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PubMed1992

Defibrase, a purified fibrinolytic protease from snake venom in acute myocardial infarction.

To investigate the thrombolytic effects of defibrase in AMI, 157 pts with AMI were studied. Of the 157 pts, 87 were assigned to defibrase thrombolysis and 70 to the conventional therapy plus heparin (control). Coronary arteriography was performed in 36 pts of the defibrase group and 26 of the control group. Pretreatment coronary arteriography was performed in 10 pts and total occlusion of infarct-related artery (IRA) was demonstrated in 7. Thirty to 45 min after either intracoronary or intravenous defibrase thrombolysis, recanalization occurred in 4 of the 7 pts. The perfusion and stenosis was improved in 2 of the 3 pts with patent IRA. Of the 10 pts who underwent emergency coronary arteriography after the onset of i.v. defibrase thrombolysis, 6 were shown to have patent IRAs. Of the 16 pts who underwent coronary arteriography two weeks after the i.v. defibrase thrombolysis, 13 were shown to have patent IRAs. In contrast, only 11 of the 26 pts in the control group had patent IRAs two weeks after admission to the hospital. Of the 36 angiographic cases of the defibrase group, 15 underwent follow-up coronary arteriography, only 1 pt showed reocclusion. In comparison to the control group, the pts in the defibrase group had earlier CPK peaking, higher percentage of pts with LVEF > 0.5, a lower mortality and complication rate. Major spontaneous bleeding complications were rarely seen with defibrase. The results indicate that defibrase is an effective thrombolytic agent with a reasonable recanalization rate, low reocclusion rate and a low rate of bleeding complications.

Batroxobin↗
PubMedDate not supplied

[Enzymes of snake venoms].

Snakes' venom is a mixture of biologically active substances, containing proteins and peptides. A number of these proteins interact with haemostasis system components. Activators and inhibitors affecting blood coagulation and fibrinolysis systems are of special interest. Venom components can be classified into three main groups, such as procoagulants, anticoagulants and fibrinolytic enzymes according to their action. This review is focused on enzymes from Agkistrodon halys halys venom. They are thrombine-like enzyme, named Ancystron-H, flbrinogenolytic enzyme, protein C activator and platelet aggregation inhibitor. Ancystron-H is used for determination of fibrinogen level in blood plasma of patients undergoing heparin treatment and blood coagulation inhibitors accumulation. The fibrinogenolytic enzyme can be used as the instrument for protein-protein interactions in fibrinogen-fibrin system. The protein C activator is used for protein C level determination in blood plasma with different pathologies. Functions of the platelet aggregation inhibitor, belonging to disintegrins group, can be used for development of antithrombotic preparations. Information about the use of snake venoms in science and medicine is presented.

Ancrod↗
PubMed1992

Hemostatic activity of the bovine parotid gland glycoconjugates.

The bovine parotid gland was studied by means of biochemical analyses and the glycoconjugates extracted were used to investigate the activity on the human hemostatic system. Thromboelastography was unable to reveal anticoagulant properties. Conversely, the Thrombin Time (TT) was prolonged in a statistically significant way and with dose-coupling response. Reptilase Time (RT) was affected by the highest concentration of extract suggesting that the bovine parotid glycoconjugates alter the fibrinogen polymerization.

Animals↗
PubMed1978

[Action of hemocoagulase on the cicatrization of the dura mater in rabbits. Preliminary results].

The present study compares the cicatrization of the dura by administration of I.M. hemocoagulase. This study was done on 6 rabbits and 6 control animals. The authors think that the cicatrization is a little slower but of better quality. The hemocoagulase seems to favorize the vasculo-exsudative process of cicatrization. The fibrinous deposits are more important too. Perhaps the occlusion of C.S. fluid fistulas could be favorized by means of the used product. Definitive conclusions are not possible for the moment but a work on a larger scale is projected.

Animals↗
PubMed2005

Effect of iontophoresis on skin permeation of defibrase.

AIM: To investigate the effect of iontophoresis on skin permeation of defibrase. METHODS: Iontophoresis was carried out in side-by-side chambers, excised rat skin membrane (RSM) or human epidermis membrane (HEM). The effects of electrode polarity, permeation medium pH and ionic strength were evaluated. RESULTS: Permeation of defibrase caused by anodal iontophoresis was more effective [the apparent permeability coefficient was (1.2 +/- 0.4) x 10(-4) cm x h(-1)] than that of cathodal iontophoresis [(4.3 +/- 1.4) x 10(-5) cm x h(-1)]. The amount of permeated defibrase caused by anodal iontophoresis in pH 7.4 medium was (25 +/- 5) x 10(-14) mol x cm(-2), which was higher than that of in pH 6. 4 permeation medium [(15 +/- 4) x 10(-14) mol x cm(-2)]. CONCLUSION: Iontophoresis could enhance skin permeation of defibrase. Electroosmotic flow effect played an important role.

Animals↗
PubMed2005

Reassessment of defibrase in treatment of acute cerebral infarction: a multicenter, randomized, double-blind, placebo-controlled trial.

OBJECTIVE: To evaluate the efficacy and safety of defibrase in patients with acute cerebral infarction by a large sample, multicenter, randomized, double-blind, placebo-controlled clinical trial. METHODS: Patients with acute cerebral infarction within 12 hours of stroke onset were randomly assigned to receive either an initial intravenous infusion of defibrase 15 U plus normal saline 250 mL or 250 mL of normal saline only. Subsequent infusions of defibrase 5 U or placebo (normal saline) were given on the 3rd, 5th, 7th, and 9th day, respectively. Both groups received standard care of acute cerebral infarction. The primary efficacy outcome was functional status (Barthel Index) at 3 months after treatment. Safety outcome were bleeding events and mortality rate. Secondary outcome included Chinese Stroke Scale (CSS) score at 14 days and recurrence rate of stroke at 1 year. RESULTS: A total of 1053 patients were enrolled at 46 centers from September 2001 to July 2003, and 527 patients were randomly assigned to receive defibrase and 526 to receive placebo. A similar proportion of patients in both groups completed a full course of treatment. There was a significantly greater proportion of favorable functional status (Barthel Index > or = 95) in defibrase group than in placebo group at 3 months (52.2% vs. 42.8%, P < 0.01), and the proportion of dependent functional status (Barthel Index < or = 60) was a little lower in defibrase group compared with placebo group (27.7% vs. 32.4%). These differences were more obvious among patients who were treated within 6 hours of stroke onset. Patients in defibrase group had better improvement with respect to CSS score than those in placebo group at 14 days (P < 0.05). Recurrence rate of stroke at 1 year was lower in the defibrase group compared with placebo group (6.2% vs. 10.1%, P = 0.053). Patients in defibrase group had higher risk of extracranial bleeding events (4.7% vs. 1.5%, P < 0.01) and a tendency of higher risk of symptomatic intracranial hemorrhage. The hemorrhage incidence was higher in patients with fibrinogen level < 130 mg/dL than > or = 130 mg/dL (10.6% vs. 3.8%, P < 0.05). Mortality rate at 3 months were slightly higher in defibrase group than placebo group (5.9% vs. 4.2%). CONCLUSIONS: The defibrase is effective to improve neurological function and function of daily living for patients with acute cerebral infarction within 12 hours of symptom onset. The efficacy was even better for acute cerebral infarction within 6 hours of onset. The increased risks of intra- and extracranial hemorrhage during defibrase administration were related to the plasma fibrinogen level.

Adult↗
PubMedDate not supplied

RBone volume reconstruction in atrophic edentulous ridges: placement method of graft-implant unity in single step together with endogenous growth factors.

AIM: The methods of inserting osseointegrated implants in atrophic edentulous ridges need first bone tissue graft and subsequently the insertion of fixtures. These methods need a long period of time before a prosthesis can be made: for this reason the researchers experimented different techniques to reduce times of prosthetic loading. Our experimented method makes it possible to shorten the prosthetic period notably. METHODS: During surgery an implant is inserted in the symphysis area and then it is removed by trephine bur having a diameter greater than 1 mm compared to the receiving site and by using irrigation with 4 degrees C physiological solution. After 75 days, the implant is loaded by temporary prosthesis and subsequently a final restoration is applied after 4-6 months, depending on bone quality. RESULTS: Our surgical method, in spite of being conditioned by the anatomical conformation of the edentulous ridge and anatomical limits, proved to be predictable and with the same success percentages as other surgical techniques used for morphological reconstruction of atrophic edentulous ridges, shortening prosthetic loading times notably. CONCLUSIONS: Despite the small number of patients treated and the short control period do not give enough elements to consider this new method applicable in all types of atrophies, our results confirm the validity of this technique if well used. In the future further studies and experimentations on greater number of patients and for at least 5 year follow-up are needed.

Adult↗
PubMed2006

Meta-analysis of defibrase in treatment of acute cerebral infarction.

BACKGROUND: Fibrinogen-depleting agents are promising in the treatment of cerebral ischemic disease. They were studied by many trials, and the outcomes were different because of different regimens and different doses. In this study, we assessed the efficacy and safety of defibrase on acute cerebral infarction in China. METHODS: A search using Chinese hospital knowledge database (CHKD) and MEDLINE database for randomized controlled trials was carried out. A CHKD (1994 June 2005) search was performed with the keyword "defibrase", then a second search for the keyword "acute cerebral infarction"; a MEDLINE search (1950 June 2005) was performed with the following keywords: [(cerebral ischemia), OR (acute cerebral infarction), OR (stroke)], AND [defibrase]. Meta-analysis was performed with RevMan software 4.2. RESULTS: Included were 14 studies comparing the efficiency and safety of defibrase with other drugs in the treatment of acute cerebral infarction. Patients' records were pooled (total 646 patients; defibrase, n = 328, no defibrase n = 318). Neurological deficit score (NDS) before treatment showed weighted mean differences (WMD) = 0.95, 95% confidence interval (CI) = (-0.60, 2.50), P = 0.23; NDS after treatment showed WMD = -2.20, 95% CI = (-4.21, -0.18), P = 0.03; Barthel index at 3 months showed WMD = 4.45, 95% CI = (-0.13, 9.03), P = 0.06; the plasma fibrinogen level before treatment showed WMD = 0.02, 95% CI = (-0.16, 0.19), P = 0.86; plasma fibrinogen level after treatment showed WMD = -1.51, 95% CI = (-1.88, -1.15), P < 0.00 001. CONCLUSIONS: With the given dose and regimen of defibrase in China, defibrase may play a role of anticoagulation. It might inhibit the progression of stroke and prevent the recurrence of stroke.

Acute Disease↗
PubMed1991

Ticlopidine selectively inhibits human platelet responses to adenosine diphosphate.

Platelet aggregation and fibrinogen binding were studied in 15 individuals before and 7 days after the oral administration of ticlopidine (250 mg b.i.d.). Ticlopidine significantly inhibited platelet aggregation induced by adenosine diphosphate (ADP), the endoperoxide analogue U46619, collagen or low concentrations of thrombin, but did not inhibit platelet aggregation induced by epinephrine or high concentrations of thrombin. Ticlopidine inhibited 125I-fibrinogen binding induced by ADP, U46619 or thrombin (1 U/ml). The ADP scavengers apyrase or CP/CPK, added in vitro to platelet suspensions obtained before ticlopidine, caused the same pattern of aggregation and 125I-fibrinogen binding inhibition as did ticlopidine. Ticlopidine did not inhibit further platelet aggregation and 125I-fibrinogen binding induced in the presence of ADP scavengers. After ticlopidine administration, thrombin or U46619, but not ADP, increased the binding rate of the anti-GPII b/III a monoclonal antibody 7E3 to platelets. Ticlopidine inhibited clot retraction induced by reptilase plus ADP, but not that induced by thrombin or by reptilase plus epinephrine, and prevented the inhibitory effect of ADP, but not that of epinephrine, on the PGE1-induced increase in platelet cyclic AMP. The number of high- and low-affinity binding sites for 3H-ADP on formalin-fixed platelets and their Kd were not modified by ticlopidine. These findings indicate that ticlopidine selectively inhibits platelet responses to ADP.

Adenosine Diphosphate↗
PubMed1990

Allosteric interaction of components of the replitase complex is responsible for enzyme cross-inhibition.

The enzymes of DNA polymerization and DNA precursor synthesis are assembled in the replitase complex during the S phase of the cell cycle. Cross-inhibition is a phenomenon shown by enzymes of the replitase complex, in which inhibition of one enzyme of the complex leads to inhibition of a second, unrelated enzyme. This inhibition occurs only in vivo and only during S phase. The second enzyme shows no inhibition in vitro. In this study, using Chinese hamster embryo fibroblast cells, we have shown that direct allosteric interactions, i.e., structural interaction from a remote site within the replitase complex, is the cause of cross-inhibition of thymidylate synthase activity by the inhibitors of ribonucleotide reductase and DNA polymerase, because disruptions of the deoxynucleotide pools, which would be predicted for alternative explantations, do not occur. Cross-inhibition of DNA polymerase by hydroxyurea is demonstrated by the cessation of DNA synthesis when ribonucleotide reductase block is circumvented by the provision of all four deoxynucleosides. In addition to the cross-inhibition for thymidylate synthase and DNA polymerase, we have also presented evidence, on the basis of alterations of the in vivo conversion of deoxyuridine to dUMP, that cross-inhibition also occurs for the enzyme thymidine kinase. This conclusion is further supported by the lack of inhibition of the similar process in RNA synthesis, because enzymes of RNA synthesis are not included in the replitase complex. To facilitate the measurements, we have introduced a novel method of distinguishing between thymidine and deoxyuridine derivatives, making use of the fact that a tritium label placed in the 5'-position of deoxyuridine is removed on conversion to thymidine by methylation, whereas a tritium placed in the 6'-position is not.

Allosteric Regulation↗
PubMed1991

[Cryofibrinogenemia--successful therapy by decreasing fibrinogen].

Six patients suffering from solitary cryofibrinogenaemia are described. In one patient idiopathic cryofibrinogenaemia was present, while the others showed secondary cryofibrinogenaemia associated with borrelia infection, chronic venous insufficiency with pulmonary embolism, primary biliary cirrhosis, diabetes mellitus or von-Willebrand syndrome. Subcutaneous injections of the thrombin-like snake poison batroxobin/ancrod were administered over a period of several weeks. Five patients experienced almost complete remission of their symptoms, especially of pain following cold exposure. In one patient partial relief was achieved. Overall we found a 75% reduction of symptoms. When blood fibrinogen levels are carefully monitored this therapy is an efficient and safe form of treatment for cryofibrinogenaemia.

Adolescent↗
PubMed1976

Dysfibrinogenaemia and primary hepato-cellular carcinoma.

The mechanisms of blood coagulation and fibrinolysis have been evaluated in 28 black adult Africans with primary hepato-cellular carcinoma (HCC). A characteristic pattern of abnormalities has been defined. Dysfibrinogenaemia appears to be a useful biological marker for the disease. The reptilase test (RT) is a simple, reliable and sensitive means of detection of this metabolic abnormality. It is suggested that the RT should be used to screen populations at high risk of developing HCC, such as cirrhotics, in conjunction with alpha fetoprotein determinations, which, alone, are inadequate for the purpose. The haemostatic defect may have relevance to the pathogenesis of HCC, and further suggests a potentially useful, additional, therapeutic modality.

Adult↗
PubMed1991

A new congenital abnormal fibrinogen Ise characterized by the replacement of B beta glycine-15 by cysteine.

A new case of heterozygous dysfibrinogenemia characterized by the replacement of NH2-terminal amino acid of fibrin beta-chain was found in a 50-year-old man. Despite a prolonged thrombin time, the propositus' fibrinogen had a normal reptilase time with the normal release of fibrinopeptide A. Release of fibrinopeptide B by thrombin was strongly affected, but a very high concentration of thrombin almost completely released fibrinopeptide B with a normal elution pattern on reversed-phase high performance liquid chromatography (HPLC). Lysylendopeptidase-cleavage of purified B beta-chains analyzed on HPLC showed the decrease of one peptide compared with the normal and the appearance of an abnormal peptide peak. These peptides were treated with thrombin and further separated on HPLC. Amino acid sequence analysis of the abnormal peptide demonstrated that B beta glycine-15, NH2-terminus of the fibrin beta-chain, was replaced by cysteine. These findings will be of particular importance because they strongly support the hypothesis that the NH2-terminal portion of the fibrin beta-chain is involved in the polymerization reaction by thrombin. The propositus' daughter and two sisters had the same abnormal fibrinogen. This unique inherited abnormal fibrinogen was designated as fibrinogen Ise. During these studies, we found that a very high concentration of thrombin cleaves not only the A alpha Arg19-Val20 bond but also the COOH-terminal region of alpha-chains, which results in the generation of further degraded alpha-chains with apparent molecular weights of 44,000 or less.

Amino Acid Sequence↗
PubMed1990

[Coronary thrombolysis with defibrase].

Clinical use of defibrase (DF), a fibrinolytic agent from venom of Agkistrodon acutus, was investigated in patients with acute myocardial infarction (AMI). Patients with AMI were randomized to tow groups, one receiving conventional therapy and DF, the other a control group having conventional treatment only. The patients in the DF group received intravenous DF 0.05 u or 0.075 u/kg over 1 hour immediately after the attack and 0.025 u/kg over 4 hours on the 5 th and 10 th day. The control patients received conventional therapy only. Of the patients randomized, 21 had coronary angiography and left ventriculography. Recanalization was seen in 10 of the 10 patients treated with DF, while only in 3 of the 11 patients in the control group. LVEF in the DF group was higher than that in the control group (61% vs 50%). However the difference was not significant. In the DF group, two patients developed petechia and blood oozing at the site of intravenous injection and one patient developed gum bleeding; all patients had transient thrombocytopnia, which returned to normal within 5 days. There was no intracranial hemorrhage, gross hematuria or hematemesis. In conclusion, DF possess thrombolytic as well as anticoagulant effects with minor bleeding complication. Early infusion of DF yields high patency rate and shows a trend toward preservation of LV function.

Batroxobin↗