胰激肽释放酶生产新工艺研究

在得到胰酶和弹性蛋白酶的同时,用国产T离子交换树脂吸附分离胰激肽释放酶,再经除盐后用离子交换纤维素(DEAE——Cellulose)精制,平均可得胰激肽释放酶4.52万u/kg胰脏,比活为25.07u/mg。     

胰激肽释放酶治疗39例冠心病临床资料分析

<正> 据有关文献报道,胰激肽释放酶是一种蛋白酶,存在于各种腺体、血液,分泌液和排泄物中,该酶在整个激肽体系中作用于激肽原产生激肽样物质,可使小动脉和微血管扩张。目前应用此药治疗周围血管疾病较多,但用于治疗冠心病报道尚属少见。现将我们应用胰激肽释放酶治疗39例冠心病(总有效率为82.05％)的资料整理报道如下。一、资料和方法一般资料病例选择:39例冠心病均按世界卫生组织(W.H.O)冠心病的诊断标准选择。来源于门     

胰激肽释放酶对糖尿病患者左心室功能的影响

目的了解胰激肽释放酶对糖尿病患者左心室功能各项参数的影响。方法在用药前和用药后 3个月用彩色多普勒超声心动图测定左心室功能参数。结果与对照组相比 ,该药对心输出量、舒张早期最大充盈速度及舒张晚期充盈加速时间 ,用药后 3个月较用药前明显增加 (P <0 .0 5或P <0 .0 1) ,而舒张晚期最大充盈速度和舒张早期充盈加速时间用药后 3个月较用药前明显降低 (P <0 .0 1或P <0 .0 5 )。结论糖尿病患者服用胰激肽释放酶可改善左室舒张功能     

电位滴定法测定胰激肽释放酶活力测试条件探讨

本文用ＦＩＰ推荐的方法，以具有国际单位的参照品为标样，滴定液为０．０１ｍｏｌ／ＬＮａＯＨ标准溶液，考查了以ＢＡＥＥ为底物的电位滴定法测定胰激肽释放酶活力的实验条件，通过正交试验得出直观和方差分析的结果，依据酶活力单位高、ＳＤ和ＲＳＤ％较小的原则，求出酶活力测定的最适条件是：酶反应温度为２５℃；缓冲液为０．００１５ｍｏｌ／ＬＮａ２Ｂ４Ｏ７－０．２５ｍｏｌ／ＬＮａＣＬ－２×１０（－４）ｍｏｌ／ＬＥＤＴＡ，ｐＨ为８．００；反应液中酶浓度为０．４８ＩＵ／ｍｌ；底物浓度为５×１０（－３）ｍｏｌ／Ｌ；胰蛋白酶抑制剂浓度为１２５μｇ／ｍｌ。胰激肽释放酶活力测定的实验数据的相对标准偏差小于５％。     

胰激肽释放酶致固定性药疹一例

1病例资料 男,73岁.因患高血压、冠心病,一直口服硝苯地平控释片、吲达帕胺片、肠溶阿司匹林等治疗.既往有呋喃西林过敏史.     

胰激肽释放酶致固定性药疹一例

1病例资料 男，73岁。因患高血压、冠心病、一直口服硝苯地平控释片、吲达帕胺片、肠溶阿司匹林等治疗。既往有呋喃西林过敏史。1999年4月因右髂股动脉粥样硬化斑块形成伴栓塞，加服胰激肽释放酶(江苏常州生化千红制药有限公司生产，批号：990127)112单位，每日3次。1999年9月初，患双足出现皮肤干燥、脱屑，尤以足跖及外侧缘为重，予外用足光粉、复方土     

Effects of epsilon-aminocaproiloaminoacids on the amidolytic activity of tissue plasminogen activator, urokinase and kallikrein

Effect of three epsilon-aminocaproylaminoacids with a significant antifibrinolytic activity on amidolytic activity of tissue plasminogen activator (t-PA), urokinase and kallikrein was examined. epsilon-Aminocaproyl-S-benzyl)-L-cysteine and epsilon-aminocaproyl-L-norleucine were weak inhibitors of kallikrein. Weak activation of t-PA activity was observed at high concentration of the tested compounds. Only one of the examined dipeptides was a weak inhibitor of amidolytic activity of urokinase.     

Effects of epsilon-aminocaproylaminoacids on prothrombin activation and thrombin activity

Influence of four epsilon-aminocaproylaminoacids on prothrombin activation and thrombin activity was examined. Only epsilon-aminocaproylnorleucine markedly inhibited the prothrombin activation in an extrinsic system.     

The influence of tetracosactide and adrenal steroids on renal kallikrein activity and urinary kallikrein excretion in rats

The effect of adrenal steroids (mineralo- and glucocorticoids) as well as that of the adrenocorticotrophic peptide tetracosactide (beta 1-24 corticotropin) on the renal kallikrein activity and on the urinary kallikrein excretion of rats was investigated. After the animals had been adapted to metabolic cages, they were injected with deoxycorticosterone acetate (15 mg/kg day), corticosterone (40 mg/kg day), both steroids combined or the vehicle (sesame oil). Additional groups of rats received tetracosactide (0.05, 0.1 or 0.2 mg/day) or the vehicle (100 microliter of 38 X 10(-3) M ZnCl2). After four days of treatment the urinary kallikrein excretion was higher in deoxycorticosterone-treated rats than in their controls. This increase was prevented when corticosterone was administered simultaneously. The renal kallikrein activity of corticosterone as well as that of deoxycorticosterone plus corticosterone-treated rats was subnormal. A dose-related reduction of both the renal kallikrein activity and the urinary kallikrein excretion was observed 2 days after starting the tetracosactide administration. It may be concluded that a stimulation of the endogenous release of glucocorticoids in the rat reduces the renal kallikrein activity and that glucocorticoids can prevent the stimulating effect of mineralocorticoids.     

制备高活力胰酶的安全低污染新工艺

目的建立安全、低污染制备高活力胰酶的方法。方法胰脏自溶水提取,以一定浓度的蛋白质沉淀剂P60在最佳筛选条件下沉淀6h,室温干燥得胰酶粉,对上清液中的P60进行回收再利用。结果收率达15%以上,胰蛋白酶、胰脂肪酶、胰淀粉胰三酶活力分别为3.70×103、2.80×104、5.30×104U·g-1,为《中国药典》要求的6～8倍。结论所建立的方法能安全简便的制备新型高活力胰酶。     

Measurement of urinary kallikrein activity by kinin radioimmunoassay

A method for measuring urinary kallikrein activity by kinin radioimmunoassay (RIA) is described. Kinins were generated by incubating urine with partially purified dog kininogen in the presence of peptidase inhibitors. Antibodies against kallidin were induced in rabbits by injecting kallidin coupled to ovalbumin. One of the antisera generated was used at a final dilution of 1:18,000 to obtain a 40 per cent binding of approximately 3000 cpm (10 pg) of bradykinin (S-tyrosin)-[¹²⁵I]triacetate ([¹²⁵I]bradykinin). Synthetic kallidin (10–500 pg) was used to construct standard curves. When kinins generated by urinary kallikrein were also used, the two displacement curves for [¹²⁵I]bradykinin were similar. The RIA was sensitive to 10 pg kinins. The antiserum cross-reacted with bradykinin, methionyl- kallidin, and kininogen, but not with angiotensin, oxytocin or SQ 20,881. To increase the specificity of the RIA, the kininogen was removed by ethanol precipitation followed by QAE-Sephadex-A50 chromatography. Kallikrein activity in 81 human urine samples and 8 samples obtained from a dog undergoing stop-flow procedure was measured by RIA and bioassay. Correlations of r = 0.81 and 0.94 were found. This RIA is useful for measuring kallikrein activity in rat, dog and human urine.     

Impaired renal kallikrein activity and elevated blood pressure normalized by orally applied kallikrein in essential hypertension

Urinary kallikrein excretion was significantly lower in patients with essential hypertension (0.48 +/- 0.05 EU/24 h) than in normotensive controls (1.26 +/- 0.14 EU/24 h). Oral administration of hog pancreatic kallikrein normalized decreased urinary kallikrein and reduced arterial pressure. The treatment-induced rise in urinary kallikrein was due to an enhanced release of endogenous enzyme, as was determined by radioimmunoassay. It is proposed that in the hypertensive patients the low urinary kallikrein excretion reflects a defect in renal kallikrein formation which is normalized by oral kallikrein. The hypotensive action of oral kallikrein, as well as its stimulating effects on renal kallikrein release, suggest that the kallikrein-kinin system is involved in blood pressure regulation and that impaired renal kallikrein activity may be a factor in the maintenance of essential hypertension.