次声对脑组织血栓素A2,前列环素代谢的影响

目的 探讨次声作用后脑皮层组织血栓素Ａ２（ＴＸＡ２）、前列环素（ＰＬＩ２）代谢改变及及代谢性谷氨酸受体拮抗剂ＭＣＰＧ的作用。方法 ４０只ＳＤ大鼠随机分为正常对照,次声作用１次、７次、１４次及代谢性谷氨酸受体拮抗剂ＭＣＰＧ治疗５组,采用第四军医大学研制的次声压力仓,用８Ｈｚ、１２０ｄＢ的次声按规定次数。每次作用２ｈ。采用蛋白定量和放免法行脑ＴＸＡ２、ＰＬＩ２稳定代谢产物血栓素Ｂ２（ＴＸＢ２）及６－酮     

支气管哮喘患者血小板活化及与肺功能的关系

花生四烯酸 (AA)的代谢产物血栓素 A2(TXA2)及前列环素 (PGI2)是调节血小板功能的重要因子 [1]。血栓素 B2(TXB2)及 6－酮－前列腺素 F1ɑ (6－ kPGF1ɑ )分别是其稳定物。血栓素 A2(TXA2)绝大部分 (80％ )以上,均来自血小板 [2];通过测定血浆中 TXB2的含量来反映 TXA2。研究证实 TXA2是支气管哮喘的重要介质之一 [3]。 TXA2/PGI2是一对平衡调节物,病理情况下, TXA2－ PGI2间失去平衡,引起支气管的收缩和肺激惹。本文通过测定支气管哮喘发作 (发作组 )和临床控制后 (缓解组 )患者的血浆 TXB2、 6－ kPGF1a含量及动…     

川芎嗪对妊娠期高血压综合征患者血浆血栓素A2/前列环素平衡的调节作用

目的 观察川芎嗪对妊娠期高血压综合征(PIH)患者血浆血栓素A2(TXA2)/前列环素(PGI2)平衡的调节作用.方法 选择50例轻中度PIH患者为川芎嗪治疗组,予以川芎嗪120 mg静脉滴注10 d,另取正常妊娠对照组50例.放射免疫法检测川芎嗪治疗组治疗前后TXA2和PGI2的稳定代谢产物血浆血栓素B2(TXB2)和6-keto-PGF1a含量的变化,正常妊娠对照组只测定1次.结果 与正常妊娠对照组相比较,川芎嗪治疗组患者血浆TXA2含量上升,而血浆PGI2含量下降(均P<0.05).经过川芎嗪治疗10 d后,患者血浆TXA2含量下降,而血浆PGI2含量上升(均P<0.05).结论 PIH患者存在TXA2/PGI2比值升高.川芎嗪治疗PIH患者的另一作用机制可能是通过降低TXA,含量和升高PGI2含量,从而纠正TXA2/PGI2比值失衡.     

支气管哮喘患者血小板活化及与肺功能的关系

花生四烯酸（AA）的代谢产物血栓素A2(TXA2）及前列环素（PGI2）是调节血小板功能的重要因子。栓素B2（TXB2）及6－酮－前列腺素F1α（6-kPGF1α）分别是其稳定物,血栓素A2（TXA2）绝大部分（80％）以上,均来自血小板;通过测定血浆中TXB2的含量来反映TXA2。研究证实TXA2是支气管哮喘的重要介质之一。TXA2／PGI2是一对平衡调节物,病理情况下,TXA2－PGI2间失去平衡,引起支气管的收缩和肺激惹。本通过测定支气管哮喘发作（发作组）和临床控制后（缓解组）患的血浆TXB2、6-kPGF1α含量及动脉血氧分压（PaO2),用力呼气1秒率（FEV1％）,以探讨支气管哮喘患血小板的活化状态。     

绝经前后妇女血浆血栓素A2和前列环素水平的变化

目的：为探讨绝经对妇女血浆血栓素A2(TXA2)和前列环素(PGI2）水平的影响。方法：将72例研究对象按月经情况分四组，即：月经正常组(Ⅰ)；月经紊乱组(Ⅱ)；绝经≤5年组(Ⅱ)；绝经>5年组(Ⅳ)。用同位素放射免疫方法集中测定各组妇女外周血浆TXA2、PGI2的稳定代谢产物血栓素B2(TXB2)及6-酮前列腺素F1。(6-K-PGF1α)的含量。结果：(1)各组妇女血浆TXB2及6-K-PGF1α水平无显性差异(P>0.05)；(2)各组妇女TXB2／6-K-PGF1α。的比值较恒定(1．04±0.05)。结论：绝经对妇女体内TXA2和PGI2的水平和稳定无明显影响。有血管舒缩不稳定症状(如潮热)的绝经前后妇女，由于其血浆TXA2／PGI2总保持动态平衡，故不会增加心血管疫病的发病风险。     

急性闭合性颅脑损伤病人脑脊液及血浆血栓素B2含量的变化及意义

原发性颅脑损伤后，神经细胞钙离子(Ca2^2)超载．膜磷脂水解，产生血栓素A2(TXA2)．TXA2(TXB2的活性前体)可引起脑血管收缩,降低脑血流量,减少脑组织对氧的摄取．引起继发性损害。我们检测了56例急性闭合性颅脑损伤病人．伤后7天由脑脊液(CSF)及血浆中血栓索B2(TXB2)含量．探讨其含量改变与继发性脑损害的关系。     

山莨菪碱对家兔全脑缺血再灌注脑组织TXA_2和PGI_2代谢的影响

目的　探讨山莨菪碱对家兔全脑缺血再灌注期间脑组织TXA2 和PGI2 代谢的影响。方法　 40只家兔随机分为假手术组、缺血组、缺血再灌注组、治疗组 ,采用“闭塞双侧颈总动脉和椎动脉 体循环低血压法”建立全脑缺血再灌注损伤模型 ,缺血 2 0min ,再灌注 2h ,通过放免法测定脑组织TXB2 、6 -keto -PGF1α含量及其比值。结果　缺血组脑组织TXB2 、6 -keto-PGF1α含量明显高于假手术组 (P <0 0 1,P <0 0 5 ) ;再灌注组脑组织TXB2 、TXB2 / 6 -keto -PGF1α比值明显高于缺血组 (P <0 0 1) ;而治疗组脑组织TXB2 及TXB2 / 6 -keto -PGF1α比值较缺血再灌注组显著降低 (P <0 0 1)。结论　脑缺血再灌注损伤与TXA2 /PGI2 比例失调有关 ;山莨菪碱具有抑制TXA2 合成 ,调节TXA2 -PGI2 平衡的作用     

久强脑立清对自发性高血压大鼠血浆血栓素A2和前列环素水平的影响

目的探讨久强脑立清 (JNQ )对自发性高血压大鼠 (SHR)血浆血栓素A2 (TXA2 )和前列环素 (PGI2 )水平的影响。方法设立JNQ低、中、高剂量 3个组 ,剂量分别为 0 13 3 g/kg、0 2 65 g/kg和 0 5 3 0g/kg ,SHR和正常Wistar大鼠对照组给予 1%羧甲基纤维素溶媒对照 ,分别灌胃给药 5周后 ,分离血浆 ,用放免法测定血浆中TXA2 和PGI2 的稳定代谢产物TXB2 和 6 keto PGF1α的水平。结果SHR血浆TXB2 及TXB2 /6 keto PGF1α(T/P)值明显上升 (P <0 0 1) ,PGI2 无明显变化 (P >0 0 5 )。经JNQ3种剂量治疗 5周后 ,SHR的血浆TXB2 均显著下降 ,并呈明显的剂量依赖关系 ,高剂量组SHR血浆 6 keto PGF1α水平也有明显提高 ,各治疗组T/P比值均下降。结论JNQ对SHR血浆TXA2 /PGI2 的平衡失调有明显的改善作用     

参麦对围手术期肝缺血再灌注损伤患者血浆血栓素A_2和前列环素I_2的调控作用

目的:观察参麦对肝缺血再灌注损伤患者血栓素A2(TXA2)和前列环素I2(PGI2)的调控作用。方法:将40例择期行肝叶切除的患者分为实验组和对照组。对照组在肝门阻断前30min静脉滴入5%葡萄糖盐水250mL,实验组在5%葡萄糖盐水250mL中加入参麦注射液2mL/kg体重。分别在肝门阻断前、肝门阻断末及肝门再开放60min时放射免疫法测定血浆血栓素B2(TXB2)和6-酮-前列腺素F1α(6-keto-PGF1α)浓度。结果:两组患者血浆TXB2、6-keto-PGF1α和TXB2/6-keto-PGF1α浓度均增加(P<0.05),但实验组增加幅度低于对照组(P<0.05),且肝门再开放60min后TXB2、6-keto-PGF1α和TXB2/6-keto-PGF1α已降到或低于肝门阻断前水平(P<0.05)。结论:血浆TXA2/PGI2比值升高,可能是肝缺血再灌注损伤机制之一。参麦对肝缺血再灌注损伤的保护作用可能与改善花生四烯酸代谢紊乱,抑制TXA2/PGI2比值升高有关。     

葛根素对心肌缺血-再灌注损伤兔乳酸脱氢酶活性变化的影响

目的:探讨心肌缺血-再灌注损伤(MIRI)时乳酸脱氢酶(LDH)活性的变化以及中医药的保护作用机制.方法:实验兔30只,随机分为对照组、盐水组和葛根素葡萄糖注射液(PGI)组,每组10只.制作MIRI模型,观察血清及心肌组织LDH活性、血栓素B2(TXB2)和6-酮-前列腺素F1α(6-keto-PGF1α)含量、TXB2/6-keto-PGF1α(T/K)比值变化及PGI对它们的影响.结果:MIRILDH活性进行性升高(P<0.05或P<0.01),心肌组织内LDH活性明显下降(P<0.01)而T/K比值显著增高(P<0.01);PGI能降低血清中升高的LDH活性,降低心肌组织中LDH活性和T/K比值,均有显著性差异(P<0.05和 P<0.01).结论:PGI可通过纠正TXA2与前列环素的平衡,对MIRI时LDH活性的异常改变起积极的调节作用,以达到心肌保护作用.     

乌司他丁对体外循环心脏手术患者TXA2和PGI2的影响

目的观察乌司他丁（UTI）对体外循环（CPB）心脏手术患者血栓素（TXA2）和前列环素（PGI2）的影响。方法将60例CPB择期心脏手术患者随机分为实验组和对照组，分别采用UTI1．2万U／kg稀释于10ml生理盐水中和等量生理盐水中，一次性加入CPB预充液中，分别于麻醉诱导后（L）、主动脉开放30min（T2）、术毕（T3）及术后6h（T4）4个时点，抽取桡动脉血用放射免疫法测定TXB2／6-keto—PGF1a浓度。结果CPB后两组患者T2、T3、T4血浆TXB2、TKG6-keto—PGF1a浓度均较T1浓度增加（P〈0．05），但实验组增加幅度低于对照组（P〈0．05），且术后6hTXB2、6-keto—PGF1a浓度己降到或低于术前水平（P〈0．05）。结论血浆TXA2和PGI2比值升高，可能是CPB后肺损伤的机制之一。乌司他丁对CPB后肺损伤的保，护作用可能与改善花生四烯酸代谢紊乱，抑制TXA2／PGI2比值升高有关。     

颌面部爆炸伤后组织血栓素A2和前列环素I2对兔脑的作用机制

Blastinjuryofneckandheadisamainwoundtypeinaccident，violenceandwarwound．Andtheskullwillbeimpactednecessarilyduringthosecourses．thromboxaneA２（TXA２）canincreaseresistingforceofcerebralbloodcirculationandprostacyclinI２（PGI２）canpre－ventthebrainviadilatingvessels犤１－２〗．ThehalflifeofTXA２andPGI２isshortinblood，andnoteasytodetectdirectly．Usuallydetectthestablenon－activityproduction－TXB２and６－ketop－PGF１αtorepresentTXA２andPGI２．HereweinvestigatethechangeofTXA２andP…     

颈髓损伤患者血小板活化因子、血栓素B_2和6-酮-前列腺素F_(1α)测定及其临床意义

目的：探讨急性颈髓损伤患者全血血小板活化因子（PAF）、血浆血栓素B2（TXB2）、6－酮－前列腺素F1a（6－keto－PGF1a）含量的动态变化及其临床意义。方法：分别采用定量生物分析法、放射免疫分析法检测了35例急性外伤性颈髓损伤患者全血PAF、血浆TXB2和6－keto－PGF1a的含量变化。结果：伤情越重、预后越差的患者，血液中PAF、TXB2含量和TXB2／6－keto－PGF1a（T／K）值在伤后早期升高越明显；8例颈髓损伤早期死于颈髓水肿、呼吸衰竭的患者，伤后当日全血PAF含量和T／K值分别为对照组的15．34倍和6．39倍。结论：伤后全血PAF、血浆TXB2和6－keto－PGF1a含量的动态变化反映脊髓损伤的严重程度及脊髓神经功能恢复状态。脂质炎性介质——PAF、TXB2和6－keto－PGF1a可能与急性颈髓水肿的病理生理过程有关。     

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。     

Effects of nitroglycerin on human vascular prostacyclin and thromboxane A2 generation

We examined the effects of NTG on human saphenous and umbilical vein PGI2 and TXA2 generation. Vascular rings from both types of vessels generated TXA2 in addition to PGI2. The treatment of vascular rings with NTG in concentrations of 5 to 1000 ng/ml and subsequent incubation with AA caused a significant increase in PGI2 in the supernatants, as identified by bioassay (platelet aggregation inhibition) and by measurement of 6-keto-PGF1 alpha (stable hydrolysis product of PGI2). The maximum increase in PGI2 was observed with therapeutic concentrations of NTG, i.e., 5 to 10 ng/ml. The levels of vessel wall-generated TXB2 (stable metabolite of TXA2) were not affected by NTG treatment. A prior incubation of vascular rings with indomethacin abolished the increase in PGI2 after NTG treatment. In contrast, incubation of vascular rings with OKY 1581 (selective TXA2 inhibitor) resulted in a significant additional increase in PGI2 release but no change in TXB2 levels after NTG treatment. These studies indicate important effects of NTG on vascular PGI2 generation but not on TXA2 generation.     

内皮素1和前列环素在脑梗死病变过程中的相互作用

Inrecentyears,theresearchoftheendocrinefunctionofvas-cularendothelialcellscausedpepole'sextensiveconcern,andal-readydiscoveredthatendothelin-1(ET-1)andprostacyclin(PGI2)ofendothelialcellssecretorytopossesregulatingthetensionofvasculardissepimentandtheproliferationofsmoothmusclecell.ThemotivethisinvestigationistryingtofindouttheclinicalsignificanceandpathogenesisofplasmaET-1andPGI2inthedevelopmentofis-chemiccerebralinfarction.1Subjectsandmethods1.1Subjects(1)Studygroup:Therewere37patients,…     

Increased renal thromboxane production in murine lupus nephritis.

To determine whether the amount of cyclooxygenase metabolites correlates with the development of lupus nephritis, intrarenal eicosanoid production was measured in autoimmune mice. Disease progression was related to the renal biosynthesis of prostaglandin (PGE2), prostacyclin (6 keto PGF1 alpha), and thromboxane (TXB2) using the MRL-lpr and NZB X NZW F1 hybrid mouse strains with predictably progressive forms of renal disease that mimic the human illness. Mice were evaluated for renal disease by measuring urinary protein excretion and renal immunopathological conditions and these features were related to renal eicosanoid production. These studies show that: (a) intrarenal synthesis of TXB2 increased incrementally in MRL-lpr and NZB X NZW F1 hybrid mice as renal function deteriorated and renal pathologic events progressed; (b) there were no consistent increases in the levels of two other cyclooxygenase metabolites, PGE2 or 6 keto PGF1 alpha; (c) increased TXB2 production occurred in the renal medulla, cortex, and within enriched preparations of cortical glomeruli; (d) when renal disease was prevented by pharmacologic doses of PGE2, intrarenal TXB2 did not increase; (e) administration of a dose of ibuprofen (9 mg/kg), a cyclooxygenase inhibitor capable of reducing 90% of platelet TXB2 without affecting intrarenal levels, did not retard the progression of renal damage. Taken together, these data indicate that the intrarenal level of TXB2 rises in relation to the severity of murine lupus nephritis. Furthermore, because of the potential deleterious effects of TXA2, enhanced production of this eicosanoid may be an important mediator of renal injury.     

Stimulation of prostacyclin synthesis by physical exercise in type I diabetes

We examined the effect of short- and long-term exercise on prostacyclin (prostaglandin I2 [PGI2]) and thromboxane A2 (TXA2) synthesis in type I (insulin-dependent) diabetic patients and healthy control subjects. PGI2 synthesis was assessed by determining the urinary excretion of 6-keto-PGF1 alpha and 2,3-dinor-6-keto-PGF1 alpha and TX synthesis by measuring TXB2 in serum and urine. In the resting state, prostanoid excretion and concentrations were similar in diabetic and control subjects. During 40 min of ergometric cycling exercise, the urinary excretion of 6-keto-PGF1 alpha (a hydration product of vasodilatory PGI2) increased 5.8-fold more in the 12 control subjects than in the 15 diabetic patients (P less than .02). Serum TXB2 concentration rose similarly in diabetic patients and control subjects (P less than .05). During a 75-km competitive cross-country ski race (7 h, 30 min), urinary excretion of 6-keto-PGF1 alpha rose 1.9-fold in 7 diabetic (P less than .05) and 3.3-fold in 10 control (P less than .001) subjects, whereas urinary dinor excretion, reflecting vascular PGI2 synthesis more closely, increased only in the control subjects (P less than .01). Urinary TXB2 excretion remained unchanged in both groups during long-term exercise. These data suggest that diabetic patients have normal PGI2 and TXA2 synthesis in the resting state but diminished PGI2 response to both acute and prolonged exercise.     

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.     

Influence of selective thromboxane synthetase blocker CGS-13080 on thromboxane and prostacyclin biosynthesis in whole blood: evidence for synthesis of prostacyclin by leukocytes from platelet-derived endoperoxides

Increase in thromboxane A2 (TXA2) generation has been proposed as a mechanism of dynamic vaso-occlusion and in vivo platelet thrombus formation. We have examined the effects of CGS-13080, an imidazole derivative, on rabbit and human TXA2-prostacyclin (PGI2) "balance." In rabbits given CGS-13080, serum levels of TXB2 (stable metabolite of TXA2) were inhibited 81% at 2 hours and 56% at 24 hours (both P less than or equal to 0.01). Collagen-induced platelet aggregation was inhibited at 2 hours after CGS-13080 administration. In contrast, serum levels of 6-keto-PGF1 alpha (stable hydrolysis product of PGI2) increased 587% compared with control values at 2 hours (P less than or equal to 0.01). Platelet and white blood cell counts were not significantly altered. In human blood incubated in vitro with CGS-13080, serum TXB2 was completely inhibited, whereas PGI2 generation was stimulated (both P less than or equal to 0.001). In other experiments, we demonstrated uptake of platelet-generated cyclic endoperoxides by leukocytes and generation of PGI2 in the presence of CGS-13080 but not indomethacin. Thus, CGS-13080 inhibits TXA2 and stimulates PGI2 production in rabbit and human blood. Increase in PGI2 generation with TXA2 inhibition may be of potential benefit in conditions characterized by platelet hyperactivity.