氨氯地平干预兔动脉粥样硬化过氧化脂质代谢、前列环素/血栓烷A2平衡异常的研究

目的 :观察动脉粥样硬化 （AS）兔过氧化脂质代谢、前列环素 （PGI2 ） /血栓烷A2 （TXA2 ）平衡异常以及氨氯地平干预作用。方法 :采用高脂饲料或高脂饲料加氨氯地平喂养家兔 6 0d ,喂养前、后抽血测生化指标 ,喂养后处死动物作组织学研究。结果 :喂养后血清总胆固醇 （TC）、主动脉和血浆丙二醛 （MDA）、全血血小板活化因子 （PAF）、血浆TXB2 、内皮素 （ET）水平显著升高 ,血小板聚集性增强 ,而主动脉组织和血浆 6 酮 前列腺素 （6 Keto PGF1α）、血浆超氧化物歧化酶 （SOD）水平显著下降 ,并且发生AS病变。氨氯地平可以降低MDA及ET含量 ,提高PGI2 /TXA2 比值 ,减轻AS病变。结论 :AS家兔体内出现脂质过氧化代谢异常、PGI2 /TXA2 平衡失调 ,而氨氯地平具有明显的拮抗作用 ,其机制可能与抗氧化有关。     

中药当归配伍丹参复方对兔髂动脉球囊内皮剥脱术后血小板粘附的影响

通过扫描电镜观察了中药复方制剂（当归配伍丹参）对兔髂动脉球囊内皮剥脱术后血小板粘附的影响，同时测定了血浆超氧化物歧化酶（SOD）活性及脂质过氧化物（LPO）、前列环素（PGI2）／血栓素A2（TXA2）和环磷酸腺苷（cAMP）水平。结果表明，当归配伍丹参有增加SOD活性、升高PGI2、cAMP水平和PGI2／TXA2比值、降低LPO和TXA2水平、抑制球囊内皮剥脱术后血小板粘附的作用，与对照组比较，有显著性差异（均P＜0．05～0．01）。结果为中药用于临床防治PTCA后急性血栓形成和慢性再狭窄等并发症提供了理论依据。     

妊娠期糖尿病患者妊娠晚期母血血栓素、前列环素及胎盘血栓素受体水平及意义

目的观察妊娠期糖尿病（GDM）患者妊娠晚期母血血栓素A2（TXA2）、前列环素（PGI2）及胎盘血栓素A：受体水平变化及意义。方法选择GDM妊娠晚期患者（GDM组）及同期正常妊娠者（对照组）各30例,用放免法检测母血TXA2、PGI2水平（分别以TXB2和6-keto—PGFlα浓度代替）,用免疫组化法检测胎盘血栓素受体（TXA2R）水平。结果实验组母血TXB2浓度、TXB2／6-keto—PGFlα明显高于对照组（P〈0．01或〈0．05）。实验组胎盘TXA2R阳性表达以强阳性为主,阳性表达率明显高于对照组（P〈0．05）。结论母血中TXA2浓度异常升高及TXA2／PGI2比例失衡与GDM胎盘TXA2R强阳性表达有关。     

川芎嗪对紫癜性肾炎患儿血浆内皮素、血栓素及前列环素水平的影响

将同期收治的48例紫癜性肾炎（HSPN）患儿随机分为观察组28例和对照组20例，两组均予常规综合治疗，观察组在此基础上予川芎嗪8～10mg／（kg·d）静滴，疗程2～4周。治疗前后测定两组血浆内皮素-I（ET-1）、血栓素A2（TXA2）、前列环素（PGI2）水平。结果两组治疗后血浆ET-1、TXA2水平均较治疗前明显下降，PGI2水平较治疗前明显升高，尤以观察组为著（P〈0．05）。认为川芎嗪能纠正TXA2、PGI2失衡，改善血液高凝状态，有利于肾损伤修复。     

脑缺血再灌注胃肠损伤老年大鼠前列腺素和肿瘤坏死因子的变化及其意义

目的：从血栓素（TXA2）与前列环素（PGI2）和肿瘤坏死因子（TNF）的变化方面研究老年大鼠脑缺血再灌注胃肠损伤的机制。方法：青年（5月龄）和老年（20月龄以上）大鼠均分为模型组和正常对照组，观察大鼠全脑缺血30min再灌注60min后胃肠组织变化和TXA2，PGI2，TNF含量。结论：青年和老年模型组胃肠组织出现明显的病理损伤，老年模型组较青年模型组严重。青年模型组胃组织中TXB2／6－Keto-PGF1α比值高于青年对照组和老年模型组，青年对照组小肠组织中TXB2／6－Keto-PGF1α低于青年模型组和老年对照组。老年模型组小肠中TNF含量高于青年模型组和老年对照组，结论：脑缺血再灌注胃肠损伤机制与以TXA2占优势的TXA2与PGI2的平衡失调和TNF增高有关，但由于老年大鼠胃肠组织前列腺素和TNF的增龄变化，使戎脑缺血再灌注胃肠组织TXA2与PGI2的平衡失调不明显，而TNF的改变较显著。     

吲哒帕胺对原发性高血压患者TXA2、PGI2含量的影响

目的研究轻中度原发性高血压患者血栓索A2(TXA2)和前列环素(PGI2)含量及二者比值的变化,评价吲哒帕胺对轻、中度原发性高血压的降压疗效以及对TXA2、PGI2和TXA2/PGI2的影响,探讨吲哒帕胺对血管内皮功能和血小板活性影响的机制.方法对30例轻、中度高血压患者和20例正常对照者的血浆采用放射免疫法测定TXA2、PGI2的水平,对高血压患者给予吲哒帕胺治疗2周,并进行治疗前、后对照比较.结果高血压组TXA2水平明显高于对照组,而PGI2水平明显低于对照组,TXA2/PGI2明显高于对照组(P均＜0.01).吲哒帕胺治疗组,降压有效率为60%,治疗后TXA2水平明显降低,PGI2水平明显升高,TXA2/PGI2明显下降(P均＜0.01).结论原发性高血压患者TXA2及TXA2/PGI2升高,PGI2水平下降.吲哒帕胺对轻、中度原发性高血压患者疗效显著,可引起TXA2水平显著下降,PGI2水平显著升高,对高血压所致的血管内皮损害具有保护作用.     

心悦胶囊对高脂血症大鼠血脂代谢的影响

目的 观察心悦胶囊对实验性高脂血症大鼠总胆固醇、脂蛋白-胆固醇代谢的影响.方法 将Wistar大鼠随机分为正常组、高脂血症模型组、心悦胶囊低、中、高剂量组及阳性药洛伐他汀组.正常组及高脂血症模型组灌胃0.5％羧甲基纤维素钠2ml· kg-1 ·d-1,心悦胶囊三个剂量组分别灌胃150、300、600mg·kg-1·d-1,洛伐他汀组灌胃30 ng·kg-1 ·d-1,连续30 d,测定血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白-胆固醇( LDL-C)、高密度脂蛋白-胆固醇(HDL-C)和血浆前列环素(PGI2)、血栓烷A2(TXA2)含量,血清和肝脏超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量,并观察肝脏脂肪沉积情况.结果 心悦胶囊能明显降低高脂血症大鼠血清TC、TG、LDL-c、TXA2和MDA含量及TC/HDL-C、LDL-C/HDL-C比值,升高血清HDL-c 、PGI2含量,SOD活性及PGI2/TXA2比值,并抑制肝脏脂肪沉积.结论 心悦胶囊可能通过增强抗氧化酶活性,调整PGI2与TXA2的平衡状态,纠正脂蛋白-胆固醇及自由基代谢紊乱等途径发挥调血脂作用,从而防止动脉硬化的形成和发展.     

肺癌患者血小板活化的临床意义

目的探讨血小板活化在肺癌患者中的临床意义。方法采用流式细胞仪和酶联免疫吸附试验法检测86例肺癌患者血小板膜蛋白P-选择素（CD62P）、血小板激活复合物（PAC-1）、血浆血栓素A2（TXA2）和前列环素I2（PGI2）及其比值。结果肺癌患者PAC-1和CD62P均明显高于正常对照组（P〈0.01）,血浆TXA2活性及TXA2/PGI2明显增高（P〈0.01）,PGI2活性无统计学变化;不同细胞类型肺癌患者各项指标均无统计学差异,但中晚期（Ⅲb＋Ⅳ）肺癌患者PAC-1、CD62P、TXA2活性及TXA2/PGI2均明显高于早期（Ⅰ~Ⅲa）患者（P〈0.01）;治疗缓解组PAC-1、CD62P、TXA2活性及TXA2/PGI2均较治疗前明显降低（P〈0.05）,而未缓解组无统计学变化。结论肺癌患者存在血小板活化现象,其TXA2活性增强可能起重要作用。血小板活性增强可能在肺癌的发生、发展、转移及预后等方面起一定作用。     

老年男性ApoA／ApoB与代谢综合征及其各组分相关性研究

目的探讨老年男性中载脂蛋白A／载脂蛋白B（ApoA／ApoB）与代谢综合征（metabolic syndrome，MS）及其相关组分的关系。方法采用横断面调查方法，选取2006年6月至2006年12月在我科进行体检的具有完整资料的老年男性共1729人，平均年龄（73．94±6．77）岁。测量身高、体质量、腰围、血压、血糖、总胆固醇（TC）、三酰甘油（TG）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、ApoA、ApoB、ApoA／ApoB。根据ApoA／ApoB四分位值将人群分为4组，以Logistic回归分析ApoA／ApoB与MS及其组分的关系。结果（1）中心性肥胖、高TG、低水平HDL-C、高血糖、MS患病率随着ApoA／ApoB降低而逐渐升高（P〈0．01）。（2）有代谢异常患者ApoA／ApoB水平较无代谢异常者低（P〈0．01）。（3）ApoA／ApoB水平随代谢异常组分增多而降低（P〈0．01）。（4）ApoA／ApoB下四分位组发生MS是ApoA／ApoB上四分位组的4．126倍（P〈0．01）。去除高血脂影响后，ApoA／ApoB下四分位组发生MS是ApoA／ApoB上四分位组的2．651倍（P〈0．01）。结论ApoA／ApoB与MS及其相关组分有密切的关系，MS、代谢异常者ApoA／ApoB较低。而低ApoA／ApoB也较易出现MS。ApoA／ApoB对MS的影响是独立于TC、TG、HDL-C、LDL-C之外的。     

重症急性胰腺炎患者早期血液流变学及血管活性指标血栓素A2、前例环素I2水平变化

目的：观察重症急性胰腺炎（SAP）患者早期血液流变学指标及血栓素A2（TXA2）、前列环素I2（PGI2）的变化。方法2012年1月至2013年9月住院的32例SAP患者为SAP组,30例体检健康人为NC组。于患者入院后治疗前即静脉采血,平行检测血液流变学指标及血浆TXA2、PGI2水平,并计算TXA2、PGI2比值。结果比较进行t检验。结果 SAP组血液流变学中除红细胞变形指数低于NC组（t＝2．185,P＜0．05）外,全血高、中、低切黏度、血浆黏度高于NC 组（t＝2．820、2．755、2．700、3．622,P＜0.05）,全血高切还原黏度、全血低切还原黏度高于NC组（t＝3．391、2．018,P＜0．05）,红细胞压积、红细胞刚性指数、红细胞聚集指数高于NC组（t＝2．980、2.209、2.004,P＜0．05）、全血高切相对指数、全血低切相对指数高于NC组（t＝2.630、2．440,P＜0．05）;SAP组TXA2、PGI2、TXA2、PGI2比值高于NC组（t＝3．256、2.589、2.640,P＜0．05）。结论 SAP患者早期即存在血液流变性异常及血管内皮细胞活性增高。     

Independent predictors of the severity of angiographic coronary atherosclerosis: the lack of association between impaired glucose tolerance and stenosis severity

Independent predictors of the severity of coronary atherosclerosis are ill defined. We sought to determine the predictors and examine the association of impaired glucose tolerance with stenosis severity. Four hundred thirty-seven patients were studied who underwent coronary angiography for suspected coronary artery disease. Serum concentrations of total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDLc), lipoprotein(a) [Lp(a)] and apolipoproteins (Apo A-I and Apo B) were measured and low-density lipoprotein cholesterol (LDLc) concentration was calculated. Except the patients treated for diabetes mellitus (DM), patients were classified into three groups such as normal glucose tolerance (NGT), impaired glucose tolerance (IGT) and DM by glucose tolerance test. Coronary atherosclerosis index (CAI) representing the severity of coronary atherosclerosis was determined by summation of the stenosis score of all lesions on coronary angiograms. Results indicated that age, total amount of cigarettes smoked, Apo B/Apo A-I, and LDLc/HDLc correlated with CAI, whereas HDLc and Apo A-I concentrations inversely correlated with CAI. TC, TG, Lp(a), LDLc, Apo B concentrations and body mass index did not correlate with CAI. One- and two-hour plasma glucose concentrations and the area of plasma glucose concentration under the curve at the glucose tolerance test did not correlate with CAI, revealing that post-challenge glycemia is not associated with stenosis severity. CAI in IGT patients was significantly lower than that in DM patients but did not differ from that in NGT patients, indicating that IGT does not affect the stenosis severity. Multivariate analysis showed that age, male gender, Apo B/Apo A-I, DM, systemic hypertension, and total amount of cigarettes smoked were independent predictors of CAI.     

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.     

Prostaglandin I2 half-life regulated by high density lipoprotein is decreased in acute myocardial infarction and unstable angina pectoris

To investigate the prostaglandin I2 (PGI2) half-life regulated by high density lipoprotein (HDL) in patients with coronary artery disease (CAD), we determined the stability of PGI2 and serum apolipoprotein A-I (Apo A-I) and apolipoprotein A-II (Apo A-II) levels in four age-matched groups of patients: controls (n = 17), angina pectoris (n = 18), unstable angina pectoris (n = 17), myocardial infarction (n = 19) (acute phase, 3.6 +/- 1.7 hours from onset; subacute phase, 75 +/- 15 hours from onset in the same patients). Serum PGI2 half-life and total serum Apo A-I levels were lower in the CAD group than in the control group. PGI2 was least stable in patients with unstable angina and the acute phase of myocardial infarction. In these patients, the molar ratio of Apo A-I to Apo A-II and HDL-associated Apo A-I levels were decreased, and free Apo A-I levels were increased. After in vitro incubation of HDL with increasing amounts of Apo A-II, Apo A-I in HDL was displaced by Apo A-II, with the parallel decrease in stability of PGI2. Free Apo A-I cannot stabilize PGI2. HDL-associated Apo A-I, whose amount is affected by Apo A-II, stabilized PGI2 and correlated well with stability of PGI2 in patients with CAD and control patients. Decreased PGI2 half-life may play an important role in the pathogenesis of atherosclerosis and thrombus formation in the coronary arteries, especially thrombus formation during an acute coronary event.     

西洋参茎叶三醇组皂苷对大鼠压力超负荷性心室重构的保护作用

目的 观察西洋参叶20s-原人参三醇组皂苷(PQTS)对压力超负荷性大鼠心室重构的保护作用.方法 Wistar大鼠随机分为假手术组、模型组、阳性药卡托普利组及PQTS低、中、高剂量组.结扎大鼠腹主动脉建立压力超负荷性心室重构模型,PQTS按12.5、25.0、50.0mg·kg-1·d-1连续腹腔注射6周,检测心室脏器系数、心肌组织病理学及血流动力学参数,测定血清丙二醛( MDA)含量及超氧物歧化酶(SOD)活性,血浆前列环素(PGI2)、血栓素A2 (TXA2)、内皮素(ET)及血管紧张素Ⅱ(AngⅡ)含量.结果 与重构模型组比较,PQTS能明显抑制心室重构大鼠心肌组织的病理性改变,降低心室质量及心脏系数,明显升高收缩压、舒张压、平均动脉压、左室收缩压及左心室内压最大上升和下降速率(±dp/dtmax),降低心率及左室舒张末压,可明显降低血清MDA含量,升高SOD活性,亦能明显降低血浆ET、AngⅡ及TXA2含量,提高PGI2含量及PGI2/TXA2比值(P＜0.05或P＜0.01).结论 PQTS对大鼠心室重构具有明显保护作用,可能与其改善心室重构大鼠的左心收缩和舒张功能,增强抗氧化酶活性,减少自由基及缩血管活性物质对心肌的损伤,纠正PGI2/TXA2失衡等机制有关.     

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.     

Ⅰ型肝肾综合征患者前列腺素I2和血栓素A2水平分析

目的 通过分析肝硬化腹水伴Ⅰ型肝肾综合征(HRS)患者的临床资料、实验室指标、前列腺素I2(PGI2)和血栓素A2(TXA2),探讨花生四烯酸代谢与Ⅰ型HRS发生的关系.方法 纳入肝硬化腹水伴Ⅰ型HRS患者38例(HRS组)及肝硬化腹水且肾功能正常患者50例(非HRS组),收集两组患者的一般资料和血液,分析肝肾功能、电解质、PGI2和TXA2水平.结果 HRS组和非HRS组的PGI2、TXA2、PGI2/TXA2水平分别为(32517±6023) pg/ml、(7432±2186) pg/ml、4.79 ±1.58和(29 597±3343) pg/ml、(5032 ±2104)pg/ml、7.50±2.38,HRS组TXA2水平高于非HRS组(t=2.385,P=0.027),而PGI2/ TXA2水平低于非HRS组(t=2.29,P=0.035),两组PGI2水平差异无统计学意义(t=1.233,P=0.23).结论 Ⅰ型肝肾综合征患者PGI2/TXA2比例失调,花生四烯酸代谢异常可能和Ⅰ型HRS发生有关.     

Effect of OKY-046, a thromboxane A2 synthetase inhibitor, on arachidonate-induced platelet aggregation: possible role of "prostaglandin H2 steal" mechanism

To clarify the mode of action of a selective thromboxane A2 (TXA2) blockade in platelet reactivity, we examined the effect of (E)-3-[4-(1-imidazolylmethyl) phenyl]-2-propenoic acid hydrochloride (OKY-046), a potent TXA2 synthetase inhibitor, on human platelet aggregation induced by arachidonic acid (1 mM) in the absence and presence of aspirin-treated aortic microsomes containing prostacyclin (PGI2) synthetase activity ex vivo. The production of TXA2 and PGI2 in platelet rich plasma was determined by the amounts of their stable catabolites, TXB2 and 6-keto-PGF1 alpha respectively, measured by radioimmunoassay. In the absence of aortic microsomes, OKY-046 (greater than 10(-5) M) produced more than 90% inhibition of TXA2 production, whereas platelet aggregation was less inhibited, about 40% inhibition over control, by OKY-046 in that concentration. In the presence of aortic microsomes, the inhibitory effect of OKY-046 on platelet aggregation was markedly augmented in a dose-dependent manner in proportion to the increment of PGI2 production, which paralleled the OKY-046-induced inhibition of TXA2. These results suggest that a selective TXA2 blockade produces effects on platelet aggregation mainly in dual fashion in the presence of PGI2 synthetase: one is due to mere inhibition of TXA2 synthetase and the other is due to the enhancement of PGI2 production probably involving "prostaglandin H2 (PGH2) steal" mechanism, in which PGH2 accumulated in platelets is partly converted to a substrate of PGI2 synthetase in aortic microsomes to produce PGI2.     

克山病病区粮饲养大鼠血栓素前列环素水平及其与硒维生素E的关系

研究了硒和维生素Ｅ（ＶＥ）对大鼠血浆和心肌血栓素（ＴＸＡ２）、前列环素（ＰＧＩ２）水平及ＴＸＡ２／ＰＧＩ２比值的影响。发现饲低硒、ＶＥ的克山病病区粮组动物在谷胱甘肽过氧化物酶降低和自由基净含量、脂质过氧化物（ＬＰＯ）浓度增高的同时，ＴＸＡ２水平增高、ＰＧＩ２水平降低、ＴＸＡ２／ＰＧＩ２比值增高；加硒或／和ＶＥ对纠正上述变化有相似而又不尽相用的效果，而以联合补充效果量佳。本研究结果提示硒和ＶＥ缺乏通过影响花生四烯酸代谢参与克山病缺血缺氧性心肌坏死的发生发展，其机制可能与二者缺乏，抗氧化能力降低，生成过量自由基和ＬＰＯ，抑制了ＰＧＩ２合成酶的作用并促进ＴＸＡ２形成有关。     

前列环素及血栓素在实验性肝肾综合征发病中的作用

采用硫代乙酰胺复制大鼠急性肝功能衰竭模型，结果大鼠在出现内毒素血症（ＥＴＭ）的同时，肾功能有明显异常，尿中ＰＧＩ２、ＴＸＡ２及其比值均有异常改变，提示ＥＴＭ的产生与肾脏ＴＸＡ２增多密切相关；ＥＴＭ及ＴＸＡ２均与肾小球滤过率（ＧＦＲ）下降有关。而丹参的防治作用似乎并非仅通过改变ＰＧＩ２、ＴＸＡ２产量及其比值这一单一途径。     

Changes of nitric oxide and endothelin, thromboxane A2 and prostaglandin in cirrhotic patients undergoing liver transplantation

AIM: To investigate the perioperative changes of nitric oxide (NO) and endothelin (ET), thromboxane Az (TXAa) and prostaglandin (PGh) during liver transplantation in end-stage liver disease patients. METHODS: Twenty-seven patients with end-stage cirrhosis undergoing liver transplantation were enrolled in this prospective study. Blood samples were obtained from superior vena at five different surgical stages. Plasma concentrations of nitrate and nitrite were determined to reflect plasma NO levels. Plasma levels of ET-1, 6-keto-PGF1 alpha and thromboxane B2 (TXB2), the latter two being stable metabolites of PGI2 and TXA2 respectively, were measured. RESULTS: The NO level decreased significantly after vascular cross-clamping and increased significantly at 30 min after reperfusion. While the ET levels at 30 min after clamping and after reperfusion were significantly elevated. The ratio of NO/ET decreased significantly at 30 min after vascular cross-clamping and at the end of surgery. The PGI2 level and the TXA2 during liver transplantation were significantly higher than the baseline level, but the ratio of TXA2/PGI2 decreased significantly at 30 min after clamping. CONCLUSION: NO/ET and TXA2/PGI2 change during liver transplantation. Although the precise mechanism remains unknown, they may play a role in the pathobiology of a variety of liver transplant-relevant processes.