关于精制蝮蛇抗栓酶的问答

于1991年5月下旬在昆明召开的中国蛇毒酶临床应用研讨会后,陆续收到许多读者来信,询问精制蝮蛇抗栓酶有关问题。为了能较全面地回答读者来信,采访了有关专家并做了某些调查,对几个共同问题公开做答,不专门复信,见谅。一、精制蝮蛇抗栓酶的本质是什么?答:根据昆明会议信息。精制蝮蛇抗栓酶就是原来的“江浙蝮蛇毒抗栓酶-3号”,由中国医科大学老年病防治中心在沈阳第一制药厂生产的江浙蝮蛇抗栓酶(Svate)基础上,经过两次分离所得的产物。经过动物实验及临床验证认为:毒副反应明显低于原江浙蝮蛇抗栓酶。为了区别于原江浙蝮蛇抗栓酶,已被辽宁省卫生厅批准正式批量生产。商品名称为“精制蝮蛇抗栓酶”。为什么要取消“江浙”二字,其     

蝮蛇抗栓酶治疗庆大霉素中毒

应用蝮蛇抗栓酶治疗庆大霉素中毒6例,其中1例由于合并严重神经症状及应用蝮蛇抗栓酶时间延长,需8个月治愈,余5例因应用蝮蛇抗栓酶及时,两周即治愈.总之,应用蝮蛇抗栓酶治疗6例庆大霉素中毒患者均获得理想效果。     

清栓酶（蝮蛇抗栓酶）的药理研究与临床应用进展

清栓酶（蝮蛇抗栓酶）的药理研究与临床应用进展中国蛇协蛇毒研究所邓禄延,覃公平,胡征林自本世纪八十年代起,蛇毒抗凝制剂在我国研制及应用于临床以来,相继有尖吻蝮蛇毒制剂去纤酶,长白山陆生白眉蝮蛇毒制剂清栓酶（蝮蛇抗栓酶）及江浙蝮蛇毒制剂江浙蝮蛇毒抗栓酶（...     

精制蝮蛇抗栓酶（Svate—3）与复方丹参低分子右旋糖酐治疗脑血栓疗效对比临床观察

精制蝮蛇抗栓酶（Ｓｖａｔｅ—３）与复方丹参低分子右旋糖酐治疗脑血栓疗效对比临床观察山东烟台东方医院马玉冰,曲元海,范雅琳山东烟台肺科医院宋雨田（指导）精制蝮蛇抗栓酶（Ｓｖａｔｅ—３）是继研制蛇岛蝮蛇抗栓酶（Ｓｖａｔｅ—１）,和江浙蝮蛇抗栓酶（Ｓｖａｔ...     

两种蝮蛇抗栓酶与传统方法治疗缺血性脑卒中146例的疗效分析

采用东北白眉蝮蛇抗栓酶、江浙蝮蛇抗栓酶、丹参加低右治疗缺血性脑卒中,以一般对症处理治疗作为对照组结果显示东北白屑蝮蛇抗栓酶治疗缺血性脑卒中与对照组比较 P 值有显著性差异,而其他两组与对照组比较 P 值无显著性差异.     

不同蝮蛇抗栓酶对动物的神经毒性敏感反应

给小鼠、家兔、豚鼠等３种动物注射不同剂量的两种蝮蛇抗栓酶,观察它们的反应。结果：东北白眉蝮蛇抗栓酶未见神经毒反应,而浙江蝮蛇抗栓酶有神经毒反应,以豚鼠的反应最为敏感,主要表现为箭毒样毒性症状     

紫外线照射和充氧自血回输加白眉蝮蛇抗栓酶治疗脑梗塞的临床实验研究

我们应用紫外线照射和充氧自血回输(简称自血回输)加白眉蝮蛇抗栓酶治疗急性脑梗塞,与单纯用自血回输及单纯用白眉蝮蛇抗栓酶治疗急性脑梗塞进行了临床实验研究.其结果自血回输加白眉蝮蛇抗栓酶疗法优于单纯自血回输疗法,更优于单纯白眉蝮蛇抗栓酶疗法.临床证明两者合用有协同作用,而且方法安全、简单、方便.     

何谓“清栓酶”“AT—3”?

編辑同志: 近来我们发现蝮蛇抗栓酶的名目较多,有“清栓酶”,报纸上又见有“AT—3”,到底是不是同一样的产品? 田阳县医院邓有辉我国从蛇毒中提取有效成份制成抗血栓药物目前有三种,即用东北白眉蝮蛇毒制成“东北蝮蛇抗栓酶”江浙蝮蛇毒制成的,“江浙蝮蛇抗栓酶”和用五步蛇毒制成的“去纤酶”。     

蝮蛇抗栓酶的临床新用途

蝮蛇抗栓酶的临床新用途苏佳广西桂林南溪山医院（５４１００２）蝮蛇抗栓酶系从蝮蛇蛇毒中提取的一种酶制剂,具有溶栓、抗凝、扩血管和改善微循环作用,被广泛用于脑、心及周围血管性疾病。近年来,随着对蝮蛇抗栓酶药理学与临床研究的进一步深入,其用途也不断扩展,现...     

蝮蛇抗栓酶对高粘血症患者血液流变与微循环影响的观察

静注蝮蛇抗栓酶并口服青龙胶囊治疗高粘血症１４０例患者。结果显示,蝮蛇抗栓酶能明显降低血液粘度,表现为全血粘度、血浆粘度、全血还原粘度及纤维蛋白原降低,同时降低甲襞微循环形态、流态及管周状态积分。探讨其改善血液粘度机制。     

蝮蛇抗栓酶对实验性动脉粥样硬化与PGI2／TXA2平衡影响的观察

通过用蝮蛇抗栓酶（Ｓｖａｔｅ）防治家兔动脉粥样硬化（ＡＳ）实验,发现Ｓｖａｔｅ能明显减轻家兔主动脉ＡＳ;同时能明显降低血液血栓素含量,能明显升高血液前列环素含量。以上血液检查结果与Ｓｖａｔｅ治疗心脑血管疾病时临床检查结果一致。说明Ｓｖａｔｅ有防治ＡＳ的作用,其机制与Ｓｖａｔｅ具有恢复前列环素／血栓素平衡的作用密切相关。     

清栓酶对过氧化脂质含量影响的研究

将５４例冠心病、高血压病、糖尿病及脑梗塞病人,随机分为对照组与清栓酶组。对照组２６例,常规药物治疗,清栓酶组２８例,在常规药物治疗基础上加用蝮蛇清栓酶０．５ｕ,稀释静脉点滴,一日一次,１４天为一疗程。观察到蝮蛇清栓酶能明显升高超氧化物岐化酶活性（Ｐ＜０．０１）,明显降低过氧化脂质的终末代谢产物丙二醛含量（Ｐ＜０．０１）,说明蝮蛇清栓酶能有效减轻自由基损伤。     

玻璃体内注射清栓酶治疗实验性玻璃体积血

清栓酶可促进玻璃体内纤维蛋白凝血块溶解,我们制作新鲜及陈旧性兔眼玻璃体积血模型,将清栓酶、尿激酶及注射用水分别注入玻璃体腔内,观察眼底、测定玻璃体出血指数、FDP含量、进行3P 试验,结果发现清栓酶有治疗效果,同对照组相比统计学上有显著差异,同尿激酶相比无差异,且未发现有毒副作用。     

蝮蛇抗栓酶对动脉粥样硬化影响的实验研究

通过用蝮蛇栓酶对家兔实验性动脉粥样硬化影响的观察,发现Ｓｖａｔｅ能明显抑制家兔主动脉ＡＳ,同时能明显降低血液丙二醛、血栓素及甘油三酯含量,能升高血液超氧化物歧２化酶活性及前列环素含量。说明Ｓｖａｔｅ能预防ＡＳ,其机制与Ｓｖａｔｅ减轻自由基损伤、恢复前列环素血检 平衡及降血脂密切相关。     

蝮蛇抗栓酶治疗银屑病产生耐受性原因探讨

目的通过治疗银屑病５０例临床观察,探讨部分病例未能治愈与机体对蝮蛇抗栓酶产生耐受性原因分析。方法用蝮蛇杭栓酶０．７５ＩＵ加入生理盐水中静滴,治疗前、后及各疗程间监测血小板计数与血浆纤维蛋白原变化。结果药效消失后,血小板计数与血浆纤维蛋白原增高超过治疗前水平。结论该类药物治疗其他血栓性疾病可将血小板计数与血浆纤维蛋白原增高作为药效消失及耐受性产生的一项指标。     

降纤酶治疗高粘血症40例报告

目的：观察降纤酶治疗高粘血症患者的临床疗效。方法用生理盐水２５０ｍｌ加降纤酶５ｕ,体重超过６５ｋｇ和１０ｕ,静脉滴注,每天１次,连用３天,第４天停用,第５天开始隔天静脉滴注降纤酶５ｕ或者１０ｕ,总量６０ｕ。结果降纤酶能明显地降低高粘血症患者的血液粘度、纤维蛋白原、红细胞聚集指数、微循环滞留时间等,同时也能使患者原有临床症状和体征以及微循环得到明显改善,结论降纤酶是治疗高粘血症的有效药物。     

Immune and autoimmune disorders in HCV chronic liver disease: personal experience and commentary on literature

HCV chronic liver disease can be associated with a plethora of immune and autoimmune perturbations and many authors claim that HCV chronic infection can play an important role in the pathogenesis of these disorders. To compare our experience with literature reports, we performed a retrospective study on the case histories of 265 patients with HCV chronic liver disease, evaluating the type and prevalence of the associated immune and autoimmune manifestations. We found that the patients with HCV chronic liver disease can present arthromyalgias (7.1% of the patients), Sj?rgen's syndrome (5.2%), thyroiditis (4.1%), rheumatoid arthritis (2.2%), autoimmune thrombocytopenia (2.6%), mixed cryoglobulinemia (1.5%), autoimmune anemia (0.3%) and oral lichen planus (0.3%). We claim that HCV liver infection is able to induce immune and autoimmune perturbations, without playing a significant role in the pathogenesis of a well-defined disorder.     

Homomeric and heteromeric interactions of the extracellular domains of death receptors and death decoy receptors

Death receptors (DRs) can induce apoptosis by oligomerization with TRAIL, whereas death decoy receptors (DcRs) cannot, due to their lack of functional intracellular death domains. However, it is not known whether DRs and DcRs can interact with one another to form oligomeric complexes prior to TRAIL binding. To address this issue, the extracellular domains (ECDs) of DR4 (sDR4), DR5 (sDR5), DcR1 (sDcR1), and DcR2 (sDcR2) were expressed in a soluble, monomeric form, and their binding interactions were quantified by surface plasmon resonance. The purified sDRs and sDcRs exhibited native-like secondary structure and bound to TRAIL with binding affinities in the nanomolar range (K(D)= approximately 10-62 nM), suggesting that they were properly folded and functional. The soluble receptors interacted homophilically and heterophilically with similar micromolar range affinities (K(D)= approximately 1-9 microM), with the exception that sDR5 did not interact with the sDcRs. Our results suggest that most DRs and DcRs can laterally interact through their ECDs to form homomeric and/or heteromeric complexes in the absence of TRAIL binding.     

Thermodynamics of RNA-RNA duplexes with 2- or 4-thiouridines: implications for antisense design and targeting a group I intron

Antisense compounds are designed to optimize selective hybridization of an exogenous oligonucleotide to a cellular target. Typically, Watson-Crick base pairing between the antisense compound and target provides the key recognition element. Uridine (U), however, not only stably base pairs with adenosine (A) but also with guanosine (G), thus reducing specificity. Studies of duplex formation by oligonucleotides with either an internal or a terminal 2- or 4-thiouridine (s(2)U or s(4)U) show that s(2)U can increase the stability of base pairing with A more than with G, while s(4)U can increase the stability of base pairing with G more than with A. The latter may be useful when binding can be enhanced by tertiary interactions with a s(4)U-G pair. To test the effects of s(2)U and s(4)U substitutions on tertiary interactions, binding to a group I intron ribozyme from mouse-derived Pneumocystis carinii was measured for the hexamers, r(AUGACU), r(AUGACs(2)U), and r(AUGACs(4)U), which mimic the 3' end of the 5' exon. The results suggest that at least one of the carbonyl groups of the 3' terminal U of r(AUGACU) is involved in tertiary interactions with the catalytic core of the ribozyme and/or thio groups change the orientation of a terminal U-G base pair. Thus thio substitutions may affect tertiary interactions. Studies of trans-splicing of 5' exon mimics to a truncated rRNA precursor, however, indicate that thio substitutions have negligible effects on overall reactivity. Therefore, modified bases can enhance the specificity of base pairing while retaining other activities and, thus, increase the specificity of antisense compounds targeting cellular RNA.