中风毒邪论与神经保护治疗的研究

中风毒邪论是一种与传统中医中风病理有所不同的理论 ,在中风毒邪论指导下形成解毒通络方是较为理想的神经保护剂 ,可解决目前神经保护治疗的主要障碍 ,有望成为提高中医治疗中风急性期疗效的关键     

云南白药对血小板活化的研究

为探讨云南白药对血小板活化的影响 ,应用单克隆抗体法 ,并用流式细胞仪对 2 0 6例男性腹股沟斜疝患者血小板活化分子标志物进行检测 ,同时检测血浆凝血物质和 D-二聚体含量。结果显示 :服药组血小板明显活化与对照组比较有显著性差异 ( P<0 .0 5 ) ,凝血物质和 D-二聚体与对照组比较无差异 ( P>0 .0 5 )。结论 :云南白药能增加血小板活化 ,促进局部止血 ,但它不影响凝血物质和 D-二聚体的含量 ,不增加血栓形成的危险。     

血小板活化因子在急性肝肾衰竭动物模型中对肾功能的影响

目的:了解血小板活化因子(PAF)在急性肝、肾衰竭动物模型中对肾功能的影响及可能的作用机制。方法:设4组大鼠,分别注射D-氨基半乳糖(D-GaLN)加内毒素(LPS),D-GaLN加PAF,D-GaLN加LPS加PAF受体拮抗剂及生理盐水,诱导急性肝、肾衰竭动物模型,测肝、肾功能指标并观察肝、肾组织病理改变。结果:注射D-GaLN大鼠的血清丙氨酸氨基转移酶、总胆红素比生理盐水组升高10倍以上,差异有显著性,病检有肝细胞坏死。注射PAF或LPS组与PAF受体拮抗剂组或生理盐水组比,肾功能指标差异有显著性。肾组织病检可见部分肾小管坏死。结论:PAF与急性肝、肾衰竭动物模型中的急性肾衰有关;PAF可能参与了内毒素相关的肝肾综合征(HRS)的形成;PAF受体拮抗剂对HRS可能有治疗作用。     

推按运经仪为主治疗结石300例

采用推按运经仪加中药、耳穴贴压等综合治疗结石３００例，６０例肝胆结石中，治愈２８例，显效２０例，无效１２例，有效率８０％；２４０例泌尿系结石中，治愈１３６例，显效８８例，无效１６例，有效率９３．３％。     

手术联合中药治疗激素性股骨头缺血性坏死的实验研究

目的 :初步探讨激素性股骨头缺血性坏死的发病机制 ,观察手术 +中药治疗本病的疗效。方法 :通过对新西兰大白兔联合应用马血清 +甲基强的松龙造模及手术处理 ,对正常组、模型组、手术组、手术 +中药组实验兔的血脂、血液流变学、血生化及股骨头标本切片观察 ,分析比较。结果 :手术 +中药治疗本病的疗效优于单纯保髋手术。结论 :手术 +活血化瘀补肾壮骨方法是股骨头缺血性坏死治疗的合理方法     

自拟白术桃花汤治疗习惯性便秘临床观察

目的　观察白术桃花汤治疗习惯性便秘的疗效。方法　自拟白术桃花汤 (白术 30g ,桃花 12g ,生地黄 30g ,枳实 10g) ,每日服 1剂 ,7d为 1个疗程。对照组服用果导片作对比观察。结果　白术桃花汤治疗习惯性便秘 117例 ,治愈 10 6例 ,好转 4例 ,总有效率 94 .0 2 %;果导片治疗 6 6例 ,治愈18例 ,好转 30例 ,总有效率 72 .73%。两组总有效率比较 ,经统计学处理P <0 0 1,差异有非常显著性意义。结论　白术桃花汤功能为补气除湿 ,增液行气 ,通调大便 ,治疗习惯性便秘疗效满意。     

海风藤酚、甲基海风藤酚、海风藤醇A和海风藤醇B对兔血小板聚集的影响

海风藤酚、甲基海风藤酚、海风藤醇Ａ和海风藤醇Ｂ均有抑制血小板激活因子（ＰＡＦ）诱导的兔血小板聚集作用，ＩＣ_（５０）分别为１７．９、９．２、１４２．０、１４．０μｍｏｌ·Ｌ~（－１）。经阿司匹林（ＡＳＡ）、磷酸肌酸／磷酸肌酸激酶（ＣＰ／ＣＰＫ）预处理的兔洗涤血小板，甲基海风藤酚和海风藤醇Ｂ仍能抑制ＰＡＦ诱导的兔血小板聚集，ＩＣ_（５０）为９．０、１６．５μｍｏｌ·Ｌ~（－１）。同时，４种成分对于二磷酸腺苷（ＡＤＰ），花生四烯酸（ＡＡ）诱导的血小板聚集抑制作用较弱，海风藤Ｂ能使ＰＡＦ诱导血小板聚集量－效曲线平行右移，ＥＣ_（５０）由１．５９ｎｍｏｌ·Ｌ~（－１）升为２０．６ｎｍｏｌ·Ｌ~（－１）。结果表明：４种成分能选择性拮抗ＰＡＦ对兔血小板的聚集作用。     

活血软坚方对大鼠膜性肾小球肾炎肾小管间质损害影响的实验研究

目的：观察活血软坚方对大鼠膜性肾小球肾炎（MN）肾小管间质损害的影响，并探讨活血软坚中药对MN伴发小管间质损伤的作用机制。方法：用阳离子化牛血清白蛋白复制大鼠MN模型，将实验动物随机分为正常组、模型组、雷公藤组、治疗组，观察24h尿蛋白、血浆白蛋白、胆固醇、三酰甘油、血肌酐、尿素氮等生化指标，并对肾组织进行光镜、电镜、免疫荧光观察；采用RT—PCR的方法检测ColⅠmRNA和ColⅢmRNA的表达。结果：本方能明显降低蛋白尿及血清胆固醇、三酰甘油、血肌酐、尿素氮，升高血清白蛋白，减少免疫复合物沉积，改善肾小球及肾小管的病理损伤。结论：活血软坚方能减轻尿蛋白对肾小管的损伤，减少细胞外基质在肾间质的积聚，减轻肾脏病理损伤，从而达到保护肾功能的作用。     

PAF antagonistic activity of 2-hydroxy-3-methoxybenzoic acid glucose ester fromGentiana scabra

In order to find out anti-platelet activating factor (PAF) from natural resources, Korean medicinal plants used for the treatments of peripheral circulation disorders were tested for their possible protective effects on PAF-induced anaphylactic shock. From the above screening, the methanol extract ofGentiana scabra showed a potent antagonistic activity against PAF. Water suspension of the extract was partitioned with CH₂Cl₂ and EtOAc, successively. The EtOAc fraction which showed the highest activity was chromatographed on silica gel to yield 6 fractions. From the fraction which showed higher PAF-antagonistic activity than the other fractions, compound1 was isolated by recrystallization. On the basis of spectral data, compound1 was identified as 2-hydroxy-3-methoxybenzoic acid glucose ester. The compound prevented the mice from the PAF-induced death at a dose of 300 μg/mouse.     

Role of neutrophils in gastric damage induced by platelet activating factor

Summary Platelet-activating factor (PAF) has recently been shown to be a potent ulcerogenic agent in the stomach and intestinal mucosa. Its exact mechanism of action is not yet known although histological studies suggest that vasocongestion is an important feature of PAF-induced damage. We have therefore studied the activity of various agents with different modes of action toward PAF-induced gastrointestinal lesions in the rat (PAF 2 g/kg i.v. ; macroscopic lesions of tissues scored 20 min later; arbitrary scale from 0 to 4). Drugs were administered either i. m., s. c. (5 min) or orally (30 min) before PAF injection. PAF-induced gastric lesions were strongly inhibited by the natural PAF-antagonist BN 52021 as well as by atropine sulphate and cimetidine which implicates cholinergic stimulation in the ulcerogenic activity of PAF. The somatostatin analog BIM 23014 was also very potent against PAF, perhaps by reducing the parasympathetic stimulation in the gastric wall as described for somatostatin. Allopurinol, which is a free radical scavenger also almost totally inhibited PAF-induced gastric damage, suggesting that neutrophils are involved in the mucosal lesions. The considerable inhibition of the gastric effects of PAF found in neutrophil-depleted animal supports this hypothesis. Theophylline and disodium cromoglycate, mast cell stabilizing drugs which were also active in our model, could act by protecting mast cell degranulation induced by free radicals released from activated neutrophils. A multifunctional process seems to determine the mucosal gastric damage induced by PAF, but parasympathetic stimulation and neutrophil activation play a major role in this pathology.Send offprint requests to A. Etienne at the above address