雌激素缺乏引起雌性SD大鼠血小板激活

目的 研究雌激素缺乏对雌性SD大鼠血小板聚集功能的影响及其与一氧化氮相关的作用机制.方法 雌性SD大鼠随机分为假手术组、卵巢切除组以及卵巢切除补充雌激素组,分别施行假手术、卵巢切除术以及在卵巢切除术后第3天开始皮下注射补充雌激素,药物补充4周后处死动物,提取血清检测血清雌激素水平,提取富小板血浆测定血小板聚集功能,并用ELISA方法测定血浆中一氧化氮生物活性指标环磷酸鸟苷的水平.结果 卵巢切除组雌性SD大鼠血清雌激素水平明显降低,雌激素补充使卵巢切除补充雌激素组动物的雌激素水平回复到假手术组状态.卵巢切除组雌性SD大鼠血小板聚集率显著升高;卵巢切除补充雌激素后血小板聚集率较前者明显回落,但仍高于假手术组聚集水平;血浆中环磷酸鸟苷水平在卵巢切除组显著下降,补充雌激素后血浆中环磷酸鸟苷水平与假手术组差异无显著性.结论 雌激素缺乏会促进雌性SD大鼠的血小板聚集,其机制可能与血浆中一氧化氮/环磷酸鸟苷水平下降有关.     

高氟摄入后大鼠骨骼肌环核苷酸的变化及镁硒的影响

雄性Ｗｉｓｔａｒ大鼠腹腔ＮａＦ实验表明，亚急性氟中毒大鼠肌骼肌组织环磷酸腺苷（ＣＡＭＰ）水平明显市长中，环磷酸鸟苷（ＣＧＭＰ）水平下降，ＣＡＭＰ／ＣＧＭＰ升高。加镁后，由于ＣＧＭＰ水平升高，使ＣＡＭＰ／ＣＧＭＰ下降，这一作用可能与镁拮抗指一有关。而硒对这一生理过程无明显影响。     

心脏环磷酸腺苷和环磷酸鸟苷的受体调节及其交互作用

环磷酸腺苷 (cAMP)和环磷酸鸟苷 (cGMP)在心脏既相互依存 ,又相互拮抗 ,共同维持着心脏信号转导和功能活动的完整性 ,本文就近年来二者的受体调节和交互作用的研究进展予以综述。     

依那普利和氯沙坦对自发性高血压大鼠肾皮质环核苷酸水平的影响

目的　观察肾脏环磷酸腺苷 (cAMP)、环磷酸鸟苷 (cGMP)和一氧化氮 (NO)水平与高血压的关系 ,以及依那普利和氯沙坦降压治疗对自发性高血压大鼠 (SHR)肾皮质cAMP、cGMP和NO水平的影响。方法　 14周龄雄性SHR分三组 (n=6) :依那普利组 15mg·kg- 1·d- 1灌胃 ;氯沙坦组 3 7 5mg·kg- 1·d- 1灌胃 ;SHR对照组以等量蒸馏水灌胃。Wistar kyoto(WKY)对照组亦以等量蒸馏水灌胃。采用放射免疫法及Griess法检测肾皮质cAMP、cGMP、血管紧张素Ⅱ (AngⅡ )和NO代谢产物亚硝酸盐 (NO3 - )水平。结果　SHR对照组肾皮质AngⅡ含量较WKY组显著升高 (P <0 0 1) ;与SHR对照组相比 ,依那普利组AngⅡ含量显著降低 (P <0 0 1) ,氯沙坦组AngⅡ含量增加 (P <0 0 5)。与WKY相比 ,SHR对照组cAMP水平低于WKY组 (P <0 0 1) ,依那普利组cAMP水平明显高于SHR对照组 (P <0 0 5) ,氯沙坦组cAMP较SHR对照组有升高趋势 ,但无显著性差异 (P >0 0 5) ;SHR对照组肾皮质NO3 - 、cGMP含量较WKY组显著减少 (P <0 0 1) ;依那普利治疗组NO3- 、cGMP含量较SHR对照组显著增加 (P <0 0 1) ,氯沙坦组与SHR对照组相比 ,NO3 - 、cGMP含量增加(分别为P <0 0 1,P <0 0 5) ,各组NO3- 水平与cGMP水平呈正相关 (r =0 8689,P <0 0 1)。结论　SHR肾     

中华分支睾吸虫和猪囊尾蚴的匀浆环磷酸腺苷(cAMP)和环磷酸鸟苷(cGMP)的测定

用放射免疫测定法测定了9份华支睾吸虫和9份猪囊尾蚴匀浆中cAMP和cGMP的含量。cAMP的平均值各为82.1±7.26PM/10mg蛋白质和58.5±4.28pM/10mg蛋自质;cGMP的平均值各为20.1±2.4PM/10mg蛋白质和18.8±2.3pM/10mg蛋白质。结果提示这两种寄生虫虫体匀浆中cAMP和cGMP的测定,可能有助于对寄生虫代谢的调节机制的了解,并为寄生虫虫体内存在着cAMP第二信使提供了有力的证据。     

雌激素对高糖环境兔血管内皮功能影响的研究

高糖组及高糖＋17β-雌二醇（E2）组分别孵育腹主动脉环6小时，结果显示高糖引起血管内皮舒张反应减弱，环磷酸鸟苷（cGMP）含量和一氧化氮合酶（NOS）活性降低（P〈0．001）；而E2使高糖作用下内皮舒张反应增强，cGMP含量和NOS活性增加（P〈0．05）。     

一氧化氮在高脂饲养兔胸主动脉的变化和意义

观察高脂饲养兔胸主动脉血管环对去甲肾上腺素（ＮＥ）的反应性及环磷酸鸟苷（ｃＧＭＰ）含量的变化。结果表明其对ＮＥ的反应性降低，组织ｃＧＭＰ的含量减少。左旋精氨酸（Ｌ－Ａｒｇ）和硝普钠（ＳＮＰ）可恢复此反应性，而一氧化氮合成酶（ＮＯＳ）阻滞剂Ｌ－硝基精氨酸（Ｌ－ＮＮＡ）却加重其降低的反应性。提示高脂饲养兔血管环中的一氧化氮（ＮＯ）减少，Ｌ－Ａｒｇ及ＳＮＰ可以逆转之，暗示Ｌ－Ａｒｇ／ＮＯ通路障碍可能是动脉粥样硬化的又一机理。     

依那普利和氯沙坦对自发性高血压大鼠肾皮质环核苷酸水平的影响

目的观察肾脏环磷酸腺苷(cAMP)、环磷酸鸟苷(cGMP)和一氧化氮(NO)水平与高血压的关系,以及依那普利和氯沙坦降压治疗对自发性高血压大鼠(SHR)肾皮质cAMP、cGMP和NO水平的影响.方法 14周龄雄性SHR分三组(n=6)依那普利组15 mg*kg-1*d-1灌胃;氯沙坦组37.5 mg*kg-1*d-1灌胃;SHR对照组以等量蒸馏水灌胃.Wistar-kyoto(WKY)对照组亦以等量蒸馏水灌胃.采用放射免疫法及Griess法检测肾皮质cAMP、cGMP、血管紧张素Ⅱ(AngⅡ)和NO代谢产物亚硝酸盐(NO3-)水平.结果 SHR对照组肾皮质Ang Ⅱ含量较WKY组显著升高(P<0.01);与SHR对照组相比,依那普利组Ang Ⅱ含量显著降低(P<0.01),氯沙坦组Ang Ⅱ含量增加(P<0.05).与WKY相比,SHR对照组cAMP水平低于WKY组(P<0.01),依那普利组cAMP水平明显高于SHR对照组(P<0.05),氯沙坦组cAMP较SHR对照组有升高趋势,但无显著性差异(P>0.05);SHR对照组肾皮质NO3-、cGMP含量较WKY组显著减少(P<0.01);依那普利治疗组NO3-、cGMP含量较SHR对照组显著增加(P<0.01),氯沙坦组与SHR对照组相比,NO3-、cGMP含量增加(分别为P<0.01,P<0.05),各组NO3-水平与cGMP水平呈正相关(r=0.8689,P<0.01).结论 SHR肾皮质cAMP、cGMP 显著低于WKY,依那普利和氯沙坦均可升高SHR的cGMP水平,依那普利还可改善SHR肾cAMP代谢.     

粘合素抑制急性心肌梗死血小板聚集抗血栓形成的研究

研究的疾病　急性心肌梗死。目　　的　为了评价急性心肌梗死患者应用ｔＰＡ、肝素和阿司匹林治疗时 ,联用血小板抑制剂粘合素对再灌注、出血和急性心肌梗死病人的临床事件的影响。设　　计　安慰剂对照 ,剂量递增 ,多中心。病人资料　 180例病人 ,18～ 75岁 ,急性心肌梗死发作 6ｈ内。排除标准 :体重 >12 5ｋｇ ,出血体质 ,严重高血压 ,当前华法林治疗 ,贫血 ,血小板减少 ,肾功能衰竭 ,最近非加压性血管穿刺 ,2周内≥ 10ｍｉｎ的心肺复苏 ,6月内的严重创伤 ,或者脉管炎。随　　访　第一个 2 4ｈ内连续 12导联数字心电图监测 ,在开始溶栓治…     

复合维生素B对糖尿病周围神经病变大鼠坐骨神经的传导速度及cAMP、cGMP含量的影响

目的探讨复合维生素B对糖尿病周围神经病变（DPN）大鼠坐骨神经的传导速度及cAMP、cGMP含量的影响。方法95只健康wistar大鼠,随机选取正常对照30只,其余65只以STZ腹腔注射建立糖尿病（DM）大鼠模型。将DM大鼠随机分为糖尿病对照组32只和复合维生素B治疗组33只,分别给予生理盐水和复合维生素B（20mg／kg）灌胃,连续8周,观察药物对DPN大鼠坐骨神经的传导速度及cAMP、eGMP含量的影响。结果复合维生素B治疗组大鼠坐骨神经传导速度明显提高,坐骨神经内cAMP、eGMP含量明显增加。结论复合维生素B对DPN大鼠周围神经功能有明显的保护作用。     

Ditazole activity and its interaction with urokinase on experimental thrombosis.

The effect of ditazole, a new antiaggregant oxazole derivative as well as its possible interaction with urokinase on the formation of electrically induced thrombus, was assayed in rabbits. The activity of ditazole in reducing thrombus weight was comparable to that of aspirin. In the ditazole- or aspirin-treated animals, the microscopical examination of the thrombus showed a reduction in the fibrin component, and well-isolated platelets not undergoing a viscous metamorphosis were present. Urokinase, administered in combination with these antiaggregant drugs, did not induce a further reduction in thrombus weight. However, this additional treatment did induce clearly visible lytic areas and histological modifications as observed with the antiaggregant drugs. These data suggest that the antiplatelet drug ditazole may be an effective antithrombotic agent in man and could facilitate the penetration of urokinase into the thrombus.     

血管抑素对新生血管的作用及其机制研究进展

血管抑素作为近年来发现的一种血管生成抑制剂,对肿瘤及眼部新生血管具有较强的抑制作用,该文就其在新生血管中的作用作简单综述。     

Effect of aspirin upon experimental coronary and non-coronary thrombosis and arrhythmia

The effect of aspirin upon platelet function led to speculation on the potential effects of salicylates upon arterial thrombogenesis, in which platelets play a primary role. Aspirin was given by mouth or intravenously before attempting induction of coronary or femoral artery thrombosis in dogs by means of a catheter electrode. The incidence of thrombus formation in all animals receiving aspirin was comparable to that of the control groups. Although in several animals of coronary thrombus group receiving aspirin, the thrombus was smaller than in the controls, this was not statistically significant. An unexpected finding was the distinct decrease in incidence of arrhythmias and ventricular fibrillation in the coronary thrombus group treated with aspirin. The reason for the differences is not clear at this time.     

大承气汤治疗大鼠实验性急性胰腺炎肠功能障碍的机制研究

目的 探讨大承气汤治疗大鼠实验性急性胰腺炎(AP)肠功能障碍的可能机制.方法 将72只成年SD大鼠随机分为假手术组(SO组)、胰腺炎组(AP组)和大承气汤治疗组,每组24只.经胆胰管内加压注射3.5%牛磺胆酸钠0.1 ml/100 g体重制备AP模型,治疗组在造模前给予大承气汤按2 g/100 g体重剂量灌胃1次,AP组和SO组则灌注等量0.9%氯化钠溶液.每组于造模后3、6、12 h各处死8只大鼠并立即心脏取血,检测血清淀粉酶水平,酶联免疫吸附试验检测血清5-羟色胺(5-HT)含量.同时取6 h时间点各组大鼠距屈氏韧带10 cm空肠、末端回肠及乙状结肠组织,采用RT-PCR和Western印迹法检测肠黏膜中5-HT_3、5-HT_4mRNA及蛋白表达情况.结果 ①造模后AP组和治疗组血清淀粉酶、5-HT水平均明显高于SO组(P<0.01),且每个时间点治疗组均较AP组显著降低(P<0.05);AP组和治疗组5-HT水平均呈现出先升后降趋势.②与SO组相比,AP组5-HT_3、5-HT_4mRNA及蛋白表达水平在空肠、末端回肠及乙状结肠均明显下降(P<0.01);与AP组比较,治疗组各部位5-HT_4mRNA及蛋白表达均增高(P<0.05),而5-HT_3 mRNA 及蛋白表达则未增加.结论 5-HT升高及其受体降低可能是AP发生肠功能障碍的原因之一,而大承气汤治疗的主要作用可能是通过增加5-HT_4表达以改善肠功能,可作为AP肠功能障碍的治疗方法之一.     

Effects of oxymatrine on experimental hepatic fibrosis and its mechanism in vivo

AIM: Hepatic fibrogenesis has close relation with hepatic stellate cells (HSC)and tissue inhibitors of metalloproteinase (TIMP). Oxymatrine (OM) is a kind of Chinese herb that is found to have some effects on liver fibrosis. We aimed to determine the effects of OM on hepatic fibrosis and explore the possible mechanism. METHODS: Thirty-two rats were randomly divided into four groups; 16 were used to develop hepatic fibrosis by carbon tetrachloride (CCI4) and treated with or without OM, and 16 were used as controls. The expression of tissue inhibitor of metalloproteinase-1 (TIMP-1) and α-smooth muscle actin (α-SMA) in the livers of rats was detected by immunohisto-chemical assay. Liver pathology was determined by H&E staining and reticulum staining. RESULTS: In CCl4-injured rats, the normal structure of lobules was destroyed, and pseudolobules were formed. Hyperplasia of fibers was observed surrounding the lobules. While the degree of fibrogenesis in liver tissues was significantly decreased in those rats with OM-treatment compared with those without OM treatment. The pseudolobules were surrounded by strong, multi-layer reticular fibers, which netted into pseudolobules in CCl4-injured rats, however, there was a significant decrease in reticular fibers in OM-treated rats. The expression of TIMP-1 in hepatic cells was weak in control groups, but strong in CCl4-injured groups, however, the expression of TIMP-1 was significantly inhibited by OM (F = 52.93, P<0.05). There was no significant change in the expression of α-SMA between CCl4-injured rats with or without OM treatment (F= 8.99, P>0.05). CONCLUSION: OM effectively inhibits CCl4-induced fibrogenesis in rat liver tissues, probably by reducing the expression level of TIMP-1.     

Effect of extra virgin olive oil on experimental thrombosis and primary hemostasis in rats

BACKGROUND AND AIM: Olive oil is a particular source of fat in the Mediterranean diet, which is associated with a lower incidence of cardiovascular disease. We investigated the possible antithrombotic role of extra virgin olive oil as a single dietary modification in experimental thrombosis and primary hemostasis models in rats. METHODS AND RESULTS: Two different groups of animals were studied: one fed a usual diet (control group) and the other a diet enriched with extra virgin olive oil (3%; weight/weight). After six weeks feeding, arterial thrombosis was initiated by inserting an artificial prosthesis (or "aortic loop") into the aorta, and venous thrombosis was induced by ligating the inferior vena cava. "Template" bleeding time (BT) was measured, as well as factor VII coagulant activity (FVII:C) and fibrinogen levels. The animals fed the olive oil enriched diet showed a significant delay in the thrombotic occlusion of the "aortic loop" (99 +/- 5 h vs 82 +/- 5 h, p < 0.04), a lower incidence of venous thrombosis (57% vs 86%; p < 0.05) and a prolonged BT (154 +/- 7 sec vs 122 +/- 4 sec; p < 0.01) in comparison with the control group. They had lower plasma fibrinogen concentrations (209 +/- 5 mg/dL vs 233 +/- 4 mg/dL; p < 0.01) but similar FVII:C levels (119 +/- 5% vs 108 +/- 5%; p = NS) despite their lower triglyceride concentrations (52 +/- 5 mg/dL vs 79 +/- 10 mg/dL; p < 0.05). CONCLUSIONS: This study provides the first in vivo experimental evidence of the thrombosis prevention properties of olive oil, which are possibly mediated by reduced fibrinogen concentrations and impaired platelet/vessel wall interactions.