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PubMed1998

Streptokinase as a mediator of acute post-streptococcal glomerulonephritis in an experimental mouse model.

Group A streptococcal infections are sometimes followed by the inflammatory kidney disease acute post-streptococcal glomerulonephritis (APSGN). To test the importance of streptokinase in the pathogenesis of this disease, isogenic strains of the nephritis isolate NZ131, differing only in the ability to produce streptokinase of the nephritis-associated ska1 genotype, were used for infection in a mouse tissue cage model for APSGN. Streptokinase production was found to be a prerequisite for the capacity of the strain to induce APSGN in mice. In addition, streptokinase was demonstrated in the kidneys of mice infected with the nephritogenic NZ131 and EF514 strains. After infection with the nonnephritogenic strain S84, neither streptokinase nor C3 deposition were observed. Deposition of streptokinase in the glomeruli was detected as soon as 4 days after infection. These findings provide support for the hypothesis that streptokinase initiates the nephritis process by glomerular deposition, which leads to local activation of the complement cascade. Detection of streptokinase in kidney tissue increased with the degree of glomerular hypercellularity. Thus, the severity of the pathological process may be a reflection of the degree of streptokinase deposition.

Animals↗

PubMed1976

Streptokinase in acute myocardial infarction: a controlled multicentre study in the United Kingdom.

In a multicentre trial of streptokinase in acute myocardial infarction 302 patients received an intravenous infusion of 2 500 000 IU of streptokinase over 24 hours, while 293 patients served as controls. Neither group received anticoagulants unless indicated by thromboembolic complications. No significant difference in mortality was evident during inpatient treatment nor at six-week or six-month follow-up. The inpatient death rate was 12-6% in the streptokinase group and 13-7% among controls. There was no significant difference in the peak levels or pattern of enzyme increase. The incidence of cardiac failure and reinfarction was similar in the two groups, but major arrhythmias were less common in those on streptokinase (P less than 0-05). In the streptokinase group there were 36 minor and six more serious haemorrhagic complications. Gastrointestinal haemorrhage may have contributed to the death of one patient in each group. There were 18 thromboembolic complications in the streptokinase group and 38 among the controls. Pathological examination of the hearts of 25 patients who had taken streptokinase and 24 controls showed no striking differences between the groups, but haemorrhagic infarcts were found in three patients who had received streptokinase. An infusion of streptokinase within 24 hours of the onset of acute myocardial infarction does not significantly affect the mortality or course of the illness up to six months.

Aged↗

PubMed1995

Effects of streptokinase in patients presenting within 6 hours of prolonged chest pain with ST segment depression.

BACKGROUND: The effects of streptokinase on the occurrence of a combined clinical outcome in patients presenting with recent chest pain and ST depression were investigated in view of the role of thrombus in the pathogenesis of acute ischaemic syndromes. METHODS: 112 patients aged < or = 75 years presenting within 6 h of the last episode of ischaemic chest pain of least 20 min duration with > or = 1 mm ST depression were randomised in a double blind manner to receive either streptokinase 1.5 million units over 30 min (n = 57) or placebo (n = 55). The primary end point was the combination of death, frequency of myocardial infarction (defined as peak creatine kinase > 600 U/ml), need for angiography because of uncontrollable ischaemia, and an exercise test within 35 days showing > or = 1 mm ST depression at < or = 6 min. The secondary end points were safety, frequency of chest pain, readmission with myocardial infarction or unstable angina, or need for revascularisation between 35 days and 1 year. The severity of ST depression on presentation was analysed with respect to clinical outcome. RESULTS: The frequency of the combined hierarchical end point of death, myocardial infarction, early angiography, and a positive exercise test was 82% (47 of 57 patients) with streptokinase and 75% (41 of 55 patients) with placebo. There were four deaths, two in each group. 27 patients (47%) receiving streptokinase and 22 (40%) receiving placebo developed myocardial infarction. 11 patients (eight streptokinase and three placebo) required coronary arteriography and subsequent revascularisation because of angina uncontrolled by medical treatment. 44 patients (22 in each group) had a positive exercise test. There were three further cardiac deaths (one streptokinase, two placebo), and three noncardiac deaths within 1 year. A conservative approach to intervention was adopted and over a period of 1 year 29 patients (26%) (13 streptokinase and 16 placebo) underwent revascularisation procedures. Three patients (two streptokinase and one placebo) required transfusion. ST depression > or = 3 mm had 90% specificity but only 60% positive predictive value for myocardial infarction at presentation (P = 0.008, stepwise logistic regression). ST depression > or = 2 mm was predictive of death, late development of myocardial infarction, or a need for angiography (P = 0.02). CONCLUSION: Patients presenting with ischaemic chest pain and ST depression frequently develop myocardial infarction. Severe ST depression is predictive of an adverse outcome. The 35 day (3.6% cardiac and total) and 1 year mortality (8.9% total, 6.3% cardiac) are low with conservative management and expeditious revascularisation. Streptokinase treatment within 6 h of the last episode of pain does not seem to be beneficial.

Aged↗

PubMed1994

Role of streptokinase in the treatment of acute loculated parapneumonic pleural effusions and empyema.

BACKGROUND: Intrapleural administration of streptokinase has been shown in a few small series to be effective treatment for complicated parapneumonic effusions and pleural empyemas, but techniques of instillation of streptokinase differ. The role of streptokinase in promoting drainage was investigated prospectively in a larger series of patients with complicated parapneumonic effusions and pleural empyemas. METHODS: Twenty consecutive patients with parapneumonic effusions, 15 with complicated parapneumonic effusions and five with pleural empyemas, drawn from 160 patients presenting with pleural effusions were studied. The age of the patients ranged from 15 to 92 years. Initial thoracocentesis showed mean (SD) values of pH 7.1 (0.15), glucose 45.9 (17.5) mg/dl, white blood cell count 12,000 (6627)/mm3. Streptokinase was administered intrapleurally in a single daily dose of 250,000 units in 100 ml normal saline via the chest tube once the drainage was < 100 ml/24 hours. Patients were treated for 3-10 (mean 6) days. RESULTS: Following administration of streptokinase a clinical and radiological improvement was noted in all but one patient who died on the fourth day of hospitalisation due to widespread adenocarcinoma. Another patient with clinical but minimal radiological improvement underwent thoracotomy, but a clear pleural space with only fibrotic changes was found. The mean (SD) volume of fluid drained 24 hours before streptokinase was 42.5 (39) ml, which increased in the first 24 hours after streptokinase to 334 (130) ml. Radiological evaluation showed an excellent improvement in 14 of the 20 patients, a moderate improvement in three, and minimal improvement in the remaining three patients. One patient developed a high fever as an adverse reaction to streptokinase. All 19 patients who completed the treatment were well at follow up 6-30 months (mean 15 months) later. CONCLUSIONS: Intrapleural instillation of streptokinase is an effective and safe mode of treatment for complicated parapneumonic effusions and pleural empyemas and alleviates the need for thoracotomy.

Adolescent↗

PubMed1994

Abrupt complement activation and transient neutropenia in patients with acute myocardial infarction treated with streptokinase.

BACKGROUND: Whether and to what extent complement is activated in acute myocardial infarction (AMI) and how it contributes to inflammation of the ischemic area are not yet clear. Fibrinolytic agents used for thrombolysis are known to activate complement in vitro and may contribute to its activation in vivo. The aim of this study was to measure the extent of complement activation in AMI patients, some treated and some not treated with streptokinase. In addition, because abrupt complement activation in vivo is usually associated with leukocyte margination, plugging of cells in the microcirculation, and hypotension, we correlated complement activation with leukocyte numbers and mean arterial pressure. METHODS AND RESULTS: Forty AMI patients were studied: 20 were treated with streptokinase (1.5 million IU IV over 60 minutes), and 20 were not given any fibrinolytic agent. The extent and severity of AMI were not significantly different in both groups. Blood samples were drawn on arrival at the hospital, during streptokinase infusion, and then daily for 1 week. Time-matched samples were also drawn from patients not treated with streptokinase. We measured plasma levels of anaphylatoxin C4a, C3a, and C5a by radioimmunoassay and membrane attack complexes SC5b-9 by enzyme immunoassay. Leukocytes and arterial pressure also were measured when samples were obtained. C4a, C3a, and SC5b-9 levels increased about 10-fold (P < .0001) during infusion of streptokinase. There were no significant increases in complement catabolic products in AMI patients not treated with streptokinase. There was a significant transient leukopenia (mean +/- SEM, -29.5 +/- 7.0%; P = .001) and decreases in systolic and diastolic pressures (systolic, -29.3 +/- 3.2%, P < .0001; diastolic, -27.5 +/- 3.4%, P < .0001) after 15 minutes of streptokinase infusion in coincidence with the peak of anaphylatoxins in plasma. CONCLUSIONS: Streptokinase treatment of AMI causes abrupt activation of the complement system, whereas no significant complement activation can be detected in plasma of AMI patients not treated with fibrinolytic agents. Complement activation causes a transient leukopenia, as reported for such other clinical conditions as dialysis and cardiopulmonary bypass, and possibly contributes to the hypotension observed during streptokinase treatment.

Aged↗

PubMed1992

Intrapleurally administered streptokinase in the treatment of acute loculated nonpurulent parapneumonic effusions.

Adequate pleural drainage is believed to be an essential component of the management of low pH-low glucose parapneumonic effusion. Parapneumonic effusions may become loculated rapidly, preventing adequate drainage with a single chest tube. Administration of intrapleural streptokinase may be effective in promoting drainage for loculated, nonpurulent low pH-low glucose parapneumonic effusions when fibrin adhesions may not yet be organized. Intrapleural streptokinase was used in 12 patients with relatively large, symptomatic, loculated, nonpurulent parapneumonic effusions in whom the initial thoracentesis demonstrated a pH less than or equal to 7.0 and/or glucose less than or equal to 40 mg/dl, and when inadequate drainage was demonstrated roentgenographically despite tube thoracostomy. Mean pleural fluid WBC was 9,750/mm3 (range, 1 to 27 K), and pleural fluid glucose and pH were 33 +/- 21 mg/dl and 6.95 +/- 0.19, respectively. A solution of streptokinase, 250,000 units in normal saline, was given intrapleurally via the chest tube. Effectiveness of intrapleural streptokinase was assessed radiographically and by monitoring the volume of fluid drained from the chest tube after streptokinase instillation. A greater than 50% improvement in the CXR was seen in nine of 12 patients after intrapleural administration of streptokinase. The volume of fluid out in the first 48 h post-streptokinase was 849 +/- 836 ml (range, 100 to 3,000). In addition, clinical improvement (decreased chest discomfort, less dyspnea, or reduced fever) was noted in eight of 12 patients after streptokinase treatment. We conclude that intrapleural administration of streptokinase is an effective adjunct to the management of nonpurulent, loculated parapneumonic effusions that may reduce the need for multiple chest tubes or surgical drainage.

Acute Disease↗

PubMed1989

Streptokinase-induced anaphylaxis.

Streptokinase is a thrombolytic agent used most commonly for the dissolution of thrombi obstructing coronary arteries during acute myocardial infarction (MI). Anaphylactic reactions induced by streptokinase occur rarely. We report the case of a patient with acute MI who developed anaphylaxis shortly after the initiation of an intravenous infusion of streptokinase. The patient became profoundly hypotensive and developed an erythematous rash that spread rapidly to cover most of his body. He required mechanical ventilation and the administration of epinephrine for blood pressure support, which succeeded after dopamine and norepinephrine had failed. Streptokinase-induced anaphylaxis is thought to be mediated by immunoglobulin E (IgE), and patients who develop this adverse reaction have been shown to have higher serum concentrations of IgE to streptokinase than those who do not. Epinephrine is the agent of choice for the management of hypotension associated with anaphylaxis. Little evidence exists to support the routine pretreatment of patients who are to receive streptokinase with corticosteroids and/or antihistamines. Streptokinase skin testing may be a useful and accurate means of identifying patients at risk for streptokinase-induced anaphylaxis. Further investigation is required to determine the appropriateness of skin testing in streptokinase therapy.

Anaphylaxis↗

PubMed1977

Activation of human plasminogen by equimolar levels of streptokinase.

Native Glu-human plasminogen (Mr approximately 92,000 with NH2-terminal glutamic acid) is able to combine directly with streptokinase in an equivalent molar ratio, to yield a stoichiometric complex. The plasminogen moiety in the complex then undergoes streptokinase-induced conformational changes. As a result of such, an active center develops in the plasminogen moiety of the complex. This proteolytically active complex then activates plasminogen in the complex to plasmin and at least two peptide bonds are cleaved in the process. The data presented in this paper reveal that initially an internal peptide bond of plasminogen (in the complex) is cleaved to yield a two-chain, disulfide-linked plasmin molecule. The heavy chain (Mr approximately 67,000 with NH2-terminal glutamic acid) of this plasmin molecule has an identical NH2-terminal amico acid as the native plasminogen. The light chain (Mr approximately 25,000 with NH2-terminal valine) of plasmin is known to be derived from the COOH-terminal portion of the parent plasminogen molecule. A second peptide is then cleaved from the NH2-terminal end of the heavy chain of plasmin producing a proteolytically modified heavy chain (Mr =60.000 with NH2-terminal lysine). This cleavage of the NH2-terminal peptide from the heavy chain of plasmin is shown to be mediated by the dissociated free plasmin present in the activation mixture. Plasmin in the streptokinase-plasmin complex is unable to cleave this NH2-terminal peptide. This same NH2-terminal peptide can also be cleaved from native Glu-plasminogen or from the Glu-plasminogen-streptokinase complex by free plasmin and not by a complex of streptokinase-plasmin. From these studies we conclude (a) in the streptokinase-plasminogen complex, the NH2-terminal peptide need not be released prior to the cleavage of the essential Arg-Val peptide bond which leads to the formation of a two chain plasmin molecule and (b) that this peptide is cleaved from the native plasminogen or from the heavy chain of the initially formed plasmin in the streptokinase complex by free plasmin and not by the plasmin associated with streptokinase. In agreement with this, plasmin associated with streptokinase was unable to cleave the NH2-terminal peptide from the isolated native heavy chain possessing glutamic acid as the NH2-terminal amino acid; whereas free plasmin readily cleaved this peptide from the same isolated Glu-heavy chain.

Amino Acids↗

PubMed1988

Immediate versus delayed coronary grafting after streptokinase treatment. Postoperative blood loss and clinical results.

Of all patients with acute evolving myocardial infarction treated surgically at Duke University Medical Center between 1984 and 1986, 27 patients given high doses (greater than 1.5 million units) of streptokinase preoperatively were studied. Eleven patients who received streptokinase had coronary bypass grafting 12 hours after thrombolytic therapy (early hours), eight patients between 12 and 72 hours (delayed), and eight patients beyond 72 hours (late hours). Seventeen patients who underwent coronary bypass grafting within 6 hours of the onset of symptoms, without preoperative streptokinase, were included as control patients. Only the patients having early operation had significantly greater postoperative blood loss; postoperative use of red blood cells; fresh-frozen plasma; cryoprecipitate; prolonged postoperative prothrombin time; and prolonged partial thromboplastin time. Patients having delayed or late operations did not differ significantly from patients not receiving streptokinase. Only the interval between time of streptokinase administration and operation could account for the coagulopathy and the postoperative bleeding complications in the early group. Patients in the early group had a higher in-hospital mortality (27% versus 6% for the non-streptokinase group) and major noncardiac morbidity (36% versus 12% for the non-streptokinase group). Patients in the delayed and late groups had minimal postoperative complications and no mortality. Observations were not explained by differences in total ischemic time, number of angioplasty failures, or number of patients with cardiogenic shock between the early group and the non-streptokinase group. Postoperative bleeding and massive use of blood products seemed to be contributory factors: Two of three deaths in the patients having early operations were associated with clinical suspicion of tamponade. Patients undergoing coronary bypass grafting within 12 hours of streptokinase therapy appear to be a high-risk group in a more emergent, uncontrolled clinical setting and require aggressive monitoring and correction of coagulopathy.

Blood Coagulation Disorders↗

PubMed1986

Intra-arterial streptokinase therapy to relieve acute limb ischemia.

One hundred two patients with acute lower limb ischemia were treated with intra-arterial streptokinase. Thirty-seven patients had occluded vascular grafts and sixty-five had had no previous vascular surgery. Eighty-six limbs were acutely threatened. Intra-arterial streptokinase was given as an initial loading dose with a lower maintenance dose given afterward. The mean duration of therapy was 59 hours and hematologic monitoring was meticulous. Indications for intra-arterial streptokinase therapy were contraindication to surgery, anticipation of technically difficult surgery, and multiple occlusions that required separate surgical approaches. Seventy-two legs were saved (71%) and 30 amputated. Morbidity was low and only 1 of the 11 deaths was attributable to streptokinase. No leg was lost that would otherwise have been saved by straightforward surgery and no leg was lost that had not been previously threatened. In 46 patients for whom emergency femorotibial bypass would have been necessary, 35 legs (76%) were saved. Forty-three patients had vascular reconstruction immediately after streptokinase therapy was stopped, to bypass occlusive lesions that had been demonstrated by the thrombolytic therapy in 28 patients, and because streptokinase had produced no response in 15 patients. The advantages of intra-arterial streptokinase in the management of the acutely ischemic leg are that the leg may be saved without surgery, that surgery is not precluded, that the patient can be made as fit as possible for surgery during the streptokinase infusion, and that streptokinase can facilitate surgery by delineating underlying vascular pathologic conditions and clearing distal runoff vessels.

Acute Disease↗

PubMed1977

[Stability of streptokinase incubated in various solvents at different temperatures (author's transl)].

Streptokinase was dissolved in various solvents and the decay recorded. The method employed was a recently described clot lysis assay for quantitative streptokinase determination. The decrease in activity of 5 u streptokinase, 1500 u streptokinase, and 50,000 u steptokinase dissolved in one milliltre of different solvents (NaCl solution, glucose solution, laevulose solution, dextran solution (Rheomacrodex), gelatin solution (Haemaccel, starch solution (Plasmasteril,albumin solution, Michaelis buffer, heparin-glucose solution) and incubated over various periods of time (15 min, 30 min, 45 min, 60 min, 4h, 8h, 12h, 48h) was investigated. Solution media tested for streptokinase-potecting quality were broken down into three groups.-Group I: Solvents displaying excellent stabilizing properties (gelatin, albumin).-Group II: Solvents displaying medium stabilizing properties (dextran, levulose)--Group III: Solvents displaying properties (starch, NaCl, glucose, Michaelis buffer).--In testing streptokinase concentrations as used for therapeutic purpose (1500 u/ml, 50,000 u/ml), no decay was found to take place over observation periods as long as 48 h. This finding was independent of the different solvents (Group I, II or III) employed. Heparin stored with streptokinase at rooom temperature did not alter the streptokinase stability. From the clinical point of view, the choice of solvents for streptokinase infusion turned out to be of minor importance.

Albumins↗

PubMed2004

Effectiveness of intrapericardial administration of streptokinase in purulent pericarditis.

BACKGROUND AND PURPOSE: Purulent pericarditis is very rare. However, among patients suffering from this disease the mortality rate is very high. The aim of this study was to evaluate the effectiveness and side effects of intrapericardial streptokinase administration in patients with confirmed purulent pericarditis. PATIENTS AND METHODS: Three patients, one 50-year-old man and two women aged 64 and 40 years, who were admitted to the intensive care unit (ICU) due to purulent pericarditis, entered the study. In all three cases a subxiphoid pericardiotomy followed by insertion of a drainage line into the pericardial space was performed. Antibiotic therapy was started immediately on admission to the hospital. Despite continued antibiotic therapy in all three patients, daily drainage from the pericardium--during several days after surgery--staggered between 50-200 ml/day. Due to considerable purulent pericardial drainage loculations and/or fibrin deposits confirmed by echocardiography, streptokinase (500,000 IU dissolved in 50 ml of normal saline) was administered into the pericardial space over 10 min, using the previously inserted drainage catheter. This regimen was repeated after 12 and 24 h. The total dose of streptokinase was 1,500,000 IU. RESULTS: The clinical effect of intrapericardial streptokinase administration was excellent. Several days after intrapericardial administration of streptokinase, drainage of purulent pericardial fluid stopped. No complications associated with intrapericardial streptokinase administration were observed. In the follow-up echocardiography (in two patients repeated 6 and 9 months after delivery of streptokinase), pericardial fluid and echocardiographic signs of pericardial constriction were not observed. CONCLUSION: Intrapericardial administration of streptokinase in purulent pericarditis is effective and safe.

Adult↗

PubMed1992

A comparison between intravenous streptokinase and tissue plasminogen activator with early intravenous heparin in acute myocardial infarction.

To compare the effects of two thrombolytic agents, streptokinase and recombinant tissue-type plasminogen activator (rTPA) with early heparinization, on left ventricular function, coronary patency and reinfarction rates, bleeding complications, and short- and long-term mortality, we studied 122 patients with acute myocardial infarction prospectively. All of them fulfilled the standard criteria for thrombolytic therapy. One group (n = 63) received 1,500,000 units of streptokinase over 1 hour, and one group (n = 59) received 100 mg of rTPA over 3 hours. Baseline data showed no significant differences between the streptokinase and rTPA groups. Results of predischarge studies 10 to 14 days after infarction revealed that there was no difference in left ventricular ejection fraction between the two groups (48.3% in the streptokinase group and 49.9% in the rTPA group; p = 0.67). The patency rate of the infarct-related artery tended to be higher in the rTPA group compared with the streptokinase group (77% vs 57%, p = 0.19). In-hospital spontaneous bleeding occurred after streptokinase in seven patients (11.1%) and after rTPA in eight (13.6%; p = 0.89). One patient had intracranial bleeding after rTPA and died 13 hours later. The early mortality rate within 30 days of acute myocardial infarction was 5 of 63 (7.9%) for the streptokinase group and 2 of 59 (3.4%) for the rTPA group (p = 0.49). During the 19.3-month follow-up period, reinfarction occurred in seven patients (11%) in the streptokinase group and in three (5%) in the rTPA group (p = 0.3). The mortality rates were 10 of 63 (16%) and 3 of 59 (5%), respectively (p = 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)

Aspirin↗

PubMed1988

Do different doses of intravenous streptokinase alter the frequency of coronary reperfusion in acute myocardial infarction?

This study assessed the relative efficacy of 3 doses of intravenous streptokinase in causing hypofibrinogenemia and coronary reperfusion in patients with acute myocardial infarction. Accordingly, 56 patients (50 men and 6 women, ages 58 +/- 10 years [mean +/- standard deviation]) with evolving acute myocardial infarction and chest pain less than or equal to 5 hours in duration were assigned to receive varying doses of streptokinase. Twenty were administered 500,000 units during 145 minutes, 18 were given 750,000 units during 30 minutes and 18 received 1.5 million units in 60 minutes of streptokinase. Serum creatine kinase was measured on admission and 6, 12, 18 and 24 hours after the initiation of streptokinase. The time intervals from onset of pain to peak creatine kinase and from streptokinase administration to peak creatine kinase were used to determine the occurrence of reperfusion. The plasma fibrinogen concentration was measured 30, 60, 90 and 120 minutes after the initiation of streptokinase. For the 3 groups, the time from onset of pain to peak creatine kinase was less than 17 hours and the time from streptokinase to peak creatine kinase was 6 or 12 hours in 15 (75%), 16 (89%) and 12 patients (67%), respectively (differences not significant). The plasma fibrinogen concentration decreased to 45 +/- 34 mg/dl, 19 +/- 14 mg/dl and 29 +/- 43 mg/dl, respectively, during the 2 hours after streptokinase was begun (p less than 0.05 for the first versus the second and third values).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1993

Comparison of results of intravenous infusion of anistreplase versus streptokinase in acute myocardial infarction.

This randomized study compares the coronary perfusion rate in patients with acute myocardial infarction (AMI) treated with 2 different intravenous thrombolytic agents: streptokinase 1.5 million U given over 60 minutes and anisoylated human plasminogen streptokinase activator complex (anistreplase) administrated as a bolus of 30 U over 5 minutes. One hundred seventy-five patients (149 men and 26 women, mean age 54 years) have been included in this study. Eighty-nine patients were treated with anistreplase and 86 patients with streptokinase. AMI was inferior in 54 patients (61%) in the anistreplase group and in 54 patients (63%) in the streptokinase group. It was anterior in 35 (40%) and 32 (37%) patients, respectively. Coronary angiography and ventriculography were performed at a mean time (+/- SEM) of 207 +/- 11 minutes after the beginning of thrombolysis in 170 patients. A perfusion score grade of 2 or 3 according to the Thrombolysis in Myocardial Infarction trial was found in 63 patients (72%) in the anistreplase group and in 56 patients (68%) in the streptokinase group (p = NS). Severe bleeding occurred in 7 patients (8%) after anistreplase and in 6 patients (7%) after streptokinase. No cerebral hemorrhage occurred. Nine patients (5%) died during their hospital stay: 6 after anistreplase and 3 after streptokinase. It is concluded that intravenous administration of anistreplase or streptokinase is efficient and safe. Coronary patency 207 minutes after fibrinolysis, incidence of adverse events and mortality are similar in both groups.

Adult↗

PubMed1990

Activation of human and bovine plasminogens by the microplasmin and streptokinase complex.

Human microplasmin is a catalytically active fragment of human plasmin. It consists of a 31-residue C-terminal peptide derived from the A chain bound through two disulfide bonds to the intact B chain of plasmin. It has similar amidolytic and proteolytic activities as the native human Lys-plasmin on a molar basis. Human microplasmin can form a complex with streptokinase, in a one to one stoichiometry, like the native human Lys-plasmin. The stoichiometric human microplasmin and streptokinase complex is an efficient activator of bovine plasminogen which can not be activated by streptokinase alone. The formation of human microplasmin.streptokinase complex was also directly demonstrated by a gel filtration column chromatography. Moreover, bovine plasminogen can not be activated by a mixture of bovine or porcine microplasmin and streptokinase. The equimolar complex of human microplasmin.streptokinase, human Lys-plasmin.streptokinase, or streptokinase alone has the same activator activity toward human Lys-plasminogen. The human microplasmin.streptokinase complex, however, has a significantly higher activator activity than human Lys-plasmin.streptokinase complex or streptokinase alone toward human Glu-plasminogen. The direct interaction between streptokinase and light chain domain of human plasmin is demonstrated in the complex formation. The difference in the activator activities of plasmins from various animal sources in complex with streptokinase therefore might be due to the difference in the compositions of light chains of plasmins.

Amino Acid Sequence↗

PubMed1990

Cellular-phase fibrinolysis and coronary reperfusion during acute myocardial infarction: a study in patients receiving intravenous streptokinase-methylprednisolone therapy.

Activation of plasma plasminogen to plasmin is the objective of current strategies for thrombolytic therapy. Although thrombolytic activity in blood involves a large cellular component as well as that in plasma, the contribution of this cellular phase to clinical thrombolysis has not been examined. Using a 125I-fibrin test tube assay, we determined blood, plasma and calculated cellular phase fibrinolytic activities in 39 patients with acute myocardial infarction before, immediately after, and at 2 hours after therapy with an intravenous streptokinase-methylprednisolone regimen. By coronary angiography and time to peak creatine phosphokinase levels, 32 patients had coronary reperfusion and 7 did not. Before streptokinase therapy, cellular phase activity of patients who reperfused was more than 2-fold greater than that of patients who did not reperfuse (p less than 0.001), while plasma activities were identical, suggesting that intrinsic cellular phase activity may be a determinant of the success of subsequent thrombolytic therapy. In both groups, in addition to the expected (and similar) increases in plasma activity, cellular phase activity increased when compared with pre-treatment values (+96% to +248%; p less than 0.001), with accompanying increase in blood granulocyte count (+23% to +65%), indicating that blood cells, as well as plasma, are major contributors to streptokinase-mediated fibrinolysis. Cellular phase stimulation was reproduced in a patient receiving streptokinase without methylprednisolone, and by addition of streptokinase to normal blood in vitro, indicating that streptokinase alone could account for these effects. Increased cellular phase activity in patients who reperfused after streptokinase was similar to that in those who did not reperfuse, when pre-treatment values were considered. These findings indicate that initial cellular phase activity in blood may determine subsequent fibrinolytic response, and that there is a significant cellular phase component to the fibrinolytic response to streptokinase, probably mediated by increased numbers of blood neutrophils, with a possible contribution from increased activity of individual neutrophils.

Blood Cell Count↗

PubMed1986

Immunotargeting of erythrocyte-bound streptokinase provides local lysis of a fibrin clot.

The creation of an anticollagen antibody-erythrocyte-streptokinase complex has been described. Immobilization of both proteins on erythrocyte membrane has been performed using an avidin-biotin interaction. Modification of streptokinase with (6-biotinylamido)hexanoic acid N-hydroxysuccinimide ester at the concentration of 1.1 mM (20% modification of protein amino groups) provides effective (up to 90%) attachment of streptokinase to an avidin-carrying erythrocyte surface. The loss of streptokinase activity due to modification under these conditions is not significant. The maximal attachment of streptokinase was equal to about 50 ng per 10(6) erythrocytes, i.e., about 5 X 10(5) molecules of streptokinase per erythrocyte. The presence of streptokinase in the incubation mixture inhibited the attachment of antibodies by about 50%. Nevertheless, co-immobilization of anticollagen antibody (1.0 X 10(5) molecules per cell) and streptokinase (2.8 X 10(5) molecules per cell) on the erythrocyte surface provided firm and specific binding of such erythrocytes to a collagen-coated surface (1.6 X 10(6) bound cells per 1 cm2 on a collagen-coated surface against 0.006 X 10(6) bound cells on a bovine serum albumin-coated surface). Targeting of such erythrocytes led to local lysis of a fibrin clot in the target zone. The properties described offer in principle the possibility of the application of this or a similar system of fibrinolytic agent targeting for the preventive therapy of rethrombosis during surgical manipulations on vessels.

Antibodies↗