BACKGROUND & AIMS: :Enzymes involved in prostaglandin I2 (PGI2) and thromboxane A2 (TXA2) synthesis were studied in maternal and fetal platelets and venous endothelium from normotensive pregnant controls (n = 70), women with mild preeclampsia (MP, n = 45), and severe preeclampsia (SP, n = 34). Activities of phospholipase A2 (PHA2), cyclooxygenase (PGHS), and PGI2 synthetase (PGIS) or TXA2 synthetase (TXAS) were determined in platelets and in endothelial cells. The PGHS enzyme was studied further by immunoblot methodology. In maternal platelets: Vmax (per 10(-10) mol/mg protein) and Michaelis-Menten constant (Km) (10(-7) mol, mean +/- SEM) of PHA2 were 3.0 +/- 0.8, 3.0 +/- 0.7, and 31.7 +/- 10.9* maximum velocity (Vmax) and 1.8 +/- 0.3, 2.0 +/- 0.8, and 0.8 +/- 0.2 (Km) in normal control (NC), mild preeclampsia (MP), and severe preeclampsia (SP), respectively (*P less than 0.05 against NC). The apparent overall PGHS plus TXAS activity was 10.2 +/- 1.8, 23.8 +/- 7.1, and 68.8 +/- 18.8* (Vmax) and 3.2 +/- 1.3, 5.4 +/- 1.4, and 6.9 +/- 1.2* (Km, *P less than 0.05 against NC). TXA synthesis in fetal platelets demonstrated PHA2 activity of 6.4 +/- 1.4, 12.0 +/- 1.3, and 17.2 +/- 3.2* (Vmax) and 3.5 +/- 0.9, 2.2 +/- 1.5, and 0.7 +/- 0.3* (Km, *P less than 0.05 against NC), respectively, whereas an apparent overall PGHS plus TXAS activity was 18.5 +/- 2.8, 87.5 +/- 12.5*, and 3.6 +/- 0.1* (Vmax) and 4.8 +/- 1.0, 8.8 +/- 1.2, and 0.8 +/- 0.3* (Km, *P less than 0.05 against NC).(ABSTRACT TRUNCATED AT 250 WORDS)

背景与目标： : 在血压正常的孕妇对照 (n = 70)，轻度先兆子痫妇女 (MP，n = 45) 和严重先兆子痫的孕妇和胎儿血小板和静脉内皮中研究了参与前列腺素I2 (PGI2) 和血栓烷A2 (TXA2) 合成的酶。子痫前期 (SP，n = 34)。在血小板和内皮细胞中测定了磷脂酶A2 (PHA2)，环氧合酶 (PGHS) 和PGI2合成酶 (PGIS) 或TXA2合成酶 (TXAS) 的活性。通过免疫印迹方法进一步研究了PGHS酶。在母体血小板中: PHA2的Vmax (每10(-10) mol/mg蛋白) 和Michaelis-Menten常数 (Km) (10(-7) mol，平均值 +/- SEM) 为3.0 +/- 0.8，3.0 +/- 0.7，和31.7 +/- 10.9 * 最大速度 (Vmax) 和1.8 +/- 0.3，2.0 +/- 0.8和0.8 +/- 0.2 (Km) 在正常对照 (NC)，轻度先兆子痫 (MP) 和重度先兆子痫 (SP)，分别 (对NC的 * P小于0.05)。表观总体PGHS加TXAS活性为10.2 +/- 1.8、23.8 +/- 7.1和68.8 +/- 18.8 * (Vmax) 和3.2 +/- 1.3、5.4 +/- 1.4和6.9 +/- 1.2 * (Km，* P对NC小于0.05)。胎儿血小板中的TXA合成显示6.4 +/- 1.4、12.0 +/- 1.3和17.2 +/- 3.2 * (Vmax) 和3.5 +/- 0.9、2.2 +/- 1.5和0.7 +/- 0.3 * (Km，* P小于针对NC的0.05)，而明显的总体PGHS加TXAS活性分别为18.5 +/- 2.8、87.5 +/- 12.5*和3.6 +/- 0.1 * (Vmax) 和4.8 +/- 1.0，8.8 +/- 1.2，和0.8 +/- 0.3 * (Km，* P小于0.05对NC)。(抽象截断在250个单词)

BACKGROUND & AIMS: :Paraquat is known to cause severe lung damage through pulmonary edema as its initial feature of toxicity. The purpose of this study was to investigate the toxicity of paraquat in rabbits intraperitoneally injected with 2 or 4 mg/kg/day of the herbicide for a period of 7 days. In the lung, prostaglandin levels of the intoxicated rabbits showed a significant increase in PGF2 alpha. This increase was dose dependent. However, a nonsignificant change in the 6-keto-PGF1 alpha was also observed. Plasma and serum levels of thromboxane-B2 were also significantly elevated but the levels of 6-keto-PGF1 alpha were affected nonsignificantly. The pathology of elevated levels of PGF2 alpha and TXB2 in the lung and blood, in response to paraquat toxicity, is discussed.

背景与目标： : 百草枯已知通过肺水肿引起严重的肺损伤，这是其毒性的最初特征。目的研究百草枯对家兔腹腔注射2或4 mg/kg/天的除草剂，为期7天的毒性。在肺中，中毒兔子的前列腺素水平显示pgf2α 显着增加。这种增加是剂量依赖性的。然而，也观察到6-keto-pgf1α 无显著变化。thromboxane-B2的血浆和血清水平也显着升高，但6-keto-pgf1α 的水平没有显着影响。讨论了响应百草枯毒性的肺和血液中pgf2α 和TXB2水平升高的病理。

BACKGROUND & AIMS: :Rabbit blastocysts recovered at 144 hours post coitum contained the prostaglandins F and E-A. We suggest that one or more of these prostaglandins act as mediators in blastocyst steroidogenesis. (In another study we have demonstrated steroidogenesis in rabbit blastocysts).

背景与目标： : 兔囊胚在coitum后144小时恢复，含有前列腺素F和E-A。我们建议这些前列腺素中的一种或多种在胚泡类固醇生成中起介质作用。(在另一项研究中，我们已经证明了兔胚泡中的类固醇生成)。

BACKGROUND & AIMS: :Amateau and McCarthy's findings published in Nature Neuroscience (June 2004) are noteworthy for suggesting a role for prostaglandins in sexual development. However, evidence suggests that in manipulating PGE2, they unknowingly implicated 3alpha-hydroxysteroid dehydrogenase [E.C. 1.1.1.50], 3(or 17)alpha-hydroxysteroid dehydrogenase [E.C. 1.1.1.209] and their respective products, androsterone (ADT) and epitestosterone (EpiT), in the developmental masculinization of sex behavior. EpiT is generally regarded as a hormonally inactive 17alpha-epimer of testosterone (T). In rats, the kidney is the primary site of EpiT formation, whereas in humans it originates from the gonads, with only a small contribution secreted by the adrenals. Because the ratio of T to EpiT is nearly constant, it is presently used for assessing steroid abuse in competitive sports, where the World Anti-Doping Agency (WADA) considers a T/EpiT ratio >4 evidence of T doping. Despite its central role in the detection of illict anabolic steroid use, our knowledge of factors effecting EpiT production is poor. Clues in the literature, however, reveal that prostaglandin-mediated processes, such as LHRH release, may influence its production. Antimycotics, NSAIDs, and opioid analgesics used in sports medicine are all known to effect prostaglandin E2 synthesis. Primary PGs are potent inhibitors of ADT oxidation, while indomethacin, a prostaglandin blocker, powerfully inhibits 3alpha-HSD reduction and ADT oxidation. This is significant because ADT inhibits the oxidation of EpiT, and may modulate its antiandrogenic and neuroprotective effects. It is hypothesized that the T/EpiT ratio is increased by COX-2 inhibitors and opiod analgesics, and decreased by antimycotics that do not impair testosterone biosynthesis. Given the devastating personal and career consequences that may result from false positive drug tests, substantive research on the effects of PGE2 manipulations on EpiT is warranted.

背景与目标： : Amateau和McCarthy发表在《自然神经科学》 (2004年6月) 上的发现值得注意，因为它暗示了前列腺素在性发育中的作用。然而，有证据表明，在操纵PGE2时，他们在不知不觉中涉及3α-羟基类固醇脱氢酶 [E.C. 1.1.1.50]，3 (或17) α-羟基类固醇脱氢酶 [E.C.1.1.209] 及其各自的产物，雄酮 (ADT) 和表甾酮 (EpiT)，在性行为的发展男性化中。EpiT通常被认为是睾丸激素 (T) 的激素不活跃的17α-epimer。在大鼠中，肾脏是EpiT形成的主要部位，而在人类中，肾脏起源于性腺，肾上腺仅分泌少量。由于T与EpiT的比率几乎是恒定的，因此目前用于评估竞技运动中的类固醇滥用，世界反兴奋剂机构 (WADA) 认为T/EpiT比率> 4是T掺杂的证据。尽管它在检测合成代谢类固醇的使用中起着核心作用，但我们对影响epi产生的因素的了解却很差。然而，文献中的线索表明，前列腺素介导的过程 (例如LHRH释放) 可能会影响其产生。运动医学中使用的抗真菌药，NSAIDs和阿片类镇痛药都可以影响前列腺素E2的合成。初级pg是ADT氧化的有效抑制剂，而前列腺素阻滞剂吲哚美辛则有效抑制3α-hsd还原和ADT氧化。这很重要，因为ADT抑制EpiT的氧化，并可能调节其抗雄激素和神经保护作用。假设COX-2抑制剂和阿片类镇痛药会增加T/EpiT比，而不会损害睾丸激素生物合成的抗真菌药会降低T/EpiT比。鉴于假阳性药物测试可能会导致毁灭性的个人和职业后果，因此有必要对PGE2操作对EpiT的影响进行实质性研究。

BACKGROUND & AIMS: :Rats have an attenuated febrile response to endogenous pyrogen near the term of pregnancy. Given the fundamental role of E-series prostaglandins (PGEs) in mediating the febrile response to blood-borne endogenous pyrogen, the present experiments were carried out to determine whether PGEs increase in the area surrounding the organum vasculosum laminae terminalis (peri-OVLT) of near-term pregnant (P) rats as in nonpregnant (NP) rats after intravenous (iv) administration of recombinant rat interleukin-1beta (rrIL-1beta). Core temperature was measured by telemetry and peri-OVLT interstitial fluid was sampled in 12 NP and 12 P chronically instrumented, Sprague-Dawley rats by microdialysis for determination of total PGEs by radioimmunoassay. Basal core temperatures were higher in NP compared with P rats (NP 37.9 degrees C +/- 0.5, P 36.9 degrees C +/- 0.4; P < 0.05), but basal peri-OVLT PGEs were similar in both groups (NP 260 +/- 153 pg/ml, P 278 +/- 177 pg/ml; P =not significant). Intravenous administration of rrIL-1beta to NP rats produced a significant increase in core temperature with a latency, magnitude, and duration of 10 min, 0.87 degrees C, and at least 170 min, respectively; peri-OVLT PGEs were increased significantly by 30 min and averaged 270% above basal levels throughout the experiment. In P rats, however, neither core temperature nor peri-OVLT PGEs increased significantly after iv administration of rrIL-1beta. Intravenous administration of vehicle did not significantly alter core temperature or peri-OVLT PGEs in either group of rats. Thus peri-OVLT PGEs do not increase in P rats as they do in NP rats after iv administration of rrIL-1beta. The mechanism of this interesting component of the maternal adaptation to pregnancy, which likely plays a major role in mediating the attenuated febrile response to endogenous pyrogen near the term of pregnancy, warrants further investigation.

背景与目标： : 大鼠在怀孕期间对内源性热原的发热反应减弱。鉴于E系列前列腺素 (PGEs) 在介导对血源性内源性热原的发热反应中的基本作用，进行了本实验，以确定在静脉内 (iv) 施用重组大鼠后，近期怀孕 (P) 大鼠的器官脉管终层 (peri-OVLT) 周围区域的PGEs是否增加 (rrIL-1beta)。大鼠interleukin-1beta)。通过遥测法测量核心温度，并通过微透析在12 NP和12 P长期仪器的Sprague-Dawley大鼠中采样周围OVLT间质液，以通过放射免疫测定法测定总PGEs。与P大鼠相比，NP的基础核心温度更高 (NP 37.9 ℃/- 0.5，P 36.9 ℃/- 0.4; P <0.05)，但两组的基础peri-OVLT PGEs相似 (NP 260/- 153 pg/ml，P 278 +/- 177 pg/ml; P = 不显着)。向NP大鼠静脉内施用rrIL-1beta会产生核心温度的显着增加，潜伏期，幅度和持续时间分别为10分钟，0.87摄氏度和至少170分钟; peri-OVLT PGEs显着增加30分钟，并且在整个实验中平均270% 高于基础水平。然而，在P大鼠中，静脉注射rrIL-1beta后，核心温度和周围OVLT PGEs均未显着增加。静脉内施用媒介物不会显着改变两组大鼠的核心温度或周围OVLT PGEs。因此，在iv给药rrIL-1beta后，P大鼠中的peri-OVLT PGEs不会像在NP大鼠中那样增加。孕产妇适应妊娠的这一有趣成分的机制可能在介导妊娠期间对内源性热原的减弱的发热反应中起主要作用，值得进一步研究。

BACKGROUND & AIMS: :Addition of substance P (SP) to astrocytes cultured from rat neonatal spinal cord evoked a time- and concentration-dependent increase in the accumulation of phosphoinositol and the release of prostaglandin (PG) D2 and PGE2. Both basal and stimulated releases were reduced to similar levels by indomethacin. In contrast, astrocytes cultured from cerebral cortex and cerebellum showed no SP-stimulated increase in phosphoinositol accumulation or release of PGs. Release of PGD2 and PGE2 was, however, stimulated by the calcium ionophore A23187, and both phosphoinositol accumulation and PG release were stimulated from cortical astrocytes incubated in the presence of serum. The results from this study suggest that SP-stimulated phosphoinositol accumulation and release of PGs from cultured rat neonatal astrocytes are regionally specialised in favour of cells derived from spinal cord.

背景与目标： : 从大鼠新生脊髓培养的星形胶质细胞中添加p物质 (SP) 引起磷酸肌醇积累和前列腺素 (PG) D2和pge2释放的时间和浓度依赖性增加。消炎痛将基础释放和刺激释放降低到相似的水平。相反，从大脑皮层和小脑培养的星形胶质细胞未显示SP刺激的磷酸肌醇积累或pg释放增加。然而，钙离子载体A23187刺激了PGD2和PGE2的释放，并且在血清存在下孵育的皮质星形胶质细胞刺激了磷酸肌醇的积累和PG的释放。这项研究的结果表明，SP刺激的磷酸肌醇积累和从培养的大鼠新生星形胶质细胞中释放的pg在区域上是专门的，有利于脊髓来源的细胞。

BACKGROUND & AIMS: :We examined the relative contribution of endothelial and vascular smooth muscle-derived prostaglandins and endothelium-derived relaxing factor in modulating both the large coronary artery and resistance vessel responses to thromboxane in vivo. Vascular responses to the thromboxane analogue U46619 were measured in four separate experimental protocols: 1) The vascular responses were measured in the presence and absence of intact endothelium to examine the role of endothelium-derived vasodilators. 2) Responses were measured in the presence of intact endothelium before and after inhibition of cyclooxygenase with indomethacin to examine the role of endothelial and vascular smooth muscle-derived prostaglandins. 3) Responses were measured after endothelial removal before and after indomethacin to examine the role of vascular smooth muscle-derived prostaglandins. 4) Responses were measured after indomethacin and before and after removal of endothelium to examine the role of endothelium-derived relaxing factor. In anesthetized dogs (n = 41) that underwent constant pressure perfusion of the left anterior descending coronary artery (LAD), LAD diameter was measured with sonomicrometer crystals, and coronary flow was measured with an electromagnetic flow probe. Intracoronary infusion of U46619 (0.01-1.0 microgram/min) produced a dose-dependent constriction of LAD. Constriction of the LAD was augmented after endothelial removal, after indomethacin treatment in both the presence and absence of endothelium, and after removal of the endothelium in the presence of indomethacin. Inhibition of prostaglandin synthesis had the greatest effect of augmenting constriction of LAD to thromboxane. Coronary flow was decreased by U46619 only in the presence of indomethacin.(ABSTRACT TRUNCATED AT 250 WORDS)

背景与目标： : 我们检查了内皮和血管平滑肌衍生的前列腺素和内皮衍生的舒张因子在体内调节大冠状动脉和阻力血管对血栓烷的反应中的相对贡献。在四个独立的实验方案中测量了对血栓素类似物U46619的血管反应: 1) 在存在和不存在完整内皮的情况下测量血管反应，以检查内皮衍生的血管扩张剂的作用。2) 在吲哚美辛抑制环氧合酶之前和之后，在完整的内皮存在下测量反应，以检查内皮和血管平滑肌衍生的前列腺素的作用。3) 在吲哚美辛前后测量内皮去除后的反应，以检查血管平滑肌衍生的前列腺素的作用。4) 在吲哚美辛之后以及去除内皮之前和之后测量反应，以检查内皮衍生的松弛因子的作用。在接受左前降支冠状动脉 (LAD) 恒压灌注的麻醉犬 (n = 41) 中，用sonomicrometer晶体测量LAD直径，并用电磁流量探针测量冠状动脉流量。冠状动脉内输注U46619 (0.01-1.0微克/分钟) 产生LAD的剂量依赖性收缩。内皮去除后，在存在和不存在内皮的情况下进行吲哚美辛处理后，以及在存在吲哚美辛的情况下去除内皮后，LAD的收缩增加。抑制前列腺素的合成具有最大的作用，可以增加LAD对血栓烷的收缩。只有在吲哚美辛存在的情况下，U46619才能减少冠状动脉血流。(摘要截短于250字)

BACKGROUND & AIMS: :Prostaglandins (PGs) are a family of lipid compounds that are derived from arachidonic acid via the cyclooxygenase pathway, and consist of PGD2, PGI2, PGE2, PGF2, and thromboxane B2. PGs signal through G-protein coupled receptors, and individual PGs affect allergic inflammation through different mechanisms according to the receptors with which they are associated. In this review article, we have focused on the metabolism of the cyclooxygenase pathway, and the distinct biological effect of each PG type on various cell types involved in allergic airway diseases, including asthma, allergic rhinitis, nasal polyposis, and aspirin-exacerbated respiratory disease.

背景与目标： : 前列腺素 (PGs) 是一类脂质化合物，通过环氧合酶途径衍生自花生四烯酸，由PGD2，PGI2，PGE2，PGF2和血栓烷b2组成。PGs通过g蛋白偶联受体发出信号，单个PGs根据与其相关的受体通过不同机制影响过敏性炎症。在这篇综述文章中，我们重点关注环氧合酶途径的代谢，以及每种PG类型对涉及过敏性气道疾病的各种细胞类型 (包括哮喘，过敏性鼻炎，鼻息肉病和阿司匹林加剧的呼吸道疾病) 的独特生物学作用。

BACKGROUND & AIMS: AIM:The effects of losartan on blood pressure and on renal function have mainly been attributed to AT1 receptor blockade. Experimental evidence suggests that these effects could also be related to the actions of angiotensin II through AT2 receptors or to vasodilatory systems. The present study was therefore designed to investigate the manner in which the acute effects of losartan on renal excretory function are affected during simultaneous administration of an AT2 receptor antagonist, a kinin B2 receptor antagonist, a cyclo-oxygenase inhibitor or a nitric oxide synthesis inhibitor.

MATERIALS AND METHODS:The AT2 receptor antagonist PD 123319 (10 mg/kg), the bradykinin B2 receptor antagonist Hoe 140 (30 mu g/kg), the cyclo-oxygenase inhibitor meclofenamate (5 mg/kg) and the nitric oxide synthesis inhibitor NG-monomethyl-L-arginine (1 mu g/kg per min) were administered separately with acute intravenous losartan (1 mg/kg) to spontaneously hypertensive rats and the effects on mean arterial pressure and renal excretory function were assessed.

RESULTS:Losartan reduced mean arterial pressure by 11.1 +/- 5.7 mmHg and increased the glomerular filtration rate, urine flow and sodium excretion rate. The decrease in mean arterial pressure was blocked in the presence of NG-monomethyl-L-arginine but not during concurrent administration of PD 123319, Hoe 140 or meclofenamate. The increase in glomerular filtration rate induced by losartan was blunted by Hoe 140, meclofenamate and NG-monomethyl-L-arginine. Co-administration of PD 123319, Hoe 140 or meclofenamate, but not of NG-monomethyl-L-arginine, partially blunted the diuresis and natriuresis induced by losartan.

CONCLUSIONS:Nitric oxide participates in the antihypertensive action of losartan. Kinins, prostaglandins and nitric oxide appear to be involved in the effects of losartan on the glomerular filtration rate. The increases in urine flow and sodium excretion rate induced by losartan depend partially on AT2 receptors, kinins and prostaglandins.

背景与目标： 目的 : 氯沙坦对血压和肾功能的影响主要归因于AT1受体阻滞。实验证据表明，这些作用也可能与血管紧张素II通过AT2受体的作用或血管舒张系统有关。因此，本研究旨在研究在同时施用AT2受体拮抗剂 (激肽B2受体拮抗剂) 期间影响氯沙坦对肾脏排泄功能的急性作用的方式，环加氧酶抑制剂或一氧化氮合成抑制剂。材料和方法: AT2受体拮抗剂PD 123319 (10 mg/kg)，缓激肽B2受体拮抗剂Hoe 140 (30 μ g/kg)，将环加氧酶抑制剂甲氯芬那酯 (5 mg/kg) 和一氧化氮合成抑制剂NG-单甲基-L-精氨酸 (1 μ g/kg/min) 与急性静脉氯沙坦 (1 mg/kg) 分别给予自发性高血压大鼠，并评估了对平均动脉压和肾脏排泄功能的影响。
结果 : 氯沙坦可使平均动脉压降低11.1/- 5.7 mmHg，并增加肾小球滤过率，尿液流量和钠排泄率。在存在NG-单甲基-L-精氨酸的情况下，平均动脉压的降低被阻断，但在同时施用PD 123319，Hoe 140或甲氯芬酯期间不被阻断。氯沙坦引起的肾小球滤过率的增加被140，甲氯芬酯和NG-单甲基-L-精氨酸抑制。同时使用PD 123319，Hoe 140或甲氯芬那酯，但不使用NG-单甲基-L-精氨酸，部分减弱了氯沙坦诱导的利尿和利尿。
结论 : 一氧化氮参与氯沙坦的降压作用。激肽，前列腺素和一氧化氮似乎与氯沙坦对肾小球滤过率的影响有关。氯沙坦诱导的尿液流量和钠排泄率的增加部分取决于AT2受体，激肽和前列腺素。

BACKGROUND & AIMS: :Our previous study showed that arteriolar tone is enhanced in Type 2 diabetes mellitus (T2-DM) due to an increased level of constrictor prostaglandins. We hypothesized that, in mice with T2-DM, hydrogen peroxide (H(2)O(2)) is involved in the increased synthesis of constrictor prostaglandins, hence enhanced basal tone in skeletal muscle arterioles. Isolated, pressurized gracilis muscle arterioles ( approximately 100 microm in diameter) of mice with T2-DM (C57BL/KsJ-db(-)/db(-)) exhibited greater basal tone to increases in intraluminal pressure (20-120 mmHg) than that of control vessels (at 80 mmHg, control: 25 +/- 5%; db/db: 34 +/- 4%, P < 0.05), which was reduced back to control level by catalase (db/db: 24 +/- 4%). Correspondingly, in carotid arteries of db/db mice, the level of dichlorofluorescein-detectable and catalase-sensitive H(2)O(2) was significantly greater. In control arterioles, exogenous H(2)O(2) (0.1-100 micromol/l) elicited dilations (maximum, 58 +/- 10%), whereas in arterioles of db/db mice H(2)O(2) caused constrictions (-28 +/- 8%), which were converted to dilations (maximum, 16 +/- 5%) by the thromboxane A(2)/prostaglandin H(2) (TP) receptor antagonist SQ-29548. In addition, arteriolar constrictions in response to the TP receptor agonist U-46619 were not different between the two groups of vessels. Endothelium denudation did not significantly affect basal tone and H(2)O(2)-induced arteriolar responses in either control or db/db mice. Also, in arterioles of db/db mice, but not in controls, 3-nitrotyrosine staining was detected in the endothelial layer of vessels. Thus we propose that, in mice with T2-DM, arteriolar production of H(2)O(2) is enhanced, which leads to increased synthesis of the constrictor prostaglandins thromboxane A(2)/prostaglandin H(2) in the smooth muscle cells, which enhance basal arteriolar tone. These alterations may contribute to disturbed regulation of skeletal muscle blood flow in Type 2 diabetes mellitus.

背景与目标： : 我们先前的研究表明，由于收缩性前列腺素水平升高，2型糖尿病 (T2-DM) 的小动脉张力增强。我们假设，在患有T2-DM的小鼠中，过氧化氢 (H(2)O(2)) 参与了收缩性前列腺素的合成增加，从而增强了骨骼肌小动脉的基础张力。具有T2-DM (C57BL/KsJ-db(-)/db(-)) 的小鼠的分离的加压gra肌小动脉 (直径约100微米) 表现出更大的基底性，以增加管腔内压力 (20-120毫米汞柱) 比对照组 (80毫米汞柱，对照: 25/- 5%; db/db: 34/- 4%，P <0.05)，其通过过氧化氢酶降低至对照水平 (db/db: 24/- 4%)。相应地，在db/db小鼠的颈动脉中，可检测到的二氯荧光素和对过氧化氢酶敏感的H(2)O(2) 的水平明显更高。在对照小动脉中，外源H(2)O(2) (0.1-100 micromol/l) 引起的扩张 (最大，58 +/- 10%)，而在db/db小鼠的小动脉中，H(2)O(2) 引起收缩 (-28 +/- 8%)，转化为扩张 (最大，16 +/- 5%) 由血栓素A(2)/前列腺素H(2) (TP) 受体拮抗剂SQ-29548。此外，响应TP受体激动剂U-46619的小动脉收缩在两组血管之间没有差异。在对照或db/db小鼠中，内皮剥脱作用不会显着影响基底音和H(2)O(2) 诱导的小动脉反应。同样，在db/db小鼠的小动脉中，但在对照组中没有，在血管的内皮层中检测到3-硝基酪氨酸染色。因此，我们提出，在T2-DM小鼠中，H(2)O(2) 的小动脉产生增强，这导致平滑肌细胞中收缩性前列腺素血栓烷A(2)/前列腺素H(2) 的合成增加，从而增强基底小动脉张力。这些改变可能有助于2型糖尿病患者骨骼肌血流的调节紊乱。

BACKGROUND & AIMS: :Prostaglandins (PG) E2,E1,6-keto-E1 and D2 at concentrations of 0.15-0.80 microM inhibited by 25% the generation of superoxide anions (O2-) in human polymorphonuclear leukocytes (PMNs) stimulated with formyl-methionyl-leucyl-phenylalanine (FMLP). The potency of that inhibition by either PGD2 or PGE1 was the same when zymosan was used as a stimulator whereas PGE2 and 6-keto-PGE1 were by 13 and 21 times less potent inhibitors of O2-) in zymosan-stimulated as compared to FMLP-activated PMNs. PGF2 alpha inhibited the generation of O2- by activated PMNs only when used at the highest concentration studied (30 microM). Prostacyclin, 6-keto-PGF1 alpha and Iloprost (a carbacyclin analogue of prostacyclin) at concentrations up to 30 microM showed no significant inhibition of O2- in human PMNs stimulated either with FMLP or with zymosan. It is concluded that PGD2 and PGEs use a common basic mechanism for inhibition of the generation of O2- by PMNs activated with FMLP or zymosan. PGD2 is most generously furnished with these properties. In addition to this basic mechanism PGE2 and 6-keto-PGE1 abrogate the FMLP-induced response by occupation of formyl peptide receptor of PMNs. It is hypothesised that inhibition of the generation of O2- in PMNs and, possibly, in other cells by PGD2, PGE2 and by products of prostacyclin biotransformation might be responsible for their cytoprotective action in myocardial infarction, stroke, liver damage and peripheral vascular disease.

背景与目标： : 前列腺素 (PG) E2、E1、6-酮-E1和D2浓度为0.15-0.80微米，通过25% 用甲酰基-甲硫酰基-亮氨酸-苯丙氨酸 (FMLP) 刺激的人多形核白细胞 (pmn) 中超氧化物阴离子 (O2-) 的产生来抑制。当酵母聚糖用作刺激剂时，PGD2或PGE1的抑制作用是相同的，而PGE2和6-酮-PGE1在酵母聚糖刺激下的O2-) 抑制剂的效力要低13和21倍FMLP激活的PMNs。Pgf2α 仅在研究的最高浓度 (30微米) 下使用时才抑制活化的PMNs产生O2。浓度高达30微米的前列环素，6-keto-pgf1α 和伊洛前列素 (前列环素的碳环素类似物) 在FMLP或酵母聚糖刺激的人pmn中没有明显抑制O2-。结论是，PGD2和PGEs使用一种共同的基本机制来抑制用FMLP或酵母聚糖激活的pmn产生O2。PGD2最慷慨地配备了这些属性。除了这种基本机制之外，PGE2和6-keto-PGE1还通过占据pmn的甲酰基肽受体来消除FMLP诱导的反应。据推测，PGD2，PGE2和前列环素生物转化产物对pmn中以及其他细胞中O2-的产生的抑制可能是其在心肌梗塞，中风，肝损伤和周围血管疾病中的细胞保护作用的原因。

BACKGROUND & AIMS: 1. Recent evidence has implicated eosinophils in the inhibition of allergen-induced rat pleurisy, but the mechanism of this negative modulation is not completely understood. This study was undertaken in order to define the potential role of prostaglandins in this phenomenon. 2. Wistar rats were actively sensitized by subcutaneous injection of a mixture of ovalbumin and AI(OH)3 and challenged with an intrapleural (i.pl.) injection of ovalbumin (12 micrograms/cavity) 14 days later. 3. Analysis of the pleural fluid effluent revealed a massive mast cell degranulation and plasma protein extravasation 4 h post-challenge. We confirmed that concurrently with selective pleural fluid eosinophilia caused by platelet-activating factor (PAF), the pleural cavity became hyporesponsive to allergen-induced protein exudation and to the parallel reduction in the number of intact mast cells. 4. These hyporesponsive animals presented a significant augmentation in the pleural effluent level of prostaglandin E2 (PGE2), which increased with increasing numbers of eosinophils in the pleural cavity. Furthermore, pretreatment with either indomethacin or aspirin failed to modify allergen-induced exudation but reversed the exudatory hyporesponsiveness associated with eosinophil recruitment. 5. Allergic exudation was clearly down-regulated by the following pretreatments(i) PGE2 (10 micrograms/cavity, i.pl.) plus rolipram (40 micrograms/cavity, i.pl.), (ii) misoprostol (200 micrograms kg-1, p.o.) or (iii) dibutyryl cyclic AMP (80 micrograms/cavity, i.pl.). 6. We conclude that prostaglandins may be implicated in the eosinophil-mediated inhibition of allergic pleurisy, probably acting via cyclic AMP signalling pathway activation.

背景与目标： 1.最近的证据表明嗜酸性粒细胞可以抑制变应原诱导的大鼠胸膜炎，但这种负调节的机制尚不完全清楚。进行这项研究是为了确定前列腺素在这种现象中的潜在作用。2. Wistar大鼠通过皮下注射卵白蛋白和AI(OH)3的混合物积极致敏，并在14天后用胸膜内 (i.pl.) 注射卵白蛋白 (12微克/腔) 攻击。3.对胸膜液流出物的分析显示，攻击后4小时，肥大细胞大量脱粒和血浆蛋白外渗。我们证实，在血小板活化因子 (PAF) 引起的选择性胸水嗜酸性粒细胞增多的同时，胸膜腔对变应原诱导的蛋白渗出和完整肥大细胞数量的平行减少具有低反应性。4.这些低反应性动物的胸膜流出物中前列腺素E2 (PGE2) 的水平显着增加，并且随着胸膜腔中嗜酸性粒细胞的增加而增加。此外，用吲哚美辛或阿司匹林进行预处理未能改变过敏原诱导的渗出，但逆转了与嗜酸性粒细胞募集相关的渗出性低反应性。5.通过以下预处理 (i) PGE2 (10微克/腔，i.pl.) 加罗利普兰 (40微克/腔，i.pl.)，(ii) 米索前列醇 (200微克kg-1，p.o.) 或 (iii) 二丁酰基环状AMP (80微克/腔，i.pl.)。6.我们得出的结论是，前列腺素可能与嗜酸性粒细胞介导的过敏性胸膜炎抑制有关，可能通过环状AMP信号通路激活起作用。

BACKGROUND & AIMS: PURPOSE:Animal studies suggest that the inhibition of nitric oxide synthase (NOS) affects blood flow differently in different skeletal muscles according to their muscle fibre type composition (oxidative vs glycolytic). Quadriceps femoris (QF) muscle consists of four different muscle parts: vastus intermedius (VI), rectus femoris (RF), vastus medialis (VM), and vastus lateralis (VL) of which VI is located deep within the muscle group and is generally regarded to consist mostly of oxidative muscle fibres. METHODS:We studied the effect of NOS inhibition on blood flow in these four different muscles by positron emission tomography in eight young healthy men at rest and during one-leg dynamic exercise, with and without combined blockade with prostaglandins. RESULTS:At rest blood flow in the VI (2.6 ± 1.1 ml/100 g/min) was significantly higher than in VL (1.9 ± 0.6 ml/100 g/min, p = 0.015) and RF (1.7 ± 0.6 ml/100 g/min, p = 0.0015), but comparable to VM (2.4 ± 1.1 ml/100 g/min). NOS inhibition alone or with prostaglandins reduced blood flow by almost 50% (p < 0.001), but decrements were similar in all four muscles (drug × muscle interaction, p = 0.43). During exercise blood flow was also the highest in VI (45.4 ± 5.5 ml/100 g/min) and higher compared to VL (35.0 ± 5.5 ml/100 g/min), RF (38.4 ± 7.4 ml/100 g/min), and VM (36.2 ± 6.8 ml/100 g/min). NOS inhibition alone did not reduce exercise hyperemia (p = 0.51), but combined NOS and prostaglandin inhibition reduced blood flow during exercise (p = 0.002), similarly in all muscles (drug × muscle interaction, p = 0.99). CONCLUSION:NOS inhibition, with or without prostaglandins inhibition, affects blood flow similarly in different human QF muscles both at rest and during low-to-moderate intensity exercise.

背景与目标：

BACKGROUND & AIMS: :The effect of prostaglandins E1, E2 and F2alpha on the gall bladder pressure was studied in anesthetized dogs with and without clamping of the cystic duct. Both PGE1 and PGE2 lowered the gall bladder pressure when the initial pressure was higher than 5 mm Hg, but caused no significant change when the initial pressure was lower than 3 mm Hg. On the other hand, PGF2alpha increased the gall bladder pressure regardless of its initial pressure. When the cystic duct was clamped, PGF2alpha markedly increased the gall bladder pressure while both PGE1 and PGE2 increased it slightly. This observation suggests that the smooth muscle in the gall bladder is markedly stimulated by PGF2alpha and stimulated to a lesser degree by PGE1 or PGE2. Furthermore, PGF2alpha appears to constrict, and PGE1 or PGE2 appears to relax the sphincter of Oddi. Pretreatment with indomethacin did not affect or slightly potentiated the cholecystokinetic effect of the three prostaglandins but abolished that of pentagastrin, suggesting that prostaglandins are possible mediators for the cholecystokinetic action of the gastrointestinal hormones.

背景与目标： : 在有和没有夹紧胆囊管的麻醉犬中研究了前列腺素E1，E2和F2alpha对胆囊压力的影响。当初始压力高于5毫米Hg时，PGE1和PGE2均降低了胆囊压力，但是当初始压力低于3毫米Hg时，PGE1和PGE2均没有显着变化。另一方面，PGF2alpha增加了胆囊压力，而不管其初始压力如何。夹紧胆囊管时，PGF2alpha显着增加了胆囊压力，而PGE1和PGE2均略微增加了胆囊压力。该观察结果表明，PGF2alpha显着刺激了胆囊中的平滑肌，而PGE1或pge2则较小程度地刺激了胆囊中的平滑肌。此外，PGF2alpha似乎收缩，PGE1或PGE2似乎放松了Oddi的括约肌。吲哚美辛预处理不会影响或略微增强三种前列腺素的胆囊动力学作用，但会消除五肽胃泌素的胆囊动力学作用，这表明前列腺素可能是胃肠道激素胆囊动力学作用的介质。

BACKGROUND & AIMS: We studied the in vitro effect of prolactin on the synthesis of prostaglandins PGE and PGF2 alpha in the rat uterus. Uterine tissue was obtained from ovariectomized adult rats with or without estradiol-17 beta treatment. Prolactin (4 IU/ml) enhanced PGE uterine synthesis. At higher concentrations (10-15 IU/ml) prolactin enhanced PGE levels and diminished PGE2 alpha production by uterine tissue from ovariectomized rats. When ovariectomized rats were injected with estradiol-17 beta, we observed a pattern of PGE and PGF2 beta uterine similar to that of ovariectomized rats. However, the stimulatory action of PRL on PGE synthesis was augmented in the estrogenized animals. These results led us to conclude that1)-PRL exerts a luteotrophic action by regulating uterine tissue PGE synthesis, 2-estradiol-17 beta potentiates this action.

背景与目标： 我们研究了催乳素对大鼠子宫中前列腺素PGE和pgf2α 合成的体外作用。从接受或不接受estradiol-17 β 处理的去卵巢成年大鼠获得子宫组织。催乳素 (4 IU/ml) 增强PGE子宫合成。在较高浓度 (10-15 IU/ml) 下，催乳素可增强去卵巢大鼠的子宫组织的PGE水平并减少pge2α 的产生。当卵巢切除的大鼠注射estradiol-17 β 时，我们观察到PGE和pgf2β 子宫模式与卵巢切除的大鼠相似。然而，在雌激素化动物中，PRL对PGE合成的刺激作用增强了。这些结果使我们得出结论，1)-PRL通过调节子宫组织PGE的合成来发挥黄体营养作用，2-estradiol-17β 增强了这种作用。