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1.
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  相似文献   

2.
J Shen 《中华医学杂志》1991,71(9):488-91, 34
We studied the effects of the calcium channel blocker, verapamil on experimental acute pancreatitis (AP) in rats. The pancreatic blood flow (PBF) and pancreatic tissue perfusion (PTP) were measured after induction of AP. At the same time, the plasma levels of TXB2 and 6-keto-PGF1 alpha were determined by radioimmunoassay. The survival rate and the mean survival time after induction of AP were determined and the pancreatic histology was examined by light and electron microscopy. The results demonstrated a significant early fall in PBF and PTP, a marked increase in TXB2 levels and a slight increase in 6-keto-PGF1 alpha after induction of AP. Treatment with 0.1 mg/100 g verapamil significantly increased PBF and PTP, and decreased TXB2, resulting in a normalization of TXB2/6-keto-PGF1 alpha ratio. The treated animals also exhibited significant increase in the survival rate and the survival time. They also showed decrease in the severity of pancreatic hemorrhage and necrosis, and in the damage to the cellular ultrastructures. These data suggest that calcium blockade increases PBF and PTP, limits the prostanoid imbalance in the early phase of AP, and may influence the development of experimental acute pancreatitis in rats.  相似文献   

3.
In the femoral head necrosis model rabbit induced by endotoxin combined with methylprenisolone, the dynamical changes of plasma TXB2 and 6-keto-PGF1αcontents were observed. As a result, microscopic examination showed that in the model group, bone trabeculae became fine, empty bone lacunae increased,and osteoblasts in number decreased; the ratio of TXB2 and 6-keto-PGF1α was out of balance, and these changes worsened gradually with the lapse of time; Compound Sheng Mai Cheng Gu Capsules (复方生脉成骨胶囊) could reverse femoral head necrosis, protect the vascular endothelial cells, recover the balance of TXB2 and 6-keto-PGF1α. It is concluded that the hormone-induced femoral head necrosis is closely related with blood stasis, and that the Chinese drugs for activating blood circulation and removing blood stasis can prevent the femoral head from development of necrosis.  相似文献   

4.
Z Liu 《中西医结合杂志》1990,10(9):543-4, 517-8
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.  相似文献   

5.
EffectsofTangshenkangCapsuleonDisbeticNephropathy¥WANGXian-bo;SANGYan;HANQingGUOBao-ruiandLIUXi-xin(TheFirstAffiliatedHospita...  相似文献   

6.
为观察先兆早产患者硫酸镁治疗前后宫颈粘液6-酮-PGF1α,TXB2变化与疗效的关系,探讨其能否作为判断早产疗效及预后的指标,采用放射免疫法检测28例先兆早产患者与硫酸镁治疗前后宫颈粘液6-酮-PGF1α和TXB2水平。结果:治疗成功的患者其宫颈粘膜6-酮-PGF1α与TXB2水平较治疗前明显下降,6-酮-GPF1α与TXB2比值明显升高;治疗失败的患者其宫颈粘液6-酮-PGF1α和TXB2水平较  相似文献   

7.
ProtectiveEffectofHerbaDracocephalionLipoperoxidationDarnageinPalientswithCoronaryHeartDiseaseYangShui-xiang(杨水祥);LiTian-de(李...  相似文献   

8.
刘泽  刘晓光 《广东医学》2000,21(9):726-727
目的 探讨抗高血压因子(AHF)对心肌缺血损伤保护的机理。方法 以导丙肾上腺素性心肌损伤大鼠为模型,观察AHF对其心肌丙二醛、钙含量、血栓素B2和6-酮-前列腺素F1a(6-keto-PGF1a)的影响,结果 AHF保护组较心肌损伤组上述指标分别减少46.0%,62.2%和58.6%,而6-keto-PGF1a增加123.4%(均P〈0.05)。心肌病理损伤程度也显著减轻(P〈0.05)。结论 A  相似文献   

9.
PGI2,TXA2与先兆早产的关系研究   总被引:1,自引:1,他引:0  
为探讨前列环酸(PGI2)和血栓素(TXA2)与先兆早产的关系,采用放射免疫法分别测定了先兆早产和足月临产孕妇血及宫颈粘液中6-酮-PGF1α、TXB2和孕酮的浓度,并与相对应孕周的孕妇进行比较。结果:与对照组相比,先兆早产组及足月临产组的血浆TXB2和6-酮-PGF1α水平明显升高(P〈0.001),6-酮-PGF1α/TXB2比值降低(P〈0.001),而孕酮水平则无显著性差异(P〉0.05)  相似文献   

10.
目的研究生理剂量二氢睾酮(dmydrotestosferone,DHT)和其受体对雄性大鼠血小板激活、TXA2/PGI2平衡与细胞内钙离子浓度的调节。方法血浆睾酮(testosterone,T)应用Advia Centaur免疫检测系统测定(Bayer,Ger-many),血浆DHT应用酶联免疫试剂盒(ELISA kit)推荐方法检测。应用血小板聚集仪测定血小板聚集、血小板黏附仪测定血小板黏附。应用放免法测定TXB2和6-Keto—PGF1α。应用流式细胞仪测定血小板内钙离子浓度。结果去势雄性大鼠每日补充DHT(0.25mg/rat)使其DHT浓度达到生理水平,而且与氟他胺(flutamide)(每两日注射1次5mg/rat)联用不影响DHT浓度达到生理水平。DHT(2nM)显著抑制二磷酸腺苷(adenosine diphosphate,ADP)诱导的血小板的聚集、黏附。氟他胺预处理血小板之后,ADP诱导的血小板的聚集、黏附再次增加。去势雄性大鼠每日补充DHT(0.25mg/rat)降低TXB2和6-keto-PGF1α。的比例,然而两日补充一次氟他胺(5mg/rat)再次增加TXB2和6-keto-PGF1α。的比例。DHT(2nM)明显降低ADP诱导的血小板内钙离子浓度。然而,氟他胺预处理血小板之后ADP诱导的血小板内钙离子浓度再次增加。结论生理水平二氢睾酮介导其受体调节雄性大鼠ADP诱导的血小板聚集、黏附与其调节TXA2/PGI2平衡和血小板内钙离子浓度有关。  相似文献   

11.
目的:观察灯盏花素治疗重症急性胰腺炎(Severe acute pancreatitis,SAP)的作用。方法:将40例SAP患者随机分为A组(20例)和B组(20例),同时以健康志愿者20例作为正常对照组。A组采用常规治疗,B组采用常规治疗+灯盏花素注射液治疗,以放射免疫法测定血浆ET、TXB2、6-keto-PGF1α浓度及TXB2/6-keto-PGF1α比值,测定A、B两组APACHEⅡ评分及胰腺Balthazar CT分级评分。结果:(1)血浆6-keto-PGF1α、ET、TXB2及TXB2/6-keto-PGF1α比值:SAP患者血浆6-keto-PGF1α浓度显著低于正常对照组,而血浆ET、TXB2浓度及TXB2/6-keto-PGF1α比值显著高于正常对照组(P〈0.01);B组入院后8天与B组入院时及A组入院后8天比较,血浆6-keto-PGF1α浓度显著上升,而血浆ET、TXB2浓度及TXB2/6-keto-PGF1α比值,均显著下降(P〈0.01~0.05)。(2)APACHE II评分和胰腺Balthazar CT分级评分:A、B两组入院后8天与入院时比较,两评分均显著下降(P〈0.01~0.05);B组入院后8天与A组入院后8天比较,两评分均显著降低(P〈0.01~0.05)。结论:灯盏花素可能通过改善SAP患者的微循环障碍,从而对SAP起治疗作用。  相似文献   

12.
目的1.观察原发性血小板增多症(primary thrombocytosis,PT)患者血小板功能指标CD62P、PAC-1、TXB2、6-keto-PGF1α及TXB2/6-keto—PGF1α比值的变化。2.观察PT患者血小板功能指标与血小板数量的相关性。3.探讨可能导致P,r患者血栓发生的机制。方法1.流式细胞仪(FCM)测定血小板表面的CD62P,PAC-1水平。2.ELISA方法测定血浆血栓素A2(TXA2)代谢产物TXB2和前列环素(PGI2)代谢产物6-keto—PGF1α水平。3.观察和比较各组血小板功能的变化及其与血小板数量变化的关系。结果1.阿患者血小板功能指标均高于正常组,P〈0.01。2.胛患者血小板功能指标变化与血小板数量相关性分析结果提示:PT患者各项血小板功能指标与血小板数目之间不存在相关性,P〉0.05。结论阴患者除血小板数量显著增多外,其血小板各项功能指标亦有明显异常。研究结果表明:PT患者发生血栓的危险因素除与其血小板数目异常增多有关外,还与血小板功能异常活化(血小板活化指标CD62P、PAC-1异常增高)及血浆TXB2、6-keto-PGF1α平衡失调(TXB2/6-keto—PGF1α比值异常增高)有关。而明患者血小板功能指标与其血小板数量之间不存在相关性,故治疗原发性血小板增多症除按常规治疗予以降低血小板数量外,还应同时注意对血小板功能的干预治疗。  相似文献   

13.
  目的观察参附注射液对局灶性脑缺血-再灌注大鼠脑组织中超氧化物歧化酶(SOD)活性及丙二醛(MDA)、血栓素B2(TXB2)、6-酮-前列腺素F1a(6-keto-PGF1a)含量的影响,探讨参附注射液对脑的保护机制。方法清洁级雄性SD大鼠60只,随机分为3组假手术组(Sham组,n=20)、脑缺血再灌注组(IR组,n=20)、参附注射液预处理组(SFI组,n=20)。采用线栓法制备大鼠大脑中动脉闭塞后再灌注(MCAOR) 模型, 观察大鼠MCAOR 时神经功能状态,TTC 染色测脑梗死面积, 同时测定血浆中MDA、SOD、TXB2、6-keto-PGF1a的变化。结果参附注射液能有效改善MCAOR大鼠神经功能缺失症状,明显减小梗死灶。IR组与假手术组比较,血清中SOD活性降低,MDA、TXB2含量增加,6-keto-PGF1a含量降低(P<0.05);参附治疗组与IR组比较,SOD活性增高,MDA、TXB2含量下降,6-keto-PGF1a含量增高(P<0.05)。结论参附注射液对脑缺血再灌注损伤引发的自由基损伤有保护作用,并且能够纠正TXB2/6-keto-PGF1a平衡,达到对脑缺血再灌注大鼠的脑保护作用。  相似文献   

14.
破瘀通脉散对缺血性脑损伤的保护作用   总被引:3,自引:0,他引:3  
为探讨破瘀通脉散对急性脑缺血的保护作用与机理。本实验观察破瘀通脉散对局灶脑缺血再灌注大鼠脑梗塞范围及6—酮前列腺素(6—keto—PGF_1α)血栓素B_2(TXB_2)与肿瘤坏死因子(TDF)的影响.结果表明缺血脑组织6—kcto—PGF_1α含量降低,TXB_2及TNF升高,破瘀通脉散通过改善脑局部TXA_2/PCI_2,比例对缺血性脑损伤起保护作用。  相似文献   

15.
本实验以大鼠中等度(50g-cm)脊髓损伤模型,研究吲哚美辛对脊髓损伤后TXA_2/PGI_2变化的影响。结果表明,于脊髓损伤后30min静脉注射大剂量吲哚美辛(10mg/kg)可显著降低TXB_2含量,使6-keto-PGF_1α含量相对升高,并可减轻和延缓脊髓损伤后脊髓血流量减少,大鼠后肢运动功能明显改善。提示吲哚美辛具有防止脊髓损伤后TXA_2/PGI_2平衡紊乱的作用,从而改善脊髓血流量,促进神经功能恢复。  相似文献   

16.
In the femoral head necrosis model rabbit induced by endotoxin combined with methylprenisolone, the dynamical changes of plasma TXB2 and 6-keto-PGF1αcontents were observed. As a result, microscopic examination showed that in the model group, bone trabeculae became fine, empty bone lacunae increased,and osteoblasts in number decreased; the ratio of TXB2 and 6-keto-PGF1α was out of balance, and these of TXB2 and 6-keto-PGF1α. It is concluded that the hormone-induced femoral head necrosis is closely related with blood stasis, and that the Chinese drugs for activating blood circulation and removing blood stasis can prevent the femoral head from development of necrosis.  相似文献   

17.
目的 观察兔肾缺血再灌注损伤时血栓素A2(TXA2)/前列环素(PGl2)的变化,探讨JII芎嗪的保护作用及其机制.方法 将30只日本大耳白兔随机分为3组:假手术对照组(对照组)、缺血再灌注组(再灌注组)、缺血再灌注+川芎嗪注射液组(川芎嗪组),同时予再灌注组和川芎嗪组复制兔肾缺血再灌注损伤动物模型,并在缺血前、缺血1h、再灌注5 h时分别经颈总动脉抽血检测TXA2和PGl2降解后的代谢产物TXB2和6-酮-前列腺素F1α(6-keto-PGF1α)含量,计算其比值;实验结束时检测肾组织TXB2和6-keto-PGF1α含量与比值,并观察超微结构变化,作对比分析.结果 再灌注组缺血后各时点的血浆TXB2水平均较对照组明显增高(均P〈0.01),川芎嗪组缺血后各时点的血浆TXB2含量均较再灌注组和对照组明显降低(均P〈0.01);川芎嗪组血浆和肾组织TXB2/6-keto-PGF1α水平均较再灌注组明显降低(均P〈0.01);再灌注组肾小球毛细血管和内皮细胞及近曲小管上皮细胞超微结构均严重受损,而川芎嗪组虽大部分肾组织上述部位均存在不同程度损伤性改变,但均较再灌注组明显减轻.结论 川芎嗪可抑制血小板释放TXA2,调控TXA2/PGl2的平衡,遏制无复流现象,对肾缺血再灌注损伤具有防治作用.  相似文献   

18.
目的探讨前列酸类(PGs)在表皮生长因子(EGF)促进急性肾小管坏死(ATN)肾小管修复过程中的作用,研究外源性EGF对大鼠庆大霉素(GM)中毒性ATN肾组织PGs变化的作用及其与肾小管上皮细胞DNA合成的关系.方法Wis-tar大鼠分为3组:正常对照组(NL组,n=7);GM组(G组,n=20):予以GM200mg/kg×3 d;GM+EGF组(G+E组,n=19):GM 200mg/kg×3 d+EGF20μg.分别在注射后第1、4、8、12、15天测定肾小管上皮细胞的3氚-胸腺核苷掺入率(3HTdR)、血清肌酐(Scr)、肾组织前列腺素2(PGE2)、前列腺素6酮(6-keto PGF1α)、前列环素(TXB2)的含量.结果G+E组动物的3HTdR掺入率均较G组动物明显增加,以在给药后第4天最为显著.G+E组动物的肾脏病理损害较G组有所改善,但Scr水平较G组无差别.G+E组动物肾组织6-keto-PGF1α水平也比G组明显增高,TXB2水平比G组动物降低.G+E组动物肾组织PGE2和6-keto-PGF1α的水平与肾小管上皮细胞的3HTdR掺入率均呈显著正相关.结论(1) ATN时肾组织PGE2、6-keto-PGF1α和TXB2水平发生的动态变化可能与肾小管修复的细胞增殖有一定关系.(2)外源性EGF可能有促进肾组织6-keto-PGF1α释放,抑制TXB2合成的作用,该作用可能与EGF促进ATN肾小管上皮细胞修复有关.  相似文献   

19.
本文对血栓素、前列腺环素在实验性呼吸窘迫综合征中的变化和相互关系进行了研究,并比较了肺动脉、左心房血浆和肺组织中的含量变化。实验分两组进行,Ⅰ组盐水对照,Ⅱ组实验组。动物注射油酸(0.045ml/kg)后,血浆及肺组织中的TXB_2(TXA_2的稳定代谢产物)立即升高,6-酮-PGF_1α(PGI_2的稳定代谢产物)则较晚上升,TBX_2/6-酮-PGF_1α先上升,后下降。结果提示:(1).TXA_2和PGI_2在油酸ARDS模型中是显著增加的;(2)血浆中与肺组织中的值有时不一致;(3)TXA_2/6-酮-PGF_1α在ARDS的发病机理中可能有重要作用。  相似文献   

20.
目的观察针刺关元穴对寒凝证类痛经大鼠三阴交穴区温度(双侧)的影响并探讨其与TXB_2/6-keto-PGF_(1a)有关的机制。方法将大鼠随机分为盐水组、寒凝证类痛经模型组(简称模型组)、针刺关元组。采用全身冷冻法结合苯甲酸雌二醇和缩宫素注射法造模,用红外热成像方法检测各组大鼠左右两侧三阴交穴区0、5、10、20、30、40、50、60 min各时间点温度,同时用ELISA法测定血浆TXB_2和6-keto-PGF_(1a)含量。结果盐水组在基础温度、0~60 min各个时间点,大鼠左右三阴交穴区温度平衡(P0.05);模型组在5~60 min各个时间点,大鼠左右三阴交穴区温度失衡(P0.05,P0.01);针刺关元组在基础温度、0~30 min大鼠左右三阴交穴区温度失衡(P0.05),40~60 min逐渐趋近平衡(P0.05)。与盐水组比较,模型组TXB_2/6-keto-PGF_(1a)比值明显升高(P0.05);与模型组比较,针刺关元组TXB_2/6-keto-PGF_(1a)比值明显降低(P0.05)。结论寒凝证类痛经大鼠左右三阴交穴区温度失衡;针刺关元穴能调节其失衡状态,且调节需要一定的时间过程,在针刺结束后10~40 min作用显著,其内在机制与针刺调节体内血管舒缩物质TXB_2/6-ketoPGF_(1a)比值的失衡有关。  相似文献   

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