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At least 325 records · Page 18Linked to original sources
PubMed1989

Intraocular infusate with hemocoagulase for the control of bleeding during vitreous surgery.

The effects of hemocoagulase in injectable form (hemocoagulating enzymatic fraction of South American snake Bothrops jararaca venom provided by Ravizza) on the control of intraocular bleeding during vitreous surgery were evaluated in rabbit eyes. Intraocular infusion solution with hemocoagulase (1 NIH thrombin unit/100 ml of BSS plus) significantly reduced the bleeding time. Electroretinogram b-wave and electroretinogram c-wave showed no abnormality. Infusate with hemocoagulase (1 NIH thrombin unit/100 ml of BSS plus) is not toxic to retinal tissue and appeared to be a useful agent for the control of intraocular bleeding during vitreous surgery.

Animals↗
PubMed1997

[Comparison of defibrase and heparin in the prevention of thrombosis after coronary intervention].

To evaluate the effects of defibrase on thrombosis after coronary intervention. 12 dogs were randomized into group to be treated with defibrase (n = 6) and another group with heparin (n = 6) after coronary intervention. After implanting stents in coronary arteries, canine platelets labeled with 99mTc-hexamethyl propylene amine oxime were re-transfused into blood circulation. The stenting vessels were imaged with gamma-camera in vivo and in vitro at the 4th and 24th hour, then the relative radioactivity of stenting vessels was quantified. The isolated stenting vessels were weighted and measured with gamma-counter and the number of deposited platelets was calculated. The relative radioactivity and the number of deposited platelets were lower in the group of defibrase than in the group of heparin (P < 0.01). Compared with heparin, defibrase has more potent effect on the prevention of thrombus formation and may reduce the early-reocclusion after coronary intervention.

Angioplasty, Balloon, Coronary↗
PubMed1975

Reptilase clot retraction test. (Its cofactors and relation to other platelet functions).

C-PRP clotted by reptilase does not retract due to the lack of activation of platelets. In order to support retraction, the platelets must undergo membrane changes resulting in contractile system activation. Only in the presence of aggregating agents capable of eliciting these membrane changes in vitro (e.g. ADP, adrenaline and collagen but not bovine fibrinogen or ristocetin), strong reptilase clot retraction (RCR) occurs. During RCR an aggregating activity, platelet factor 4, and retraction stimulating factor (RSF) were released, but acid phosphatase was not available. Not only inhibitors of platelet adhesion-aggregation reaction (PAAR) but also specific blockers of release are capable of inhibiting RCR. In coagulation disorders RCR was normal in most cases, but in thrombopathies different abnormalities of RCR were found. The RCR defect may be associated not only with a defect in the initial stages of PAAR, but in some instances also with a specific defect in release reaction. Besides inducer--"activated" platelets and their adhesion to polymerizing fibrin, the presence of divalent cations and free thrombocytar--SH groups is necessary for the retraction of reptilase clots.

Adenosine Diphosphate↗
PubMed2001

Fibrinogen Matsumoto V: a variant with Aalpha19 Arg-->Gly (AGG-->GGG). Comparison between fibrin polymerization stimulated by thrombin or reptilase and fibrin monomer polymerization.

Fibrinogen Matsumoto V (M-V) is a dysfibrinogen identified in a 52-year-old woman with systemic lupus erythematous. The triplet AGG encoding the amino acid residue Aalpha19 was replaced by GGG, resulting in the substitution of Arg-->Gly. Residue Aalpha19 has been shown to be one of the most important amino acids in the so-called 'A' site or alpha-chain knob. The thrombin-catalyzed release of fibrinopeptide A from M-V fibrinogen was only slightly delayed yet release of fibrinopeptide B was significantly delayed. Both thrombin-catalyzed fibrin polymerization and fibrin monomer polymerization were markedly impaired compared to normal fibrinogen. In addition, reptilase-catalyzed fibrin polymerization of M-V was much more impaired than thrombin-catalyzed fibrin polymerization. These results indicate 'B' and/or 'b' site of M-V fibrinogen play a more important role in thrombin-catalyzed fibrin polymerization than that of normal control fibrinogen.

Batroxobin↗
PubMed1975

[Klobusitsky's hemocoagulase in plastic surgery].

Klobusitzsky haemocoagulase, a haemostatic drug obtained from snake poison, was administered prior to surgery in 35 cases of harelin, cleft palate, hypospadias and deviation of the nasal septum. Treatment was carried out from 2 to 6 days, doses and i.m. or i.v. administration being determined on the basis of age. Objective and subjective results were good, particularly in cases of cleft palate and septum deviation. In all cases, there was a significant shortening of bleeding time after treatment with the drug.

Adolescent↗
PubMed1999

[The effect of defibrase in prevention of experimental atherosclerosis in rabbits].

OBJECTIVE: To study the anti-atherosclerosis effect of difibrase in rabbits. METHODS: Use of computer, light microscope, electron microscope, biochemistry and histochemical methods to identify the total cholesterol (TC) content, mean plaque area in aorta and its cholesterol content, degree of stenosis of coronary arteries of the experimental animals and control animals. RESULTS: Defibrase could decrease the mean plaque area of aorta and the TC content in the experimental animal group was less than that in the control group (P < 0.01). The findings in aortic arches and thoracic aorta were similar to those in the aorta (P < 0.05, P < 0.01). The number of plaques at the small artery openings in the thoracic aorta and abdominal aorta of the experimental group were less than that of the control group (P < 0.01). The cross sections made at the upper third of all hearts showed that the degree of stenosis of coronary artery branches in the heart wall of the experimental group was much less than that of the control group. CONCLUSION: Defibrase can significantly inhibit atherosclerosis.

Animals↗