美洛昔康对兔急性肺损伤保护作用的研究

目的观察内毒素致兔急性肺损伤（ALI）时肺组织血栓素B2（TXB2）／6-酮-前列腺素F1α（6-keto—PGF1α）和内皮素-1（ET-1）变化及美洛昔康的影响，探讨美洛昔康对急性肺损伤干预的机制。方法将24只日本大耳白兔随机分为对照组（A组）、致伤组（B组）、美洛昔康干预组（C组）。各组分别于0、0．5、2、4h观测动脉血气、呼吸变化，4h处死动物，用放射免疫分析方法检测肺组织TXB2、6-keto—PGF，d、ET-1含量，行肺组织病理学观察并评分。结果静注内毒素后，B组动物呼吸显著加快，氧舍指数下降，肺组织TXB2／6-keto—PGF1α、ET-1均高于A组（P〈0．01），病理检查见肺水肿、出血等病理改变，病理评分也显著高于A组。C组呼吸稍增加，氧合指数稍降，肺组织TXB2／6-keto—PGF1α、ET-1、病理评分均低于B组（P〈0．01）。结论美洛昔康可通过降低肺中TXB2／6-keto—PGF1α比值和ET-1的含量，在一定程度上减轻内毒素对肺的损伤作用。     

水蛭提取液对凝血酶诱导血管内皮细胞释放血栓素B2和6-酮-前列腺素F1α的影响

目的探讨水蛭提取液对凝血酶诱导血管内皮细胞（VEC）释放血栓素B2（TXB2）和6-酮-前列腺素F1α（6-keto-PGF1α）的作用机制。方法体外培养人脐静脉内皮细胞（HUVEC）,将2～3代生长良好的细胞分为空白对照组、凝血酶刺激组和水蛭提取液低、中、高剂量组。将生药浓度分别为150、300、600 mg/L的水蛭提取液加入到10 kU/L凝血酶刺激的细胞中培养12 h,空白对照组加入等量RPMI 1640培养液。取上清液,采用酶联免疫吸附试验（ELISA）检测TXB2和6-keto-PGF1α的含量。结果与空白对照组比较,凝血酶刺激组TXB2含量（ng/L）明显升高（206.53±18.60比115.21±12.31,P＜0.01）,6-keto-PGF1α含量（ng/L）明显降低（21.31±1.12比30.54±1.11,P＜0.01）;与凝血酶刺激组比较,水蛭提取液各剂量组TXB2（ng/L）含量均明显降低,6-keto-PGF1α（ng/L）含量均明显升高,且以高剂量组变化更显著（TXB2：109.18±9.72比206.53±18.60;6-keto-PGF1α：58.67±3.24比21.31±1.12,均P＜0.01）。结论水蛭提取液能明显减弱凝血酶诱导HUVEC释放6-keto-PGF1α的抑制作用,并能对抗凝血酶诱导HUVEC释放TXB2,其作用机制可能与其调节血栓素/前列环素平衡有关。     

缺氧时ET-1、NO、TXA_2、PGI_2的变化及对心肌血流量的调节作用

目的本文旨在探讨ET-1、NO、TXA2和PGI2在缺氧时对心肌血流量的调节作用。方法大鼠随机分为平原组和急性缺氧组,用99mTc标记蟾蜍红细胞测定心肌血流量,用Gess法测量NO-、用放免法分别测量ET-1、TXA2、PGI2的含量。结果急性缺氧导致左、右心室心肌血流量、心肌NO2-、ET-1、血浆TXB2含量、TXB2/6-keto-PGF1ɑ比值明显增高(P0.05),左、右心室心肌血管阻力、ET-1/NO2-比值明显下降(P0.05),血浆6-keto-PGF1ɑ无明显变化。结论急性缺氧时,左、右心室心肌血流量增加,ET-1/NO、TXA2/PGI2参与了急性缺氧时心肌血流量的调节,以NO的扩血管作用为主。     

有氧运动对高血压大鼠血浆6-酮-前列腺素F1α、血栓素B2含量和PGI2／TXA2系统的影响

目的：探讨运动对自发性高血压大鼠（SHR）血浆6-酮-前列腺素F1α（6-keto-PGF1α）、血栓素B2（TXB2）含量和前列环素，血栓烷A2（PGI2／TXA2）系统的影响。方法：雄性SHR大鼠随机分为对照组和运动组。运动组大鼠进行60min/d无负重游泳运动，每周5d，实验共10周。实验期间，每2周测定大鼠血压，10周后，采用放射免疫非平衡法测定血浆TXB2和6-keto—PGF1α含量。结果：对照组大鼠血压较试验前显著性升高（P〈0．01），而运动组大鼠血压较试验前显著性下降。与对照组相比，运动组大鼠血压、TXB2含量显著下降（P〈0．01），血浆6-keto-PGF1α含量，6-keto—PGF1α／TAB，比值显著提高（P〈0．01）。结论：适宜的运动可以降低SHR大鼠血压水平，改善PG12／TXA2失衡，预防高血压及血栓形成。     

ω-3鱼油脂肪乳剂对急性肺损伤兔肺组织TXB2、6-keto-PGF1α表达的影响

【目的】探讨ω-3鱼油脂肪乳剂对内毒素脂多糖（LPS）致兔急性肺损伤（ALI）急性肺损伤兔肺组织中血栓素B2（TXB2）、6酮前列腺素F1α（6-keto-PGF1α）表达的影响。【方法】清洁级新西兰兔24只,随机分为对照组（A组）、LPS致伤组（B组）、ω-3鱼油脂肪乳剂预处理＋LPS致伤组（C组）,每组8只,记录0h、0．5h、1h、2h、4h时间点氧和指数（PaO2/FiO2）的改变,4h点处死动物,取肺组织测定TXB2和6-酮-前列腺素F1α（6-keto-PGF1α）含量、观察病理变化,并做病理评分。【结果】注射LPS0．5h、1h后B、C两组0．5h、1h兔肺组织TXB2、6-keto-PGF1α均较A组明显升高（P＜0．05）,B、C两组比较有统计学意义（P＜0．05）,注射LPS2h、4h后三组比较无统计学意义（P＞0．05）;B组TXB2/6-keto-PGF1α（T/P）明显高于A、C两组（P＜0．05）,A组与C组T/P均有增高趋势（0．75VS0．73）,但两组比较无显著差异（P＞0．05）;A组、C组肺损伤病理组织评分均低于B组（P＜0．05）。【结论】ω-3鱼油脂肪乳可明显减少LPS致ALI的肺组织TXB2含量,对6-keto-PGF1α最终合成无明显抑制,从而显著下调T/P,对内毒素致兔ALI具有一定保护作用。     

参附注射液对犬急性心肌缺血再灌注血浆NO、ET、6-keto-PGF1α、TXB2的影响

目的：探讨参附注射液（SF）预处理对犬急性心肌缺血再灌注血浆一氧化氮（N0）、内皮素（ET）、6-酮-前列腺素F1α（6-ke-to-PGF1α）、血栓素B2（TXB2）浓度的影响。方法：结扎犬冠状动脉左前降支建立急性心肌缺血再灌注模型。检测不同时间点4种血浆活性物质含量，并对心肌组织行电镜观察。结果：与空白对照组（生理盐水）相比，SF高剂量组（4ml／kg）血浆NO、ET和TXB2水平显著降低（P〈0．05），6-keto-PGF1α的水平显著升高（P〈0．05）；心肌组织病理学损伤程度明显减轻。结论：SF预处理能通过显著降低犬血浆NO、ET和TXB。水平，显著升高6-keto-PGF1α水平，从而对缺血再灌注心肌起到保护作用。     

急性胰腺炎胰腺一氧化氮合成酶和内皮素mRNA表达与肠道损伤的关系及丹参的影响

目的探讨重症急性胰腺炎（SAP）时胰腺组织的诱导型一氧化氮合成酶（iNOS）、内皮素（ET-1）mRNA表达状态,以及与血浆中NO、ET-1浓度和肠道损伤的关系及丹参治疗的影响。方法Wistar大鼠45只随机分为3组：SAP模型组（A组）,SAP丹参治疗组（B组）,假手术组（C组）,进行不同治疗和观察分析。结果A组血中淀粉酶（AML）、ET-1、NO、内毒素（LPS）含量、^125I-白蛋白累积指数及腹水量均显著高于C组（P〈0.01）;与A组比较,B组胰腺ET-1和iNOSmRNA表达较弱,血中AML、ET-1、NO、LPS及腹水量显著下降（P〈0.01）,125I-白蛋白累积指数较A组也有下降,但无差异（P〉0.05）。结论SAP时存在肠道损伤,胰腺组织ET-1、iNOSmRNA的过度表达,使血中ET-1、NO浓度升高,造成肠道屏障功能受损,肠通透性增加,引起内毒素血症。丹参注射液通过减轻SAP时胰腺的病理损害程度,下调胰腺ET-1和iNOSmRNA的表达,使血中ET-1、NO浓度下降,对SAP及其肠道损伤有一定治疗作用。     

针刺对大鼠颅脑损伤后血浆中血栓烷B2和6-酮-前列腺素F1α的影响

目的颅脑损伤后脑血液循环障碍是病情发展的主要病理生理基础之一,在继发性颅脑损伤中起着重要作用.观察针刺对大鼠颅脑损伤后血浆中血栓烷B2(thromboxane B2,XB2)、6-酮-前列腺素F1α(6-keto prostaglandin F1α,-keto-PGF1α)的影响.方法实验于2002-05/09在甘肃中医学院中心实验室、兰州医学院第一附属医院内分泌科完成.56只Wistar大鼠随机分为假手术组、模型组(24,72 h)、针刺治疗组(24,2h)、药物治疗组(24,2 h),每组8只.参照Feeney自由落体法致大鼠左侧颅脑损伤.按预定时间采集静脉血,将标本作相应处理,用放射免疫分析法测定血浆中TXB2,-keto-PGF1α的含量.结果①大鼠颅脑损伤后,血浆中TXB2的含量显著升高,且随着病情的发展上升更高,4,2 h分别为(3 420.71±1 153.16),3 701.21±1 133.67)ng/L;血浆中6-keto-PGF1α的含量下降,在72 h后缓慢恢复,4,2 h分别为(18.91±12.19),21.99±9.45)ng/L;TXB2/6-keto-PGF1α(T/K)值明显升高,在72 h缓慢恢复,4,2 h分别为(204.28±76.28),176.07±57.94).②24 h针刺组血浆中TXB2的含量下降,为(2 935.32±1 166.47)ng/L,6-keo-PGF1α的含量逐渐恢复,为(27.56±14.17)ng/L;T/K值升高,为108.04±41.71,与假手术组比较差异有显著性意义(P＜0.01),但低于模型组,与模型组比较差异有显著性意义(P＜0.01).③72 h针刺组血浆中TXB2的含量下降,为(1 409.48±675.55)ng/L,与模型组相比差异有显著性意义(P＜0.01),与假手术组比较差异已没有显著性意义(P＞0.05);6-keto-PGF1α的含量上升,为(39.30±22.65)ng/L;T/K值(42.66±25.47)ng/L,虽仍高于假手术组,但与假手组比较差异已没有显著性意义(P＞0.05).结论针刺可使颅脑损伤后血浆中升高的TXB2含量下降,降低的6-keto-PGF1α含量升高,可恢复T/K的失衡水平;针刺可改善血管的异常收缩状态,缓解痉挛,抑制血小板的异常聚集,保证脑的能量供应,促使损伤组织的修复,抑制继发性颅脑损伤.     

针刺对大鼠颅脑损伤后血浆中血栓烷B2和6-酮-前列腺素F1α的影响

目的：颅脑损伤后脑血液循环障碍是病情发展的主要病理生理基础之一，在继发性颅脑损伤中起着重要作用。观察针刺对大鼠颅脑损伤后血浆中血栓烷B2(thromboxane B2，TXB2)、6-酮-前列腺素F1α(6-keto prostaglandin F1α，6-keto-PGF1α)的影响。方法：实验于2002-05／09在甘肃中医学院中心实验室、兰州医学院第一附属医院内分泌科完成。56只Wistar大鼠随机分为假手术组、模型组(24，72h)、针刺治疗组(24，72h)、药物治疗组(24，72h)，每组8只。参照Feeney自由落体法致大鼠左侧颅脑损伤。按预定时间采集静脉血，将标本作相应处理，用放射免疫分析法测定血浆中TXB2，6-keto-PGF1α的含量。结果：①大鼠颅脑损伤后，血浆中TXB2的含量显著升高，且随着病情的发展上升更高，24，72h分别为(3420．71&;#177;1153．16)，(3701．21&;#177;1133．67)ng／L；血浆中6-keto-PGF1α的含量下降，在72h后缓慢恢复，24，72h分别为(18．91&;#177;12．19)，(21．99&;#177;9．45)ng／L；TXB2／6-keto-PGF1α(T／K)值明显升高，在72h缓慢恢复，24，72h分别为(204．28&;#177;76．28)．(176．07&;#177;57．94)。②24h针刺组血浆中TXB2的含量下降，为(2935．32&;#177;1166．47)ng／L，6-keto-PGF1α的含量逐渐恢复，为(27．56&;#177;14．17)ng／L；T／K值升高，为108．04&;#177;41．71，与假手术组比较差异有显著性意义(P&;lt;0．01)，但低于模型组，与模型组比较差异有显著性意义(P&;lt;0．01)。③72h针刺组血浆中TXB2的含量下降，为(1409．48&;#177;675．55)ng／L与模型组相比差异有显著性意义(P&;lt;0．01)，与假手术组比较差异已没有显著性意义(P&;gt;0．05)；6-keto-PGF1α的含量上升，为(39．30&;#177;22．65)ng／L；T／K值(42．66&;#177;25．47)ng／L，虽仍高于假手术组，但与假手组比较差异已没有显著性意义(P&;gt;0．05)。结论：针刺可使颅脑损伤后血浆中升高的TXB2含量下降，降低的6-keto-PGF1α含量升高，可恢复T／K的失衡水平；针刺可改善血管的异常收缩状态，缓解痉挛，抑制血小板的异常聚集，保证脑的能量供应，促使损伤组织的修复，抑制继发性颅脑损伤。     

芪蛭降糖胶囊治疗糖尿病肾病Ⅲ期的临床研究

目的观察芪蛭降糖胶囊治疗糖尿病肾病（DN）Ⅲ期的临床疗效,并探讨其作用机制。方法将符合DN Ⅲ期诊断标准的患者按照随机数字表法分为试验组和对照组。两组患者先给予2周的洗脱期治疗,然后给予西医基础治疗;同时对照组给予缬沙坦80 mg、每日1次,试验组给予芪蛭降糖胶囊每次2.5 g、每日3次。于治疗前和治疗后4、8、12周观察尿微量白蛋白（mALB）、mALB/肌酐（UCr）、β2-微球蛋白（β2-MG）、α1-微球蛋白（α1-MG）,同时测定血中内皮素-1（ET-1）、一氧化氮（NO）、血栓素B2（TXB2）、6-酮-前列腺素F1α（6-keto-PGF1α）、血肌酐（SCr）、尿素氮（BUN）、血清胱抑素-C（Cys-C）、视黄醇结合蛋白（RBP）、β2-MG 水平变化。结果最终纳入有效病例试验组96例、对照组95例。两组治疗前尿mALB、mALB/UCr、β2-MG、α1-MG 及血ET-1、NO、TXB2、6-keto-PGF1α比较差异均无统计学意义（均P＞0.05）;随治疗时间延长,两组治疗后mALB、mALB/UCr、β2-MG、α1-MG 及ET-1、TXB2均降低,NO、6-keto-PGF1α均升高,且以试验组变化更显著,治疗12周时两组mALB、mALB/UCr、β2-MG、α1-MG 及TXB2、6-keto-PGF1α比较差异均有统计学意义〔 mALB（mg/L）：36.6±9.2比78.6±16.5,mALB/UCr（mg/mmol）：3.90±1.97比9.70±2.90,β2-MG （mg/L）：0.25±0.10比0.40±0.12,α1-MG（mg/L）：8.40±2.26比12.50±3.21,TXB2（ng/L）：75.8±18.7比 94.7±21.7,6-keto-PGF1α（ng/L）：73.4±15.2比65.2±11.5,P＜0.05或P＜0.01〕,而ET-1、NO 比较差异均无统计学意义〔 ET-1（ng/L）：57.6±6.9比59.1±6.2,NO（μmol/L）：68.9±11.6比65.4±10.7,均P＞0.05〕。两组 SCr、BUN 治疗后各时间点与治疗前比较,两组间相同时间点比较差异均无统计学意义（均P＞0.05）;对照组治疗后Cys-C、RBP、β2-MG 均较治疗前有降低趋势,但差异均无统计学意义（均P＞0.05）;试验组治疗后12周 Cys-C、RBP、β2-MG 均明显低于治疗前〔 Cys-C（mg/L）：0.72±0.07比0.89±0.12,RBP（mg/L）：53.0±14.2比66.1±16.5,β2-MG（mg/L）：1.86±0.71比2.79±0.82,均P＜0.05〕。结论芪蛭降糖胶囊能明显降低DN Ⅲ期患者的尿mALB 及mALB/UCr,稳定肾功能,疗效优于缬沙坦,其作用机制与降低ET-1、升高NO,维持血栓素A2/前列环素（TXA2/PGI2）动态平衡、保护血管内皮细胞有关。     

The behaviour of prostanoids during the course of acute experimental pancreatitis in rats

The behavior of two vasoactive prostanoids was studied in experimental acute pancreatitis (AP) in rats. The stable metabolites of prostacyclin (PGI2) and thromboxane A2 (TXA2), 6-keto-PGF1 alpha and TXB2, respectively, were measured during the course of experimental AP. Blood samples were taken at 3, 6, and 8 h after the induction of AP. In AP both plasma 6-keto-PGF1 alpha plasma TXB2 and serum TXB2 increased up to 6 h simultaneously (6-keto-PGF1 alpha from 271.1 +/- 77.2 pg/ml (mean +/- SD) to 459.4 +/- 192.6 pg/ml, plasma TXB2 from 752 +/- 350 pg/ml to 3640 +/- 2160 pg/ml and serum TXB2 from 22.3 +/- 14.8 micrograms/ml to 140.8 +/- 52.8 micrograms/ml). After 6 h 6-keto-PGF1 alpha remained elevated, whereas serum TXB2 dropped significantly. We suggest that in AP the balance of PGI2 and TXA2 is initially maintained, but later on an imbalance appears to favor vasodilatory PGI2. These agents may contribute to the regulation of the blood flow in the pancreas and thus play a role in the pathophysiology of AP.     

The effect of parenteral feeding on the metabolism of arachidonic acid in patients with cancer of the esophagus and the stomach

Blood plasma and erythrocyte level of arachidonic acid (C20:4) and blood plasma level of its two metabolites (6-keto-PGF1 alpha and TXB2) have been investigated in 24 patients with esophageal and gastric cancer. In the preoperative period and during 8-10 days postoperatively 12 patients were on "glucose" energy supply (group I) and 12 patients were on "lipid" energy supply (group II). Daily calorie intake was 30-35 kcal/kg. In the preoperative period Lipofundin-S infusions produced a significant increase in C20:4 blood plasma and erythrocyte levels. An increase in TXB2 concentration was accompanied by a certain increase in 6-keto-PGF1 alpha content. At the same time in group I parenteral feeding caused no significant changes in the above parameters. Surgical trauma and anesthesia caused a considerable increase in 6-keto-PGF1 alpha blood plasma level in both groups (P less than 0.05), with a certain decrease in TXB2 level (P greater than 0.05). In the postoperative period, unlike "glucose", "lipid" energy supply stabilized C20:4 content in the erythrocyte membrane and favourably affected 6-keto-PGF1 alpha/TXB2 ratio. This is confirmed by a considerable increase in 6-keto-PGF1 alpha/TXB2 ratio, which in the course of the postoperative period was significantly higher in group II than in group I.     

Heparin-enhanced plasma phospholipase A2 activity and prostacyclin synthesis in patients undergoing cardiac surgery.

Although eicosanoid production contributes to physiological and pathophysiological consequences of cardiopulmonary bypass (CPB), the mechanisms accounting for the enhanced eicosanoid production have not been defined. Plasma phospholipase A2 (PLA2) activity, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and thromboxane B2 (TXB2) levels were measured at various times during cardiac surgery. Plasma PLA2 activity increased after systemic heparinization, before CPB. This was highly correlated with concurrent increases in plasma 6-keto-PGF1 alpha, TXB2 concentrations did not increase with heparin administration but did increase significantly after initiation of CPB. High plasma PLA2 activity, 6-keto-PGF1 alpha, and TXB2 concentrations were measured throughout the CPB period. Protamine, administered to neutralize the heparin, caused an acute reduction of both plasma PLA2 activity and plasma 6-keto-PGF1 alpha, but no change in plasma TXB2 concentrations. Thus the ratio of TXB2 to 6-keto-PGF1 alpha increased significantly after protamine administration. Enhanced plasma PLA2 activity was also measured in patients with lower doses of heparin used clinically for nonsurgical applications. Human plasma PLA2 was identified as group II PLA2 by its sensitivity to deoxycholate and dithiothreitol, its substrate specificity, and its elution characteristics on heparin affinity chromatography. Heparin addition to PMNs in vitro resulted in dose-dependent increases in cellular PLA2 activity and release of PLA2. The PLA2 released from the PMN had characteristics similar to those of post-heparin plasma PLA2. In conclusion, plasma PLA2 activity and 6-keto-PGF1 alpha concentrations are markedly enhanced with systemic heparinization. Part of the anticoagulant and vasodilating effects of heparin may be due to increased plasma prostacyclin (PGI2) levels. In addition the pulmonary vasoconstriction sometimes associated with protamine infusion during cardiac surgery might be due to decreased plasma PLA2 activity, with an associated increased TXB2/6-keto-PGF1 alpha ratio.     

急腹症并发多器官功能障碍综合征细胞因子及炎症介质与肽类激素的变化

目的：探讨细胞因子及其他炎症介质与肽类激素在急腹症所致多器官功能障碍综合征（MODS）中的作用。方法：动态观察19例MODS患者血浆肿瘤坏死因子-α（TNF-α），白介素-6（IL-6），血栓素B2（TXB2），6-酮-前列腺素F1α（6-keto-PGF1α），内毒素，内皮素-1（ET-1），降钙素基因相关肽（CGRP），P物质（SP）及血清脂质过氧化物（LPO）和一氧化氮9NO）水平。结果；MODS患者的TNF-α主IL-6均显著增高；入院当天未治疗者IL-6高于经布什镜逆行胆管引流（ERBD）或激素等处理者，重症胆管炎高于重症胰腺炎，并发中毒性休克者高达24000ng/L。早期MODS患者的TNF-α和IL-6均显著高于全身炎症反应综合征（SIRS）者；MODS者的内毒素及LPO均显著程式高；MODS急症住院者NO升高，某些重症胰腺炎，肝癌及高龄肝脓肿长期发热者NO降低；TXB2和6-keto-PGF1α先升后降；ET-1和CGRP早期明显增高；SP于入院当天达峰值。结论；急腹症患者IKL-6持续高于300ng/L，提示MODS时IL-6和TNF-α可区别全身炎症反应程度；NO存在升高和降低两种情况；ET-1，CGRP，TXB2，6-keto-PGF1α，内毒素和LPO增高并促进MODS的形成与发展。     

The prostacyclin-thromboxane system and platelet hemostasis following aortocoronary bypass with an uncomplicated postoperative course]

Prostacyclin-thromboxane system and platelet hemostasis have been studied in 56 patients upon aortocoronary bypass surgery with uncomplicated early postoperative period. It has been established that cardiopulmonary bypass surgery leads to a considerable increase in 6-keto-PGF1 alpha and TXB2 levels per platelet, as compared to preoperative values. By hour 18 postoperatively 6-keto-PGF1 alpha to platelet number ratio returns to baseline, while TXB2 to platelet number ratio remains higher than preoperative values, which determines a shift in 6-keto-PGF1 alpha to TXB2 ratio towards TXB2, thus ensuring, probably, enhanced platelet aggregation properties. Thrombocytopenia, a decrease in platelet aggregation properties and elevated blood plasma level of beta-thromboglobulin were observed upon aortocoronary bypass surgery. By hour 18 postoperatively the number of platelets increased significantly, their aggregation properties were enhanced, beta-thromboglobulin blood plasma level was reduced, however, the parameters under study did not reach normal values at that time. Increased levels of 6-keto-PGF1 alpha and TXB2 per platelet in the early postoperative period are considered an important component of compensatory-adaptive body reactions directed to normalization of the damaged body functions, namely hemostasis and microcirculation.     

Functional significance of renal prostacyclin and thromboxane A2 production in patients with systemic lupus erythematosus.

We have examined the urinary excretion of stable immunoreactive eicosanoids in 23 female patients with systemic lupus erythematosus (SLE), 16 patients with chronic glomerular disease (CGD), and 20 healthy women. SLE patients had significantly higher urinary thromboxane B2 (TXB2) and prostaglandin (PG) E2 excretion and significantly lower 6-keto-PGF1 alpha than did healthy women. In contrast, CGD patients only differed from controls for having reduced 6-keto-PGF1 alpha excretion. The group of SLE patients with active renal lesions differed significantly from the group with inactive lesions for having a lower creatinine clearance and urinary 6-keto-PGF1 alpha and higher urinary TXB2. Higher urinary TXB2 excretion was associated with comparable platelet TXB2 production in whole blood, undetectable TXB2 in peripheral venous blood, and unchanged urinary excretion of 2,3-dinor-TXB2. A significant inverse correlation was found between urinary TXB2 and creatinine clearance rate (CCr). In contrast, the urinary excretion of 6-keto-PGF1 alpha showed a significant linear correlation with both CCr and para-aminohippurate clearance rate (CPAH). In four SLE and seven CGD patients, inhibition of renal cyclooxygenase activity by ibuprofen was associated with a significant reduction in urinary 6-keto-PGF1 alpha and TXB2 and in both CCr and CPAH. However, the average decrease in both clearances was 50% lower in SLE patients than in CGD patients, when fractionated by the reduction in urinary 6-keto-PGF1 alpha or PGE2 excretion. We conclude that the intrarenal synthesis of PGI2 and TXA2 is specifically altered in SLE. Such biochemical alterations are associated with changes in glomerular hemodynamics and may play a role in the progression of SLE nephropathy.     

急性脑血管病患者血浆血栓素B2和6-酮-前列环素的动态分析

目的动态测定急性脑血管病患者血浆中的血栓素B2(TXB2)、6-酮-前列环素(6-keto-PGF1α)及TXB2/6-keto-PGF1α(T/6-K)比值,为临床积极干预提供参考依据。方法急性脑血管病患者300例,分为3组:CI组205例、TIA组70例、CH组25例,正常对照组120例。ELISA双抗体夹心法测定TXB2,ELISA竞争抑制法测定6-keto-PGF1α。测定急性脑血管病患者发病24h内、1周时、2周时的血浆TXB2、6-酮-前列环素1α及TXB2/6-K比值,同时将其动态值变化与正常对照组进行统计分析。结果 3组患者发病24h内、1周时、2周时的血浆TXB2、6-keto-PGF1α的含量均高于正常对照组(P<0.01),TXB2到一周时最高,到二周时下降,6-keto-PGF1α逐渐增高,到2周时最高。3组患者TXB2/6-K在发病24h内、1周时均高于正常对照组(P<0.01),1周时最高,CI组,TIA组到2周时下降基本和正常对照组相似(P>0.05),CH组下降比正常对照组低(P<0.01)。结论维持TXB2/6-keto-PGF1α的平衡有助于血流通畅,TXB2、6-keto-PGF1α水平可反映急性脑血管患者血小板活化功能状态和血管内皮细胞损伤情况。临床常规测定有助于急性脑血管病事件的综合评估。对于TIA患者患者进一步发展为脑梗死有重要的警示价值。     

The effect of ageing on human platelet sensitivity to serotonin

Twelve healthy young volunteers (mean age 21, range 18-27 years) and 12 elderly people (mean age 77, range 72-86 years) were tested regarding platelet aggregation induced by adrenaline, ADP and serotonin. The serum levels of thromboxane B2 (TXB2) and serum 6-keto-PGF1 alpha and the plasma level of adrenaline and cyclic AMP (cAMP) were also measured. Platelet aggregation induced by adrenaline and ADP increased significantly in the elderly compared with the young group (P less than 0.05 and P less than 0.02, respectively). There was a substantial and highly significant increase in the response of platelets from elderly people to serotonin (P less than 0.01). No alteration was observed in the serum level of TXB2 or 6-keto-PGF1 alpha. Plasma adrenaline increased in the old group, but plasma cAMP was unaffected. As serotonin is known to amplify adrenaline- and ADR-induced platelet aggregation, the considerable increase in platelet sensitivity to serotonin could be an important factor in the increased adrenaline and ADP-induced platelet aggregability of elderly people.     

Plasma renin activity, angiotensin II, prostacyclin and thromboxane A2 concentrations in 139 preeclamptic patients

Plasma renin activity, plasma concentrations of angiotensin II (AngII), stable metabolites (6-keto-prostaglandin F1 alpha: 6-keto-PGF1 alpha) of prostacyclin (PGI2) and a metabolite (thromboxane B2: TXB2) of thromboxane A2 (TXA2) were measured with radioimmunoassay(RIA) in 107 normal pregnancy (control) and 139 preeclamptic patients in 28-41 gestational weeks. PRA and 6-keto-PGF1 alpha were significantly higher and AngII was slightly higher in preeclampsia than in control, and TXB2 was significantly lower in preeclampsia in control. The ratio of 6-keto-PGF1 alpha/TXB2 was significantly lower in preeclampsia than in control. These data suggest that the changes in the renin-angiotensin system may not be primary alterations in preeclampsia. It can be speculated that in preeclampsia the changes in absolute concentrations of 6-keto-PGF1 alpha and TXB2 are less important than the decrease in the ratio of the 6-keto-PGF1 alpha/TXB2.