA2 during severe hemorrhagic hypotension and after blood transfusion. The imbalance may contribute to the development of irreversible hemorrhagic shock and reperfusion injury.     

左旋精氨酸对缺血—再灌注损伤肝脏的保护作用

目的探讨左旋精氨酸（L-arginine,L-Arg）对肝缺血－再灌注损伤（hepaticischemia-reperfusioninjury,HIRI）的防治作用及其机理。方法选择HIRI家兔及肝手术患者,观察一氧化氮水平、丙二醛浓度、血栓素B     

花生四烯酸细胞色素p450表氧化酶基因对肺动脉高压大鼠血浆和组织中ET-1、NO、TXA2和PGI2变化的影响

目的观察野百合碱(MCT)诱导的肺动脉高压大鼠中花生四烯酸色素p450表氧化酶CYP2J2基因过表达时血浆和肺组织中内皮素-l(ET-1)、一氧化氮(NO)血栓素A2(TXA2)和前列腺素I2(PGI2)的水平及肺组织中一氧化氮合酶(NOS)活性的变化。方法成年雄性SD大鼠60只随机分为正常对照组(n=30)和MCT模型组(n=30),皮下注射MCT(60mg/kg)建立肺动脉高压模型。三周后尾静脉分别注射生理盐水和质粒分为6组:NS组,pCDNA3.1(n=10),pcDNA3.1-CYP2J2(n=10),MCT+NS(n=10),MCT+pCDNA3.1(n=10),MCT+pCDNA3.1-CYP2J2(n=10)。三周后,检测大鼠肺动脉压(mPAP),测定血浆和肺组织中ET-1和NO水平,检测肺组织中NOS和eNOS的活性,检测血浆和肺组织TXA2代谢产物TXB2和PGI2代谢产物6-酮-前列腺素1α(6-keto-PGF1α)水平及TXB2/6-keto-PGF1α的比值。结果 MCT模型组mPAP,血浆和肺组织中ET-1水平和TXB2含量和TXB2/6-keto-PGF1α比值均明显高于正常对照组(P<0.05),而pCDNA3.1-CYP2J2治疗组与MCT模型组比均显著降低(P<0.05),但仍高于正常对照组(P<0.05);MCT模型组血浆和肺组织中NO和6-keto-PGF1α含量,肺组织eNOS和NOS活性,TXB2/6-keto-PGF1α比值均明显低于正常对照组(P<0.05),而pCDNA3.1-CYP2J2治疗组均明显增高(P<0.05),但仍低于正常对照组(P<0.05)。结论花生四烯酸色素p450表氧化酶基因CYP2J2可逆转MCT诱导的肺动脉高压,其机制可能与降低肺组织和血浆中的ET-1和TXA2含量,升高PGI2含量,上调TXA2/PGI2比值,上调机体内eNOS和总NOS活性,增加体内NO水平有关。CYP2J2基因治疗对肺动脉高压有积极的治疗作用。     

Effect of palm oil on oxidative stress-induced hypertension in Sprague-Dawley rats

BACKGROUND: Oxidative stress, associated with increased plasma isoprostane (ISO) and reductions in plasma glutathione (GSH), has been shown to cause severe hypertension in normal rats. Palm oil (PO), with an unsaturated-to-saturated fatty acid ratio close to one and rich in antioxidant vitamins, has been investigated for its beneficial effects on arterial thrombosis and atherosclerosis. In this study, the effect of PO on oxidative stress induced by inhibition of GSH synthesis (using buthionine sulfoximine [BSO]) was examined. METHODS: Sprague-Dawley rats were separated into two groups and received either natural vitamin-rich PO (Carotino, 5 g/kg daily) or water by gavage. After 4 weeks, they were further divided between receiving either BSO (30 mmol/L/day in the drinking water) or drug-free water for an additional week. Mean arterial pressure (MAP), heart rate (HR), and body weight (BW) were measured before and weekly during the experiment. The levels of plasma ISO, nitric oxide (NO), prostacyclin (PGI2), and thromboxane A2 (TXA2) were determined by enzyme immunoassay, and plasma, heart, and kidney GSH by high-performance liquid chromatography. RESULTS: The PO reduced the age-dependent increase in MAP, and the pressor response to BSO, without changing the HR or BW compared to the BSO and control groups. It also elevated PGI2, NO, and aortic cGMP, but decreased TXA2 and aortic cAMP. In addition, the BSO-induced increase in ISO and TXA2, and the reduction in kidney GSH were attenuated by PO. However, the PO effect on NO, PGI2, cGMP, and TXA2 was partly counteracted by BSO. CONCLUSIONS: Palm oil reduces BSO-induced oxidative stress and attenuates hypertension by mechanisms involving changes in endothelium-derived factors.     

血管内皮功能在良性前列腺增生症和冠心病之间的作用

目的 探讨良性前列腺增生症(BPH)和冠心病(CHD)两者之间的内在联系和发病机制。方法 测定56例BPH患者手术前后血浆血栓素(TxA2)、前列环素(PGI2)及其比值和一氧化氮(NO)、内皮素(ET)及其比值的动态变化，将其中伴有CHD和无CHD者分组比较。结果 BPH患者术后PGI2和NO明显下降，ET明显升高，TxA2／PGI2比值明显升高，NO／ET比值明显下降；与无CHD者相比，伴有CHD者术后不仅PGI2明显降低，且TxA2显著升高，手术后两者之间TxA2、PGI2水平及其比值和ET水平及其NO／ET比值变化均有显著差异。结论 BPH患者前列腺切除术后存在着直管内皮功能障碍，以伴有CHD的患者为甚，推测血管内皮功能失调可能是CHD和BPH两种疾病的内在联系和共同的发病机制之一。     

缬沙坦和卡托普利对缺血再灌注纤溶活性、内皮血管活性物质的影响

目的　探讨缬沙坦和卡托普利对缺血再灌注纤溶活性、内皮血管活性物质的影响。方法　新西兰大白兔 6 0只 ,随机分为五组 ,每组 12只 , 组 :假手术组 , 组 :急性心肌梗死 (AMI)组 , 组 :缺血再灌注 (ischem ic reperfu-sion,IR)组 , 组 :IR+卡托普利组 , 组 :IR+缬沙坦组 ;各组 (除 组外 )分别结扎冠状动脉左心室支中点 ,缺血6 0 min,松开结扎线再灌注 2 4 0 min后 ( 组不进行再灌注 ) ,分别取结扎前、再灌注前、再灌注 2 4 0 min血测定内皮素 (endochelin ,ET)、一氧化氮 (nitric oxide NO)浓度和组织型纤溶酶原激活剂 (tissue- type plasminogen activa-tor,t- PA )、纤溶酶原激活剂抑制物 (,plasm inogen activator inhibitor PAI)活性。结果　冠状动脉结扎后 ,血浆ET、NO浓度和 PAI活性显著升高 (P<0 .0 1) ,t- PA活性显著下降 (P<0 .0 1) ,再灌注后 ,血浆 ET、NO浓度和 PAI活性进一步升高 ,t- PA活性进一步下降 ,与再灌注前对比均有显著性差异 (P<0 .0 1)。再灌注后 ,与 IR组对比 ,卡托普利、缬沙坦均能显著的升高 t- PA活性 ,降低血 PAI活性和 ET、NO浓度 (P<0 .0 1)。结论　卡托普利、缬沙坦有改善缺血再灌注过程中纤溶活性、抑制内皮细胞释放 ET、NO的有益作用     

Increased prostacyclin and thromboxane A2 biosynthesis in atherosclerosis.

It has been proposed that atherosclerotic arteries produce less prostacyclin (PGI2) than nonatherosclerotic arteries do, thereby predisposing arteries to vasospasm and thrombosis in vivo. We reexamined this concept by measuring spontaneous as well as arachidonate-induced PGI2 biosynthesis in aortic segments from nonatherosclerotic and cholesterol-fed atherosclerotic New Zealand White rabbits. Thromboxane A2 (TXA2) generation was also measured. Formation of PGI2, as well as TXA2, as measured by radioimmunoassay (RIA) of their metabolites, was increased in atherosclerotic aortic segments relative to nonatherosclerotic segments (P less than or equal to 0.05) at 0, 5, 10, 15, and 30 min of incubation with arachidonate. Pretreatment of arterial segments with indomethacin inhibited PGI2 as well as TXA2 formation, whereas pretreatment with the selective TXA2 inhibitor OKY-046 inhibited only TXA2 release, thus confirming the identity of icosanoids. To confirm the RIA data, aortic segments were incubated with [14C]arachidonate prior to stimulation with unlabeled arachidonate. The uptake of arachidonate was similar, but the release of incorporated [14C]arachidonate was significantly (P less than or equal to 0.05) greater in atherosclerotic segments than in nonatherosclerotic ones. Conversions of released [14C]arachidonate to 6-keto[14C]prostaglandin F1 alpha and [14C]thromboxane B2 were similar in the two types of aortic segments. Thus, synthesis of PGI2 as well as TXA2 is increased in atherosclerosis, and this alteration in arachidonate metabolism is related to increased release of arachidonate.     

苯扎贝特联合降压治疗对高血压合并高甘油三酯血症患者内皮功能和血压的影响

目的 用随机、对照的方法观察苯扎贝特联合降压治疗对高甘油三酯血症合并高血压患者内皮功能和血压的影响。方法 58例高甘油三酯血症伴原发性高血压患者随机分为苯扎贝特组(A组)和对照组(B组)，通过治疗前后血压、血脂、血浆内皮素(endothelin，ET)、一氧化氮(nitric oxide，NO)、血栓烷A2(thromboxane A2，TXA2)、前列环素I2(PGI2)和降钙素基因相关肽(calcitonin gene-related peptide，CGRP)等指标的变化，来观察苯扎贝特对患者血管内皮功能和血压的影响。结果 A组在治疗后血甘油三酯、总胆固醇、低密度脂蛋白胆固醇水平明显降低．高密度脂蛋白胆固醇显著升高；NO显著升高．ET、TXA2／PGI2明显降低；而且A组舒张压降低较B组显著，并与血甘油三酯水平及内皮功能的变化有关。结论 苯扎贝特可能通过调整血脂代谢紊乱，对患者的血管内皮功能有改善作用，并且在降压药物的基础上．可能对患者舒张压有额外降低作用．     

不同海拔地区健康成年男性6种血激素水平的变化

人类急进高原后或高原人群会出现较多消化道症状,并伴发多种胃肠病.激素在高原胃肠病发生中所起的作用值得进一步研究.目的：研究高、中、低海拔地区健康成年男性血清胃泌素（GAS）和血浆胃动素（MTL）、前列环素（PGI2）、血栓素（TX）A2、内皮素（ET）、降钙素（CT）水平的变化,探讨上述激素与高原胃肠病发生的可能关系.方法：选取广州市（海拔2 m）、西宁市（海拔2 260 m）和青藏铁路雁石坪（海拔4 750 m）三个不同海拔地区的健康成年男性共68例,分别采血,以放射免疫测定检测上述6种激素水平.结果：雁石坪地区健康成年男性的血GAS水平显著高于广州市和西宁市（P＜0.05）,三地间MTL水平均无显著差异（P＞0.05）.雁石坪地区的PGI2和TXA2水平显著高于西宁市（P=0.006和P=0.000）,但两地ET和CT水平无显著差异（P＞0.05）.结论：随着海拔的升高,健康成年男性的血GAS水平逐渐升高,可能与人急进高原后胃黏膜病变的发生有关.高海拔地区男性的血PGI2、TXA2水平也明显升高,可能与人进入高原后胃肠的适应性和高原胃黏膜病变的病理生理有关.     

Drug modulation of thromboxane A2/prostacyclin balance and lipid peroxidation in patients with coronary artery disease

Sixty patients with coronary artery disease (CAD) were investigated in a randomized, placebo-controlled study. Therapeutic dose of diltiazem markedly inhibited the production of whole blood thromboxane A2(TXA2), but had no effect on the production of prostacyclin(PGI2). Both aspirin 20mg/d and diltiazem plus aspirin had marked inhibitive effects on both TXA2 and PGI2. The order of potency of the three regimens in decreasing TXA2/PGI2 ratio was diltiazem plus aspirin greater than diltiazem greater than aspirin. Diltiazem, aspirin and combination of both all decreased significantly serum lipid peroxides level, but had no effect on serum superoxide dismutase concentration. The results indicate that both therapeutic dose of diltiazem and low-dose of aspirin may modulate TXA2/PGI2 balance and inhibit lipid peroxidation in CAD and that the combination of both drugs may result in best therapeutic effect.