毛冬青甲素调节花生四烯酸代谢的机理探讨

毛冬青甲素(ilexonin A)是从冬青科植物毛冬青中分离出的一种有效成分,分子式为C_(34)H_(48)O_6Na,临床上初步试用于治疗脑血栓、心肌梗塞等心血管疾病。药理实验表明,毛冬青甲素在体外有抗血栓形成,抑制血小板粘附、聚集和释放功能及抑制TXA_2样物质的生成。最近研究结果表明,其抑制血小     

参附注射液对肝缺血再灌注大鼠血浆前列环素和血栓素A2及肝组织ATP酶的影响

目的:探讨参附注射液对大鼠肝缺血再灌注损伤的保护作用及其机制。方法:24只Wistar大鼠随机分为模型组和参附注射液(Shenfu Injection,SF)治疗组。SF治疗组大鼠腹腔注射参附注射液10ml/kg。模型组大鼠给予相同剂量的生理盐水。两组均采用Pringle's法阻断肝门缺血15min再灌注1h和3h,测定血浆血栓素B2(thromboxane B2,TXB2)和6-酮-前列腺素F1α(6-keto-prosta-glandin F1α,6-keto-PGF1α)以及肝组织匀浆Na -K -ATP酶、Ca2 -Mg2 -ATP酶的变化,并观察肝组织形态学改变。结果:再灌注3h SF治疗组血浆TXB2低于模型组,6-keto-PGF1α高于模型组,两者比值TXB2/6-keto-PGF1α低于模型组;再灌注1h、3h SF治疗组Na -K -ATP酶和Ca2 -Mg2 -ATP酶活性高于模型组。SF治疗组肝实质细胞和线粒体损伤明显减轻。结论:参附注射液对肝缺血再灌注损伤有保护作用,其机制与降低TXA2/PGI2比值,提高Na -K -ATP酶和Ca2 -Mg2 -ATP酶活性有关。     

Effects of nitric oxide inhibitor on prostacyclin biosynthesis in portal hypertensive rats

ＯｂｊｅｃｔｉｖｅＴｏｅｖａｌｕａｔｅｔｈｅｅｆｅｃｔｓｏｆｎｉｔｒｉｃｏｘｉｄｅｉｎｈｉｂｉｔｏｒｏｎｐｒｏｓｔａｃｙｃｌｉｎ（ＰＧＩ２）ｂｉｏｓｙｎｔｈｅｓｉｓａｎｄｔｈｅｒｏｌｅｏｆＰＧＩ２ｉｎｈｙｐｅｒｈｅｍｏｄｙｎａｍｉｃｓｏｆｐｏｒｔａｌ...     

Clinical Implication of the Changes of cAMP, TXA_2 and PGI_2 in CSF of Asphyxiated Newborns

Summary:To evaluate the changes of 3',5'-cyclic adenosine monophosphate(cAMP),thromboxane A_2(TXA_2)and prostacyclin(PGI_2)in cerebrospinal fluid(CSF)in the asphyxiated newborn andexplore their roles in hypoxic-ischamic brain damage(HIBD).Thirty-six full term newborns were di-vided into 3 groups,including 12 with moderate-severe hypoxic-ischaemic encephalopathy(HIE),13with mild HIE,11 without HIE(control group).The levels of cAMP,TXB_2(TXA_2 metabolite)and6-keto-PGF_(1α)(PGI_2 metabolite)in CSF and plasma were measured 36—72h after birth by RIA.andthe concentrations were expressed as nM/L(cAMP),ng/L(TXB_2 and 6-keto-PGF_(1α)).The infantswere followed-up at 6 and 12 month of age and Mental Development Index(MDI)and PsychomotorDevelopment Index(PDI)were measured using Bayley Scales of Infant Development(BSID).TheCSF cAMP level in moderate-severe HIE group was 8.60±2.40,significantly lower than that of themild HIE group(14.83±2.84)and the control group(24.43±2.39)(for both P<0.01).The lev-els of TXB_     

Prostacyclin and thromboxane A2 in thrombotic thrombocytopenic purpura

A study was conducted to find whether a deficiency in prostacyclin (prostaglandin I2; PGI2) is implicated in the pathogenesis of thrombotic thrombocytopenic purpura. Plasma samples from two patients with the disease before treatment and from 22 healthy controls were therefore assayed for concentrations of 6-oxo-PGF1 alpha and thromboxane B2, the stable metabolites of PGI2 and thromboxane A2, respectively. Neither of the patients responded to treatment, which in one case included an infusion of PGI2. Both patients had normal concentrations of 6-oxo-PGF1 alpha and thromboxane B2, thus implying that circulating amounts of PGI2 and thromboxane A2 were also normal. These findings suggest that 6-oxo-PGF1 alpha may be detectable in normal amounts in thrombotic thrombocytopenic purpura and that the condition need not be associated with a high concentration of thromboxane A2.     

A study on the optimal dose of aspirin therapy in Kawasaki disease--clinical evaluation and arachidonic acid metabolism

Aspirin is the basic treatment for Kawasaki disease, however its optimal dose is controversial. We investigated the therapeutic efficacy of high-dose (100 mg/kg/day, n = 30) versus low-dose (30 mg/kg/day, n = 30) aspirin. Duration of fever, transaminase, plasma thromboxane B2 (TxB2) and 6-keto-prostaglandin F1 alpha (PGF1 alpha) levels were compared before enrollment and on days 4, 7 and 14. In the high-dose group, duration of fever was significantly shorter than that of low-dose group (3.2 +/- 1.8 versus 5.4 +/- 4.3 days, p less than 0.05), however, serum glutamic pyruvic transaminase levels were elevated (157.4 +/- 187.7 versus 48.0 +/- 58.2I.U./liter, p less than 0.005). No differences in the incidence of coronary artery lesions were observed (5 of 30 versus 7 of 30). Plasma TxB2 production was completely blocked in both groups, plasma 6-keto-PGF1 alpha levels in the high-dose group on day 14 was lower than that in the low-dose group (39 +/- 26 versus 160 +/- 207 pg/ml, p less than 0.05). This latter observation suggest that high-dose therapy may be disadvantageous as anti-thrombotic treatment, and supports the notion that low dose therapy is safe in the acute stage of Kawasaki disease.     

肝炎后肝硬化患者尿血栓素B_2和6-酮-前列腺素F_(1α)与肾功能的关系

用放射免疫法测定了45例肝炎后肝硬化患者尿血栓素B_2和6-酮-前列腺素F_(1α)的排泄率。结果,肝硬化患者尿血栓素B_2排泄率较正常对照明显升高;肝硬化无并肾衰者尿6-酮-PGF_(1α)较对照组升高;但并有肾衰者尿6-酮-前列腺素F_(1α)排泄率比无并肾衰者则显著降低(P<0.01),尿TXB_2/6-酮-PGF_(1α)比值明显上升(P<0.001)。肝硬化患者尿6-酮-PGF_(1α)与血肌酐呈负相关关系,与肌酐清除率呈正相关关系。提示肾脏前列环素对维持肝硬化病人的肾功能是很重要的;肾脏TXA_2和PGI_2的平衡失调在肝肾综合征发病中可能具有重要意义。     

Anti-angina effect of puerarin and its effect on plasma thromboxane A2 and prostacyclin

Plasma concentrations of thromboxane B2 (TXB2) and 6-keto-prostaglandin Fl alpha(6-K-PGFl alpha), the stable nonenzymatic metabolites of TXA2 and prostacyclin were assayed in 30 patients suffering from angina pectoris before and after administration of puerarin. In addition, serum lipids and HDL were also measured at the same time. 20 healthy subjects were chosen as the control group. Two weeks before and during administration of puerarin, aspirin, calcium-antagonists, all kinds of hypotensors and drugs relieving chest pain of angina pectoris were strictly prohibited. Puerarin was intravenously given, 500 mg daily for 7 days, which was considered as a therapeutic course. Besides relieving of chest pain, decreasing of heart rate and reduction of blood pressure clinically, it was also found that plasma 6-K-PGFl alpha concentrations were significantly elevated from 38.32 +/- 15.40 to 158. 79 +/- 98.62 pg (P less than 0.01) after administration of puerarin, but there was no significantly difference between plasma TXB2 concentrations before and after administering the drug. In addition, serum HDL was apparently enhanced as compared with that before the administration of puerarin (P less than 0.01). The results indicated that puerarin has the function of anti-angina, reducing both systolic and diastolic blood pressure and diminishing myocardial oxygen consumption.     

室间隔缺损合并重度肺动脉高压患者围术期肺损伤的临床研究

目的　探讨室间隔缺损合并重度肺动脉高压患者围术期肺损伤的发生机制。方法　对31例先心病室间隔缺损直视修补术患者分组 (非肺动脉高压 16例 ,重度肺动脉高压 15例 )进行临床研究 ,在麻醉后 (AA) ,体外循环停止 (OEC) ,体外循环后 1h(PEC1)、6h(PEC6 )、2 4h(PEC2 4 )、4 8h(PEC4 8)、72h(PEC72 )对血栓素B2 (TXB2 )和 6 酮 前列腺素F1α(6 keto PGF1α)、丙二醛 (MDA)、IL 6、IL 8的变化进行研究 ,并结合体外循环前、后肺病理改变对肺损伤程度进行分析。结果　重度肺高压组 6 keto PGF1α与TXB2 的比值 (P/T)在OEC时下降至最低 ,于PECl时丙二醛 (MDA) (7 3μmol/L± 0 9μmol/L)和IL 6 (0 5 0ng/L± 0 19ng/L)达到最高峰 ,在PEC6时IL 8(183ng/L± 6 3ng/L)明显增高。肺动脉压在PECl～PEC6时变化最大。TXB2 与全肺阻力呈正相关性 (γ =0 2 83,P <0 0 5 ) ,呼吸指数(RI)与全肺阻力呈正相关性 (γ =0 4 0 3,P <0 0 5 ) ,RI与MDA呈正相关性 (γ =0 .5 90 8,P <0 0 5 )。体外循环后肺病理改变有明显的血管内皮细胞脱落、炎症细胞浸润、肺血管的白细胞栓塞和肺泡上皮细胞的脱落及肺泡内出血。结论　室间隔缺损合并重度肺动脉高压患者体液因素变化及肺病理改变是引起围术期严重肺损伤的机制之一     

Mechanism of overproduction of plasma prostacyclin in portal hypertensive rats

OBJECTIVE: To evaluate the role of increased portal pressure and portosystemic shunting in elevated level of prostacyclin (PGI2) in portal hypertension. METHODS: Thirty-six male Sprague-Dawley rats were divided into four groups: prehepatic portal hypertension (PHPH, 8 rats), intrahepatic portal hypertension (IHPH, 9), end-to-side portacaval shunt (PCS, 8), and sham-operated controls (SO, 11). Two weeks after surgery, free portal pressure (FPP) was measured; systemic and splanchnic hemodynamics was studied by radioactive microsphere technique and blood sample from the femoral artery was obtained to measure the level of plasma 6-keto-PGF1 alpha with radioimmunoassay. RESULTS: The FPP (mmHg) in IHPH, PHPH, PCS and SO rats was 13.10 +/- 1.02, 12.10 +/- 1.52, 3.0 +/- 0.82 and 6.86 +/- 0.69, respectively. The value of FPP was significantly increased in IHPH, PHPH rats and significantly decreased in PCS rats when compared to SO rats. Cardiac index (CI) and portal venous inflow (PVI) were in the order of PCS > PHPH > IHPH > SO rats. Portosystemic shunting (PSS) in PCS, PHPH, IHPH was 99.7 +/- 0.29%, 76.02 +/- 20.62% and 30.34 +/- 10.18%, respectively. The concentrations of plasma 6-keto-PGF1 alpha (ng/ml) in PHPH, IHPH, PCS and SO rats were 6.93 +/- 2.43, 5.09 +/- 2.27, 2.36 +/- 1.01 and 1.56 +/- 0.61, respectively. The concentrations of plasma PGI2 in PHPH, IHPH and PCS rats were significantly higher than those in SO rats. Furthermore, the concentrations of plasma PGI2 in PHPH and IHPH rats were also significantly higher than those in PCS rats. Moreover, a closed positive correlation existed between plasma PGI2 and FPP (r = 0.67, P < 0.001). CONCLUSIONS: The results of the present study suggest that the elevated PGI2 in portal hypertension is mainly due to the overproduction of PGI2 in vascular epithelium cells induced by increased portal pressure, whereas portosystemic shunting and liver dysfunction play a secondary role. In addition, the results of this study do not support that PGI2 mediated the hyperhemodynamics in portal hypertension.     

Effects of Medicinal Cake-Separated Moxibustion on Plasma 6-Keto-PGF1α and TXB2 Contents in the Rabbit of Hyperlipemia

Hyperlipemia rabbit models established with high cholesterol and fat diet were treated vith directmoxibustion and medicinal cake-separated moxibustion. The post-treatment plasma 6-keto-prostaglandin F_(1α)(6-keto-PGF_(1α)) and thromboxane B2 (TXB_2) contents were determined by radioimmunoassay. Resultsindicated that the plasma 6-keto-PGF_(1α) content significantly increased,the TXB_2 level decreased (P<0.05)and the TXB_2 /6-keto-PGF_(1α) ratio also decreased (P<0.01) in the medicinal cake-separated moxibustiongroup as compared with those in the model group respectively,but there was no significant differencebetween the medicinal cake-separated moxibustion group and the direct moxibustion group (P>0.05),suggesting that both the medicinal cake-separated moxibustion and direct moxibustion can regulate theplasma 6-keto-PGF_(1α) and TXB_2 contents,and the TXB_2/6-keto-PGF_(1α) ratio with similar actions,and have acertain protective action on endothelial cells of the aorta in the rabbit of hyperlipemia     

鼻咽癌患者前列环素及血栓素与外周血细胞免疫状况

应用间接免疫荧光法和放射免疫法分别检测了 34例鼻咽癌患者外周血中淋巴细胞的数量和血浆前列环素(PGI2 )及血栓素 (TXA2 )的含量 ,并与正常对照组对比研究。结果显示 :鼻咽癌患者外周血中 CD4细胞减少 (P<0 .0 1) ,而 CD8细胞则明显升高 (P<0 .0 5 )。同时鼻咽癌患者血浆中 PGI2 和 TXA2 的稳定代谢产物 6 - keto- PGF1α及 TXB2分别比对照组升高 ,以 TXB2 升高更明显 (P<0 .0 5 )。提示鼻咽癌患者体内前列腺素类物质 PGI2 和 TXA2 与鼻咽癌患者机体细胞免疫功能有关 ,并对其作为一种可能性抑制因素在鼻咽癌细胞免疫中的作用进行了讨论     

环孢素A肾中毒时大鼠尿中前列腺素的变化

该实验探讨了环孢素Ａ（ＣｓＡ）肾中毒与肾脏血栓素Ａ２（ＴＸＡ＿２）、前列环素（ＰＧＩ＿２）的关系。实验中将ＳＤ雄性大鼠２０只随机分为二组，Ｉ组为正常对照组；Ⅱ组为ＣｓＡ中毒组。于实验前后分别检测大鼠的肾功能、尿酶以及尿中血栓素Ｂ＿２（ＴＸＢ＿２）、６－酮－前列腺素Ｆ１ａ（６－ｋｅｔｏ－ｐＧＦ１ａ）等指标，最后进行肾脏光镜检查。结果发现，ＣｓＡ中毒组大鼠尿中的ＴＸＢ＿２显著升高，而尿中６－ｋｅｔｏ－ｐＧＦ１ａ稍低于正常对照组，ＴＸＢ＿２／６－ｋｅｔｏ－ｐＧＦ１ａ比值明显升高。实验证实，中毒剂量的ＣｓＡ引起肾脏ＴＸＡ＿２／ＰＧＩ＿２平衡常数明显升高。     

Clinical Observation on Treatment of Pediatric Intractable Nephropathy with Modified Taohong Siwu Decoction(桃红四物汤)

Ｐｅｄｉａｔｒｉｃｉｎｔｒａｃｔａｂｌｅｎｅｐｈｒｏｐａｔｈｙ（ＰＩＮ）ｉｓａｋｉｎｄｏｆｃｏｍｐｌｅｘｉｍｍｕｎｅｒｅａｃｔｉｖｅｄｉｓｅａｓｅｓｏｆｋｉｄｎｅｙ,ｔｈｅｍａｉｎｔｈｅｒａｐｙｉｎｍｏｄｅｒｎｍｅｄｉ ｃｉｎｅｉｓｔｈｅｃｏｍｂｉｎｅｄａｄｍｉｎｉｓｔｒａｔｉｏｎｏｆａｄｒｅｎａｌｃｏｒｔｅｘｈｏｒｍｏｎｅａｎｄｉｍｍｕｎｏｓｕｐｐｒｅｓｓｏｒ．Ｉｔｉｓｄｉｆｆｉｃｕｌｔｔｏｂｅｔｒｅａｔｅｄｂｅｃａｕｓｅｏｆｉｔｓｒｅｓｉｓｔａｎｃｅｔｏａｎｄｄｅｐｅｎｄｅｎｃｅｏｎｈｏｒｍ…     

Effects of Ligusticum wallichii on the plasma levels of beta-thromboglobulin, platelet factor 4, thromboxane B2 and 6-keto-PGF1 alpha in rabbits under acute experimental cerebral ischemia

By occluding the bilateral carotid arteries of rabbits to produce bilateral partial cerebral ischemia, and by using RIA and ELISA to measure the levels of Beta-thromboglobulin (beta-TG), platelet factor 4 (PF4), thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in plasma, the authors found that the levels of beta-TG, PF4 and TXB2 in plasma had significantly increased (P less than 0.01), but the level of 6-keto-PGF1 alpha in plasma showed no change (P greater than 0.05) after cerebral ischemia appeared. The results of the Ligusticum wallichii (Ligusticum) pre-treatment to the test-group showed that the levels of beta-TG, PF4 and TXB2 in plasma had significantly decreased (P less than 0.01), and the level of 6-keto-PGF1 alpha in plasma had significantly increased (P less than 0.05). This suggested that the Ligusticum treatment could effectively inhibit the platelet activation in vivo and correct the TXA2-PGI2 imbalance in blood after cerebral ischemia. In this study, some new approaches were explored to explain the mechanisms of Ligusticum for preventing and treating cerebral ischemia.     

Effects of nifedipine and Paeonia lactiflora on plasma TXB2 and 6-Keto-PGF1 alpha in cholesterol-fed rabbits

The authors examined the influences of nifedipine and Paeonia lactiflora (PL) on plasma LPO, TXB2 and 6-keto-PGF1 alpha in cholesterol-fed rabbits. In this study, oral administration of nifedipine (15 mg/kg per day) and PL (0.5 g/kg per day) with 2% cholesterol diet for 15 weeks caused 60.75% and 74.24% reduction in the lesion area of aorta respectively. The levels of plasma LPO, TXB2, cholesterol, phospholipid and calcium of the intimalmedia of the aorta in the treated groups were significantly lower than those in the control group, but the level of 6-keto-PGF1 alpha in the treated groups was significantly higher. The durations of TXB2 elevation and 6-keto-PGF1 alpha reduction were delayed. The ratio of TXB2/6-keto-PGF1 alpha tended to balance. The ratio of TXB2/6-keto-PGF1 alpha was significantly positive correlation with the percentage of lesion area of the aorta. It is demonstrated that calcium metabolism plays an important role in thromboxane, prostaglandin, and LPO synthesis. In conclusion, the inhibition of LPO production and the regulation of TXA2-PGI2 balance may be one of the mechanisms of anti-atherogenesis of calcium antagonists and PL.     

Relation of pale tongue, purple tongue and TXA2-PGI2 regulation system

This paper analysed the relationship between pale tongue, purplish tongue and TXB2, 6-keto-PGF1 alpha levels in plasma of 70 cases with coronary heart disease (CHD) and 45 normal subjects. The results showed the following characteristics: The pale tongue group (217.76 +/- 30.5 pg/ml) showed no significant difference in TXB2 level compared with the normal group (164.49 +/- 10.85 pg/ml, P greater than 0.05), while both showed significant difference compared with the purplish tongue group (360.1 +/- 31.3 pg/ml) and that with purple spots (485.07 +/- 106.1 pg/ml, P less than 0.01). The pale tongue group (179.29 +/- 9.08 pg/ml) showed a significant difference in 6-keto-PGF1 alpha level compared with the normal group (244 +/- 19.31 pg/ml, P less than 0.01), but it showed no significant difference compared with the purplish tongue group (185.08 +/- 17.07 pg/ml) and that with purple spots (229.3 +/- 33.2 pg/ml, P greater than 0.05). The comparison between the groups of purplish tongue and that with purple spots and the normal group showed no significant difference (P greater than 0.05). The pale tongue group (1.33 +/- 0.18) showed a marked difference in TXB2/6-keto-PGF1 alpha ratio compared with the normal group (0.72 +/- 0.04, P less than 0.01), the purplish tongue group (2.12 +/- 0.22, P less than 0.01) and that with purple spots (2.25 +/- 0.55, P less than 0.05). The purplish tongue group and that with purple spots showed significant difference compared with the normal group (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of Codonopsis pilosulae on the synthesis of thromboxane A2 and prostacyclin

24 angina pectoris patients were treated with Codonopsis pilosulae (CP) oral solution 20 ml (containing crude CP 20 g) thrice daily for 7 days, other 10 cases were treated by aspirin 0.5 g per day for a week as the control group. After treatment, in the CP group, the plasma level of TXB2 was obviously reduced from 156.76 +/- 11.87 pg/ml to 125.01 +/- 8.85 pg/ml (means +/- S means), the inhibitory rates was 15. 67% (P less than 0.05), and of 6-keto-PGF1 alpha (6-K) was not markedly changed (P greater than 0.05). In the aspirin group, TXB2 was also reduced significantly (P less than 0.05); 6-K was reduced more than that of CP group, the inhibitory rate was 24.33 +/- 9.40% (P less than 0.05). To reveal the mechanism of CP action on the synthesis of TXA2 and PGI2, the porcine lung microsome was used as the donor of cyclooxygenase, thromboxane synthase and prostacyclin synthase, the effects of CP on the formation of TXB2 and 6-K from arachidonic acid (AA) or endoperoxides were measured by RIA respectively. The results showed that both the levels of the formation of TXB2 from AA or endoperoxides were markedly reduced by CP in a dose-dependent (at doses of 3-300 mg/ml). The synthesis of TXB2 was distinctly inhibited alone with a dose of 100 mg/ml CP, which suggested that CP might be an inhibitor of TXB2 synthase at that dose; while at a dose of 300 mg/ml CP, the synthesis of TXB2 and 6-K were inhibited simultaneously (P less than 0.001). It showed that a larger dosage of CP, which could inhibited the synthesis of both TXA2 and PGI2, its mechanism of action needs further study.     

老年高血压病患者纤溶功能及血小板活化状态的改变

采用抗人活化血小板α颗粒膜蛋白（ＧＭＰ－１４０）单克隆抗体ＳＬ－５ｌ和１２５Ｉ－Ｓ１２以及单克隆酶联免疫法、发色底物法测定５８例老年高血压（ＥＨ）患者血浆ＧＭＰ－１４０、血栓素Ｂ２（ＴｘＢ２）、６酮－前列腺素Ｆ１α（６－ｋｅｔｏ－ＰＧＦ１α）浓度、组织型纤溶酶原激活物（ｔ－ＰＡ）含量及活性以及纤溶酶原激活抑制物（ＰＡＩ）活性，并与２０例健康人作对照。结果表明，ＧＭＰ－１４０、ＴｘＢ２、ＰＡＩ活性显著高于对照组，６－ｋｅｔｏ－ＰＧＦ１α、ｔ－ＰＡ显著低于对照组。将所得血浆各值与动态血压（ＡＢＰ）监测各指标作单相关分析，提示ＰＡＩ、ＧＭＰ－１４０、ＴｘＢ２与２４小时收缩压、舒张压、白昼收据压、舒张压呈显著正相关，６－ｋｅｔｏ－ＰＧＦ１α与２４小时收缩压、白昼收缩压呈显著负相关。     

Platelet aggregation, platelet cAMP levels and thromboxane B2 synthesis in patients with diabetes mellitus.

Platelet aggregation, platelet cAMP levels and thromboxane B2 (TXB2) synthesis had been investigated in 40 diabetics (20 with microangiopathy and 20 without) and 24 normal controls. The washed platelets, but not platelet rich plasma (PRP), from the diabetics show greater sensitivity to aggregation in response to thrombin, collagen and arachidonic acid than controls (P less than 0.05). Platelets from the diabetics contain the significantly decreased cAMP levels (P less than 0.01) and synthesize the significantly greater amount of TXB2 (P less than 0.01) when induced by thrombin or collagen. Conversion of exogenously added arachidonic acid to TXB2 remained unchanged (P greater than 0.05). cAMP levels in platelets from the diabetics exhibited a significant negative linear correlation with thrombin- and collagen-induced TXB2 synthesis. There was no significant difference in platelet aggregation, platelet cAMP levels and platelet TXB2 synthesis between the diabetics with and without microangiopathy. It was suggested that in the diabetic platelets: The observed increase in platelet thromboxane A2 (TXA2) synthesis should be due to the increased activity of arachidonic acid-metabolizing system, most likely at phospholipase site; the elevated platelet TXA2 levels should inhibit platelet membrane-associated adenylate cyclase which lowered the cAMP levels in platelets; and this alternation should be the mechanism of platelet hyperaggregability, which might contribute in some way to diabetic microangiopathy.