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At least 811 records · Page 45Linked to original sources
PubMed1988

Immunovisualization of fibrinogen A alpha-chain heterogeneity in normal plasma and plasma from patients with DIC or on streptokinase therapy.

Purified fibrinogen as well as normal plasma, or plasma from patients with DIC or undergoing streptokinase(SK)-therapy was subjected to 1D- and 2D SDS-electrophoresis under reducing conditions. The pattern was revealed either by Coomassie-staining or immunostaining after Western-blotting and then compared. The use of polyclonal antibodies to fibrinogen as well as two monoclonal anti-bodies reacting with FPA and C-terminal part of the A alpha-chain confirmed immunologically the previously reported molecular weight heterogeneity of the A alpha-chain of the fibrinogen molecule as being a constituent of normal plasma, and lead to the following conclusions: 1. The MW-heterogeneity is observed in the fibrinogen pool of normal plasma as well as in DIC-plasma, SK-plasma and in purified fibrinogen, being the least noticeable in normal plasma and most advanced in SK-plasma. Patterns obtained using immunostaining with monoclonal anti-FPA confirm that the MW-heterogeneity of fibrinogen is mainly due to C-terminal degradation of the A alpha-chain. 2. Numerous A alpha-chain remnants (at least 9), with intact N-terminal ends, are found to be present in normal plasma, with a MW range from 66,200 to 36,000 Da, demonstrating that each of the "classical" HMW, LMW, LMW' subgroups consist of fibrinogen molecules which are very heterogeneous. 3. Two populations of A alpha-chains in purified fibrinogen and in fibrinogen in plasma react with the C-terminal specific Mab G-8. This is in contrast to the findings in plasma from streptokinase-treated patients, where several bands of lower molecular weights than the gamma-chain can be seen, suggesting the presence of free, circulating A-alpha chains split in the N-terminal half of the chain beyond the last inter-chain disulphide bond. 4. 2D electrophoresis disclosed substantial deviations in the patterns obtained with DIC-plasma, SK-plasma and with fibrinogen purified by beta-alanine-precipitation from that observed with normal plasma. The present technique allows selective characterization of fibrinogen independently of the other proteins present in plasma and offers extreme sensitivity.

Blotting, Western↗
PubMed1990

Regulation of plasmin, miniplasmin, and streptokinase-plasmin complex by alpha 2-antiplasmin, alpha 2-macroglobulin, and antithrombin III in the presence of heparin.

The regulation of plasmin, miniplasmin, and streptokinase-plasmin complex (SkPm) was studied in vitro in the presence of unfractionated porcine intestinal heparin using purified plasma proteinase inhibitors. Heparin enhanced the reaction of antithrombin III (AT) with plasmin (up to 40-fold with 20 units/ml). The rate of plasmin inhibition by alpha 2-antiplasmin (alpha 2AP) and by alpha 2-macroglobulin (alpha 2M) was not changed by heparin (0.5-100 units/ml); the rank-order of plasmin-inhibitory activity remained alpha 2AP greater than alpha 2M greater than AT. The reaction of miniplasmin with AT was studied also. The second order rate constant was 9.2 x 10(2) M-1s-1 without heparin and 2.6 x 10(4) M-1s-1 in the presence of 20 units/ml heparin. Heparin did not affect the rank-order of miniplasmin-inhibitory activity; it remained alpha 2M greater than alpha 2AP greater than AT. While the reaction of AT with SkPm was negligible, heparin stimulated this reaction dramatically. The SkPm-inhibitory activity of alpha 2AP was not changed by heparin. When plasma concentrations of alpha 2AP (1.05 microM) and AT (4.76 microM) were compared, AT inhibited greater amounts of SkPm in the presence of more than 5 units/ml of heparin. The increased SkPm-inhibitory activity of AT in heparin did not result from SkPm dissociation, and heparin did not decrease the rapid rate of streptokinase association with plasmin. These studies demonstrate that heparin can affect the regulation of fibrinolysis at multiple levels of the enzyme cascade.

Animals↗
PubMed1978

Intra-arterial streptokinase and renal artery embolization.

An animal experiment was constructed to simulate the clinical entity of renal artery embolization. Because of the high morbidity and mortality rates associated with the current methods of treatment, percutaneous infusion of the renal artery with streptokinase was evaluated as a new method of therapy. Results were analyzed by the following criteria: (1) arteriography, (2) gross pathology, and (3) differential renal function studies. In 12 dogs whose left kidney was embolized without treatment, renal function was 38 per cent of the contralateral normal kidney twenty-one days later. Seven dogs were embolized but treated immediately with intra-arterial streptokinase for six hours; renal function was increased to 58 per cent of the contralateral normal kidney. Various fibrinolytic agents and their possible clinical application in embolism are discussed.

Animals↗
PubMed1987

Iatrogenic superior vena cava syndrome treated with streptokinase.

The development of an iatrogenic superior vena cava syndrome secondary to a thrombosis from an indwelling Hickman catheter in a patient with ovarian carcinoma is presented. The patient was treated with a combination of streptokinase and heparin with successful and dramatic results. Streptokinase appears to be highly effective in the treatment of iatrogenic superior vena cava syndrome from Hickman catheters. It appears that the Hickman catheter may be safely left in situ post-treatment.

Catheterization↗
PubMed1991

Fibrinolytic behaviour of streptokinase-immobilized poly(methacrylic acid-g-ethylene oxide).

Streptokinase was immobilized on poly(methacrylic acid-g-ethylene oxide) surfaces by means of a modified coupling reagent method. The surfaces were activated with a carbodiimide to form an O-acyl isourea derivative, which, upon addition of the enzyme, condensed to form the corresponding amide. The quantity of enzyme immobilized on the surface increased as the reaction time with carbodiimide and streptokinase increased. The fibrinolytic activity of the immobilized enzyme systems was measured by a clot lysis assay. The dynamics of fibrin clot lysis was investigated for a period of up to 500 min. The lysis reaction mechanism was found to approximate a first-order fibrin degradation. In addition, the kinetic rate constant was found to increase with increasing immobilized enzyme content.

Drug Carriers↗
PubMed1994

Different effect of 5,6-trans-prostaglandin E2 on plasminogen activation by urokinase and streptokinase.

We examined the effects of 5,6-trans-prostaglandin E2 (trans-PG E2) on fibrinolysis and plasminogen activation by either urokinase or streptokinase. trans-PG E2 was found to enhance fibrinolysis induced by urokinase and inhibit the one by streptokinase. These effects were also appeared in the method using synthetic chromogenic substrate S-2251, which suggested that the effects of trans-PG E2 were induced in the circumstances without coagulation factors such as fibrinogen, thrombin or fibrin. Moreover, the enhancement effect of trans-PG E2 on fibrinolysis by urokinase was investigated. The result of SDS-PAGE indicated that plasmin formation rate from plasminogen by urokinase was accelerated in the presence of trans-PG E2. As trans-PG E2 increased the hydrolyzing rate of S-2288 by urokinase, trans-PG E2 directly interacted with urokinase. Therefore, the enhancement effect of trans-PG E2 on plasminogen activation by urokinase could be explained, at least in part, as follows: at first trans-PG E2 directly exerts its effect on urokinase, then it causes the increase of generation rate of plasmin from plasminogen.

Amino Acid Sequence↗
PubMed1989

Streptokinase in the management of arterial thrombosis in infancy.

Fourteen children with a mean age of 9.7 months (range 0.1-34.0 months) and a mean weight of 5.4 kg (range 2.5-10.0 kg) received intravenous streptokinase following arterial thrombosis. A median loading dose of 1000 U/kg (range 750-4000 U/kg) was given followed by an initial median infusion rate of 1000 U/kg/hr (range 750-1000 U/kg/hr). If thrombolysis did not occur and the fibrinogen level remained within the normal range (1.5-4.5 g/l) the infusion rate was increased to a maximum of 3000 U/kg/hr. Thrombolysis was achieved in all cases a mean of 16.7 hours (range 2-44 hours) after the start of treatment. The mean fibrinogen level at thrombolysis was 1.11 g/l (range 0.28-2.25 g/l) compared with pretreatment levels of 2.12 g/l (range 1.4-3.05 g/l). Minor bleeding from arterial puncture sites occurred in 6 children (43%). Streptokinase is a safe and effective treatment for arterial thrombosis in children.

Arterial Occlusive Diseases↗
PubMed1993

Acute myocardial infarction treated with intravenous streptokinase: 6-year follow-up.

Our objective was to investigate variables which, although occurring during the acute period, could influence the medium (1st year) and long-term (6th year) survival of infarcted patients. Of a total of 332 patients treated consecutively and prospectively according to the same protocol which included intravenous streptokinase, 305 survived the hospital phase and represent the study population. Mean patient age was 55.6 +/- 10 years and mean follow-up time was 3.33 years, with 1008.59 patient-years. The clinical course of the group was analyzed according to the following variables: left ventricle ejection fraction, hypotension per/peri streptokinase infusion, CK-MB peak, previous myocardial infarction, number of obstructed coronaries, reinfarction, sex, 'definitive' treatment, residual obstruction, age, pain/streptokinase infusion interval, patency of the 'culprit' coronary and infarct location. Overall, patient survival was 93.8 +/- 1.4% during the 1st year and 83.7 +/- 2.6% at the 6th. The following groups showed significantly different (log-rank) survivals: (a) 1st year: 94.6% for absence and 82.6% for presence of reinfarction (P = 0.0451); 97.9% for inferior and 91.4% for anterior infarct location (P = 0.044); 96.4% for ejection fraction > 50% and 90.6% for ejection fraction < or = 50% (P = 0.0187); 96.5% for angioplasty/surgery and 90.1% for clinical treatment (P = 0.0028); 95.5% for absence and 80.6% for presence of previous infarct (P = 0.0001). (b) 6th year: 88.3% for ejection fraction > 50% and 73.9% for ejection fraction < or = 50% (P = 0.028); 87.4% for < or = 65 and 66.4% for > 65 years (P = 0.0114); 89.6% for aggressive and 76.8% for conservative treatment (P = 0.013); 86.6% for absence and 60.7% for presence of previous infarct (P = 0.0009).

Actuarial Analysis↗
PubMed1991

The use of streptokinase in replant salvage.

This is the first report of the clinical use of direct intra-arterial streptokinase infusion to promote the salvage of a failing thumb replant. Anastomotic revision was performed on two occasions following thrombosis in the vein grafts used to replant an avulsed thumb. Recurrent thrombosis was treated successfully with conservative thrombolytic therapy consisting of a direct infusion of streptokinase, 20,000 I.U. per hour into the radial artery for 32 hours, followed by intravenous heparin, 40,000 I.U. for 24 hours. The thumb survived, with no tissue loss. Thrombolytic therapy is the only non-surgical means of dissolving intraluminal thrombus, and should be considered when thrombosis occurs in a replanted extremity.

Amputation, Traumatic↗
PubMed1990

Study of the structure of streptokinase conjugates with a hydrophilic vinylpyrrolidone copolymer.

The modification of streptokinase by a synthetic N-vinylpyrrolidone copolymer leads to formation of conjugates varying in structures according to the proportions of the components in the reaction medium. Based on data obtained from spectrophotometry, as well as sedimentation and diffusion analyses, it is shown that in the presence of excess protein in the reaction medium, formation of the main chain takes place via the copolymer associated with several protein globules. Under conditions of excess modifier copolymer, either single-site and/or multiple-site bonding is possible for the protein backbone, depending on the molecular weight of the copolymer. One of the models for the conjugates obtained in this manner has been corroborated by small-angle X-ray scattering data. CD spectral analyses has been performed in order to demonstrate that covalent modification does not alter the secondary structure of streptokinase in the conjugate whereas the tertiary structure undergoes local changes in conformation.

Circular Dichroism↗
PubMed1989

Novel shuttle vectors for improved streptokinase expression in streptococci and bacterial L-forms.

Novel shuttle vectors of small size and increased copy number capable of replication in Escherichia coli, L-forms of Proteus mirabilis, and streptococci were constructed from a streptococcal erythromycin-resistant plasmid and an Escherichia coli phasmid. The streptokinase gene, skc, was inserted into one of them, and skc expression was studied in Streptococcus sanguis, Streptococcus lactis, and in an L-form strain (LVI) of Proteus mirabilis. The new streptokinase shuttle plasmid, pMLS10 (7.3 kb), specified higher Skc yields in all hosts when compared to pSM752 constructed previously. In particular Proteus mirabilis LVI(pMLS10) proved to be the most productive host, exhibiting complete secretion of the active protein at yields as high as 24000 unit per ml.

Electrophoresis, Polyacrylamide Gel↗
PubMed1992

Evaluation of thrombolytic and systemic effects of the novel recombinant plasminogen activator BM 06.022 compared with alteplase, anistreplase, streptokinase and urokinase in a canine model of coronary artery thrombosis.

The thrombolytic and systemic effects of BM 06.022 were evaluated and compared with those of alteplase, anistreplase, streptokinase and urokinase in a canine model of coronary artery thrombosis. BM 06.022 consists of the kringle-2 and protease domains of human tissue plasminogen activator (t-PA) and is unglycosylated because of its expression in Escherichia coli cells. Thrombus formation in anesthetized open chest dogs was induced by electrical injury to the intimal surface of the left circumflex coronary artery at a high level site of obstruction. In heparinized dogs, none of six vehicle-treated animals exhibited reperfusion. Reperfusion was achieved in four of six dogs at 18.3 +/- 6 min after intravenous bolus injection of 140 kU/kg (0.24 mg/kg) of BM 06.022, whereas four of six dogs exhibited reperfusion later (p less than 0.05) at 76.5 +/- 16.1 min during infusion of 1.33 mg/kg of alteplase (0.13 mg/kg as initial bolus injection, followed by 0.66 mg/kg over 1 h and 0.53 mg/kg over 2 h). Significantly later (p less than 0.05) reperfusion than that achieved with BM 06.022 was achieved in five of six dogs at 57.8 +/- 12.1 min after intravenous injection of 0.4 U/kg of anistreplase. Streptokinase (21,000 IU/kg over 60 min) and urokinase (20,000 IU/kg as an intravenous bolus injection, followed by 20,000 IU/kg over 89 min) each induced reperfusion in three of six dogs but at 67 +/- 12 and 84.3 +/- 17.1 min (p less than 0.05 vs. BM 06.022), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Noninvasive assessment of speed and stability of infarct-related artery reperfusion: results of the GUSTO ST segment monitoring study. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries.

OBJECTIVES: The ST segment monitoring substudy of the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) trial compared the speed and stability of ST segment recovery among four thrombolytic strategies for acute myocardial infarction. BACKGROUND: Rapid resolution of ST segment elevation has been suggested as a noninvasive marker of infarct-related artery patency. We expected that patients treated with accelerated recombinant tissue-type plasminogen activator (rt-PA) would show a quicker recovery than that of other patients but that those treated with streptokinase would show greater stability of recovery. METHODS: ST segment monitoring was initiated in 1,067 patients within 30 min of the start of thrombolysis and continued for > 18 h with the use of a three-channel continuous vectorcardiographic monitor, a 12-lead continuous electrocardiographic (ECG) monitor or a three-channel (V2, V5, aVF) Holter ambulatory ECG monitor. RESULTS: Time to 50% recovery could be assessed in 618 patients and was similar in the four treatment groups: median 45 min with streptokinase/subcutaneous heparin, 45 min with streptokinse/intravenous heparin, 42 min with accelerated rt-PA and 47 min with combination therapy (p = 0.7). No significant difference among the thrombolytic regimens was shown with the three monitors used. Time to initiation of ST segment analysis was directly related to time to 50% recovery (p = 0.0001) and was its best predictor in a multiple regression model. ST segment elevation recurred equally in each treatment group (approximately 36%, p = 0.9) but was significantly more common in patients with a patent infarct-related artery (p = 0.033) or a low ejection fraction (p = 0.001). CONCLUSIONS: The greater 90-min patency seen with accelerated rt-PA in the angiographic substudy did not correlate with a shorter time to 50% ST segment recovery, possibly because of technical limitations and study design. The similar rates of recurrent ischemia (as assessed by ST elevation) among the regimens support the similar infarction and reocclusion rates seen in the main trial and angiographic substudy.

Drug Therapy, Combination↗
PubMed2006

Hydrophobic interaction expanded bed adsorption chromatography (HI-EBAC) based facile purification of recombinant streptokinase from E. coli inclusion bodies.

The downstream processing of recombinant streptokinase (rSK), a protein used for dissolution of blood clots has been investigated employing Escherichia coli inclusion bodies obtained after direct chemical extraction followed by expanded bed adsorption chromatography (EBAC). Streptokinase was over-expressed using high cell density (final OD(600)=40) culture of recombinant E. coli, and an SK protein concentration of 1080 mg l(-1) was achieved. The wet cell pellet after centrifugation was re-suspended in 8M urea containing buffer resulting in direct extraction of almost 97% of cellular proteins into solution. Compared to mechanical disruption using sonication, the direct extraction helped in simultaneous cell lysis and inclusion body (IB) solubilization in a single integrated step. The post-extraction solution containing cell debris and cellular proteins was diluted and directly loaded on to an EBAC column containing Streamline phenyl, without clarification. By passing the solution four times through the column and using 1M NaCl during loading, 82.7% rSK activity could be recovered in the 10mM sodium phosphate buffer used for elution. A 3-fold increase in specific activity of rSK, from 0.18 x 10(5) in cell lysate to 0.53 x 10(5)IU mg(-1) resulted after this step. rSK was further purified to near-homogeneity (specific activity=0.96 x 10(5)IU mg(-1)) by a subsequent ion-exchange step operated in packed bed mode. An overall downstream recovery of 63% rSK was achieved after EBAC and ion exchange chromatography. The paper thus describes the purification of rSK using a three-step regime involving simple, efficient and highly facile steps.

Adsorption↗
PubMed1983

Angiographic evidence of hemorrhagic myocardial infarction after intracoronary thrombolysis with streptokinase.

The reperfusion of acutely ischemic myocardium by intracoronary streptokinase thrombolysis is an exciting new therapy for acute myocardial infarction (MI). It appears that successful thrombolysis and reperfusion in the first few hours after acute coronary occlusion may salvage myocardium and possibly improve prognosis. A potential adverse effect of reperfusion is the production of hemorrhage in the area of myocardial necrosis. We report on a patient with prompt, successful coronary thrombolysis by streptokinase infusion who showed angiographic evidence of a hemorrhagic MI.

Aged↗
PubMed1996

Reduction of reinfarction and angina with use of low-molecular-weight heparin therapy after streptokinase (and heparin) in acute myocardial infarction.

This study examined whether extending the anticoagulation effect of heparin by low-molecular-weight heparin (clexane) can prevent recurrent myocardial infarction (AMI) treated by streptokinase. On the fifth day after AMI and after heparin therapy cessation, 103 patients were randomly assigned to either treatment with low-molecular-weight heparin (40 mg subcutaneously per day for 25 days, n=43) or control (no treatment, n=60). All patients were followed carefully for 6 months after the infarction date. A total of 32 patients (31%) sustained a cardiac event during the 6-month observation period. There were 12 patients (20%) with reinfarction in the control group versus 2 patients (4.6%) in the low-molecular-weight heparin group during the first 30 days of the study (p=0.02). One additional patient sustained reinfarction at 3 months of followup in the control group, which yielded a total of 13 patients (21.6%) sustaining reinfarction in the control group versus 2 patients (4.6%) in the low-molecular-weight heparin group during 6 months of followup (p=0.01). Angina pectoris after AMI was diagnosed in 13 control patients (21.6%) versus 4 low-molecular-weight heparin-treated patients (9.3%) (p=0.078) during the study period. No major bleeding events were reported in either low-molecular-weight heparin-treated or control patients. Among patients with recently diagnosed AMI treated by streptokinase, extending the anticoagulant effect of heparin for 25 days may prevent recurrent coronary events for at least one month.

Adult↗