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PubMed1988

Protection of myocardial function and coronary vasculature by streptokinase.

Coronary artery reperfusion established by thrombolytic agents early in the evolution of an acute myocardial infarction is known to result in the salvage of otherwise jeopardized heart muscle. Recently, experimental evidence has suggested that reactive products of oxygen are formed as a result of reperfusion and can increase the amount of myocardial tissue that becomes irreversibly damaged. The purpose of the present study was to determine if the thrombolytic agent, streptokinase, could serve to scavenge reactive species of oxygen, thereby protecting the myocardium by a mechanism independent of its ability to lyse an occlusive thrombus. Rabbit isolated hearts were perfused at a constant rate with Krebs-Henseleit buffer (25 ml/min, 31 degrees C, pH 7.4) using a modified Langendorff method. Changes in the permeability of the coronary vascular bed were determined with 125I-labeled albumin added to the perfusion buffer. An intraventricular fluid-filled latex balloon connected to a pressure transducer maintained the left ventricle in an isovolumic state and was used to detect changes in myocardial contractility throughout the study protocol. Electrolysis of the oxygenated Krebs-Henseleit perfusion buffer with a 20 mA direct current for 2 min, delivered with a stainless-steel anode (proximal) and a platinum cathode (distal), resulted in the generation of reactive products of oxygen. Perfusion of the isolated heart with buffer containing the products of electrolysis resulted in an increase in mean coronary artery perfusion pressure, from 48 +/- 3 to 121 +/- 6 mm Hg [mean +/- SEM (n = 17)], and an increase in the left ventricular end-diastolic pressure, from 10 +/- 1 to 54 +/- 6 mm Hg. The addition of streptokinase (150 U/ml) or heparin (20 U/ml) to the perfusion medium attenuated the observed increase in coronary artery perfusion pressure from 42 +/- 3 to 73 +/- 9 mm Hg (n = 9) or from 43 +/- 2 to 98 +/- 9 mm Hg (n = 9), respectively. In addition, streptokinase prevented the increase in the left ventricular end-diastolic pressure (11 +/- 1 to 36 +/- 5 mm Hg, n = 9) and preserved left ventricular function as determined by the pressure-volume relationship. Myocardial accumulation of 125I-labeled albumin after exposure of the heart to the reactive products of oxygen was attenuated by the addition of streptokinase or heparin to the buffer solution. The data suggest that streptokinase and, to a lesser extent, heparin may preserve myocardial and coronary vascular function by scavenging reactive oxygen species.

Animals↗

PubMed2002

Improving the quality of kidneys from non-heart-beating donors, using streptokinase: an animal model.

BACKGROUND: Non-heart-beating donors (NHBD) offer a promising potential to increase the cadaveric organ donor pool, especially for kidneys. However, almost half of NHBD kidneys are discarded after viability assessment. This wastage is costly in both human and monetary terms. Intravascular thrombosis at the time of donor death is an event leading to failure in the viability assessment. We have developed an animal model to investigate the effects of the addition of streptokinase to the in situ flush medium before transplant in an attempt to redress the situation. METHODS: Two groups of eight healthy young Landrace Yorkshire white pigs were entered into the study. Both groups were subjected to approximately 70 min warm ischemia. Both groups received an intravascular flush with 4 L of Marshall's solution with heparin (1000 IU/L); one group of pigs also had streptokinase (1.5 MIU/L) added. After donor nephrectomy, all kidneys were machine perfused for 4 hr. Data on perfusion characteristics were taken and samples of kidney effluent were assayed for tissue damage biomarkers, glutathione S-transferase (GST) and alanine aminopeptidase (Ala-AP). Wedge sections of porcine kidneys were taken at the end of perfusion, for histological analysis. RESULTS: Data on machine perfusion parameters (temperature, mean pressure index, resistance) indicate better cooling, lower resistance, and lower mean pressure index in the streptokinase-treated group of pigs. GST and Ala-AP levels were increased in the nonstreptokinase group perfusates. Histopathological analysis of porcine kidneys indicated more ischemic injury and tissue damage in the nonstreptokinase group. CONCLUSION: The use of streptokinase in this porcine NHBD model conferred benefits to donor kidneys when assessed by machine perfusion. Markers of biochemical injury indicated that less renal tissue damage occurred with the incorporation of streptokinase in the in situ flush medium.

Animals↗

PubMed1993

Use of creatine kinase isoforms for diagnosis of infarct artery patency after thrombolytic therapy with streptokinase.

BACKGROUND: We investigated whether the proportion of creatine kinase (CK) MM3 to total MM isoform, measured in a single blood specimen taken at 3 hours after starting intravenous administration of streptokinase to patients with developing myocardial infarction, would give reliable information on patency or occlusion of the infarct-related coronary artery. METHODS: Fifty-nine patients received streptokinase 1.5 x 10(6) U intravenously within 6 hours of onset of prolonged chest pain and ST-segment elevation. Patency of the infarct-related coronary artery was assessed by arteriography at 2.6 +/- 0.3 (SD) hours after starting streptokinase. Creatine kinase MM isoforms were measured by chromatofocusing in blood taken at 3 hours after streptokinase. RESULTS: A proportion of CKMM3 to total CKMM of greater than 50% was present in 34 of 34 patients (100%) with a patent, infarct-related artery at arteriography and whose peak total CK activity reached twice the upper normal limit for our laboratory (600 U/L). CKMM3/total CKMM was less than 50% in 14 of 18 patients (78%) in whom the infarct-related artery was occluded. In five of six patients with a nondiagnostic total CK rise (peak < 600 U/L), 3-hour CKMM3/total CKMM was less than 50% despite a patent artery. CKMM3 was not measurable in one patient. CONCLUSIONS: A proportion of CKMM3/total CKMM of greater than 50% is highly sensitive for prediction of infarct artery patency at 3 hours after administration of streptokinase. However, the test used in this way is not reliable for patients with "prevented" myocardial infarction. Also, positive tests do occur in patients with angiographically occluded arteries, possibly signifying intermittent reperfusion and occlusion.

Adult↗

PubMed1976

Is streptokinase useful in the treatment of deep vein thrombosis?

Because of its fibrinolytic action, streptokinase is believed to reduce the severity of the postthrombotic syndrome in patients with deep vein thrombosis. A prospective and a retrospective study have been undertaken in an attempt to determine when this therapy is useful for patients with deep vein thrombosis. The prospective study included 15 patients with deep vein thrombosis: 5 were treated in the hospital with streptokinase and heparin and 5 only with heparin, 5 were treated at home with only phenprocoumon. All the patients received oral anticoagulant therapy for at least 6 months. Three to four months after the acute episode, phlebography and venous pressure measurements were carried out. Streptokinase appeared to give the best results but with more side-effects. In the retrospective study, 51 patients who had had deep vein thrombosis in 1969 were reexamined 31-47 months later. It was found that more than 50% of the patients with a thrombosis in the femoral and/or iliac vein developed a severe postthrombotic syndrome, in contrast to only 9% of those with a thrombosis in the popliteal vein or lower. It is recommended, on the basis of both the prospective and the retrospective study, that patients with a thrombosis in the femoral and/or iliac vein should be treated with either heparin or streptokinase during the early stage. It is probable that streptokinase will significantly decrease the frequency and severity of the postthrombotic syndrome in these patients in particular, although this has not yet been proven.

Adult↗

PubMed1978

A prospective study of streptokinase and heparin in the treatment of deep vein thrombosis.

In a prospective trial, 42 medical patients with a history of deep vein thrombosis of less than five days were allocated at random to treatment with streptokinase or heparin. Only patients with extensive thromboses were included. Streptokinase was given in a loading dose of 250 000 IU and a maintenance dose of 100 000 IU/hour for 4 days as a mean. Heparin was given in a loading dose of 15 000 IU and a maintenance dose of 20 000-50 000 IU/day. The therapeutic results were evaluated by phlebography. Significant thrombolysis occurred in 71.4% of 21 patients treated with streptokinase and in 23.8% of the 21 heparin-treated patients. Using the chi2-test for overall association, this difference was statistically highly significant (p = 0.002). Three patients in each treatment group experienced major bleeding, two in each group requiring blood transfusions. Minor bleeding and slight rise in temperature were encountered more often in the streptokinase than in the heparin group. It is concluded that patients with acute deep vein thrombosis with proximal extension of the thrombus beyond the calf veins should be offered a therapeutic trial with streptokinase.

Acute Disease↗

PubMed1979

Rapid thrombolysis and preservation of valvular venous function in high deep vein thrombosis. A comparative study between streptokinase and heparin therapy.

The results of streptokinase and heparin treatment are compared in a 4-year prospective study with special reference to preservation of high valvular venous function. An objective assessment was based upon phlebographic examinations before, during and 1-2 months after therapy. Complete lysis was demonstrated in 44% of high thromboses treated with streptokinase and in 6% treated with heparin. Retrograde phlebography revealed normal function of the proximal femoral valves in 92% of streptokinase-treated high thromboses, compared with 13% of those treated with heparin. These phlebographic results were considered to be a valid prognostic indicator of the eventual development of the postthrombotic syndrome. Allergic reactions were seen in 39% and minor haemorrhagic complications in 18% of the streptokinase-treated cases. The therapeutic benefit of streptokinase therapy in this study was found to outweigh any disadvantages incurred by observed complications.

Drug Evaluation↗

PubMed1990

Serum sickness and acute renal failure after streptokinase therapy for myocardial infarction.

A patient developed serum sickness and acute renal failure following therapy with streptokinase for myocardial ischaemia. There was a previous history of a cellulitic infection of the leg, and antibodies to streptokinase were measurable in a serum sample taken from the patient before therapy. A cryoglobulin was detected at the time of presentation with serum sickness. This contained polyclonal IgG (with anti-streptokinase activity), streptokinase, and C3. Circulating immune complexes were demonstrated by C1q-binding assay. Deposition of C3 was observed in skin and renal biopsies, and bound to erythrocytes. Renal histology, however, showed acute tubular necrosis, with no vasculitis or inflammatory cell infiltrate. This case provides an unusual example of the characterization of an immune complex comprising a specific antibody and an exogenous antigen, and has clinical implications for the use of streptokinase.

Acute Kidney Injury↗

PubMed1989

The streptokinase gene of group A streptococci: cloning, expression in Escherichia coli, and sequence analysis.

The gene specifying the group A streptokinase (ska) gene was cloned from an M type 49 strain of Streptococcus pyogenes and shown to express in Escherichia coli. The nucleotide sequence of the DNA fragment carrying ska was determined and compared to that of the group C streptokinase gene (skc). There is 90% sequence identity between the two genes, with highly conserved transcription and translation control regions. The deduced amino acid sequence of the group A streptokinase (SKA) contains the same number of amino acids as that of group C streptokinase, with 85% sequence identity between the two proteins. Among 440 amino acid residues specified by the coding sequence, there are 62 non-identical residues with 45 conserved and 17 non-conserved residues. The non-identical residues are located in two major regions, spanning residues 174 to 244 and 270 to 290, with 40 and 10 amino acid changes, respectively. The sequence differences provide an explanation at the molecular level for the previous findings of immunological and chemical heterogeneity among streptokinase produced by pathogenic streptococci.

Amino Acid Sequence↗

PubMed1996

Domain structure, stability and interactions in streptokinase.

The structural organization of streptokinase was established through detailed study of its denaturation by differential scanning calorimetry. Streptokinase exhibited a complex endotherm whose shape was sensitive to changing pH. In all cases the endotherms were easily described by four two-state transitions indicating unambiguously the presence of four independently folded domains in the molecule. Two of them were slightly destabilized by lowering pH from 7.0 to 3.8 while the other two were stabilized in this pH range. Two proteolytic fragments of streptokinase were examined, a 37-kDa fragment beginning at Ile1 with a cleavage following Phe62, and a 17-kDa fragment beginning at Lys 147. At pH 8.5, three two-state transitions were observed in the former and two in the latter indicating this many domains in each and suggesting that the fragments are formed by a step-wise removal of individual domains from the parent molecule. Comparison of the melting of these fragments with that of streptokinase allowed the first two transitions in the parent protein to be assigned to the melting of two NH2-terminal domains and the two higher-temperature transitions to the melting of the two COOH-terminal domains. The latter two domains strongly interact with each other since the absence of the most stable extreme COOH-terminal domain in both fragments resulted in a strong destabilization of its neighbor whose melting occurred with a midpoint near room temperature. The two NH2-terminal domains seem to be more independent. One of them melts similarly in the parent protein and both fragments while the other, formed by the 1-146 region, is less stable in the 37-kDa fragment. This destabilization is most probably due to the cleavage after Phe62 which, based on the sequence similarity of streptokinase with serine proteases, may be part of a surface-oriented loop.

Calorimetry, Differential Scanning↗

PubMed1997

Streptokinase, complement activation and hypotension.

The purpose of this study was to establish whether complement activation is the cause of transient hypotension during streptokinase infusion in patients with acute myocardial infarction. Thirteen patients with suspected acute myocardial infarction and treated with streptokinase were included. Complement 3d (C3d) as an indicator of complement activation was assessed in venous blood and blood pressure was measured. Ten patients had verified myocardial infarction. Three patients did not. Five patients developed an increase in C3d blood levels of more than 200% within 30 min. All patients developed a transient fall in blood pressure during infusion of streptokinase. This was related neither to presence of myocardial infarction nor to degree of complement activation. The mechanism of hypotension observed following the administration of streptokinase is not through complement activation, and thus how streptokinase induces hypotension is still obscure.

Acute Disease↗

PubMed1998

Crystal structure of the catalytic domain of human plasmin complexed with streptokinase.

Streptokinase is a plasminogen activator widely used in treating blood-clotting disorders. Complexes of streptokinase with human plasminogen can hydrolytically activate other plasminogen molecules to plasmin, which then dissolves blood clots. A similar binding activation mechanism also occurs in some key steps of blood coagulation. The crystal structure of streptokinase complexed with the catalytic unit of human plasmin was solved at 2.9 angstroms. The amino-terminal domain of streptokinase in the complex is hypothesized to enhance the substrate recognition. The carboxyl-terminal domain of streptokinase, which binds near the activation loop of plasminogen, is likely responsible for the contact activation of plasminogen in the complex.

Binding Sites↗

PubMed1968

Production of streptokinase in continuous culture.

A method for continuous cultivation of a beta-hemolytic streptococcus, strain H 64, is described. The production of cells and streptokinase at various dilution rates, pH, and temperature were studied in a complex medium supplied with excess glucose. At pH 7.0, productivity of cells and streptokinase, as well as the yield constant with respect to glucose, all increased with increasing dilution rate in the range of 0.1 to 0.5 hr(-1). The production of streptokinase was found to be a function of both growth rate and cell concentration. Although higher concentrations of streptokinase were obtained in experiments with batch cultures, the production of streptokinase in continuous cultures was found to be 2.3 times higher. The possible industrial application of a continuous production method is considered.

Bacteriological Techniques↗

PubMed1975

Treatment of deep vein thrombosis with streptokinase.

From September 1962 to May 1972 145 patients with acute or subacute deep vein thrombosis confirmed by phlebography were treated with streptokinase. During the same period 42 patients considered unfit for thrombolytic therapy were treated with herapin and oral anticoagulants. The results, assessed by repeat phlebography, in 93 of the patients treated with streptokinase were compared with those in 42 patients treated with heparin. The age, sex, and severity of occlusion were roughly similar in both groups. Streptokinase treatment was successful in 42 per cent, partially successful in 25 per cent, and unsuccessful in 32 per cent of the 93 patients compared with none, 10 per cent, and 88 percent respectively in the 42 patients treated with heparin. Streptokinase was more effective when the thrombus was in proximal rather than calf veins. Thrombi of more than six days old were readily lysed. Plasma fibrinogen levels were below 0-8 g/1 (80 mg/100 ml) in nearly all patients successfully treated. The incidence of pulmonary embolism was no greater with streptokinase than with heparin treatment. Only prolonged follow-up would show whether thrombolytic treatment would be effective in preventing late complications of deep vein thrombosis such as chronic venous insufficiency.

Adult↗

PubMed1998

ISIS-2: 10 year survival among patients with suspected acute myocardial infarction in randomised comparison of intravenous streptokinase, oral aspirin, both, or neither. The ISIS-2 (Second International Study of Infarct Survival) Collaborative Group.

OBJECTIVE: To assess effects of intravenous streptokinase, one month of oral aspirin, or both, on long term survival after suspected acute myocardial infarction. DESIGN: Randomised, "2 x 2 factorial," placebo controlled trial. SETTING: 417 hospitals in 16 countries. SUBJECTS: 17 187 patients with suspected acute myocardial infarction randomised between March 1985 and December 1987. Follow up of vital status complete to at least 1 January 1990 for 95% of all patients and to mid-1997 for the 6213 patients in United Kingdom. INTERVENTIONS: Intravenous streptokinase (1.5 MU in 1 hour) and oral aspirin (162 mg daily for 1 month) versus matching placebos. MAIN OUTCOME MEASURES: Mortality from all causes during up to 10 years' follow up, with subgroup analyses based on 4 year follow up. RESULTS: After randomisation, 1841 deaths were recorded in days 0-35, 991 from day 36 to end of year 1, 1478 in years 2-4, and 1230 in years 5-10. Allocation to streptokinase was associated with 29 (95% confidence interval 20 to 38) fewer deaths per 1000 patients during days 0-35. This early benefit persisted (death rate ratio 0.98 (0.92 to 1.04) for additional deaths between day 36 and end of year 10), so that there were 28 (14 to 42) and 23 (2 to 44) fewer deaths per 1000 patients treated with streptokinase after 4 years and 10 years respectively. There was no evidence that absolute survival benefit increased with prolonged follow up among any category of patient, including those presenting early after symptoms started or with anterior ST elevation. Nor did the early benefits seem to be lost in any category (including those aged over 70). Allocation to one month of aspirin was associated with 26 (16 to 35) fewer deaths per 1000 during first 35 days, with little further benefit or loss during subsequent years (death rate ratio 0.99 (0.93 to 1.06) between day 36 and end of year 10). The early benefit obtained with combination of streptokinase and one month of aspirin also seemed to persist long term. CONCLUSIONS: The early survival advantages produced by fibrinolytic therapy and one month of aspirin started in acute myocardial infarction seem to be maintained for at least 10 years.

Administration, Oral↗

PubMed1968

Streptokinase therapy in acute major pulmonary embolism: effectiveness and problems.

Eighteen patients with major pulmonary embolism were treated with streptokinase infused by a catheter or given intravenously. Fourteen showed clinical improvement and 12 out of 16 patients investigated showed definite angiographic improvement after 24 to 48 hours of treatment with streptokinase. The angiographic improvement following streptokinase contrasted with the lack of this in three patients after 24 hours of heparin treatment.Resolution following streptokinase therapy was most noticeable in patients treated shortly after a single embolic episode, and was least marked in those with recurrent embolism complicated by associated cardiac or pulmonary disease. Of the four patients who failed to improve, two died and two had pulmonary embolectomy and survived.The results suggest that streptokinase therapy is practicable provided that adequate laboratory control is available, and that it hastens early resolution in acute major pulmonary embolism.

Acute Disease↗

PubMed1989

Plasma atrial natriuretic peptide in patients with acute myocardial infarction: effects of streptokinase.

Plasma concentrations of immunoreactive atrial natriuretic peptide (mean (SEM] were measured in 135 patients admitted to two coronary care units with myocardial infarction, ischaemic chest pain, or non-ischaemic chest pain. Concentrations were significantly higher in patients with acute myocardial infarction not treated with systemic thrombolysis (60.4 (14.3) pg/ml) than in patients with non-ischaemic chest pain (21.1 (4.3) pg/ml). Patients with ischaemic chest pain had intermediate values (39.3 (7.1) pg/ml). Patients with acute myocardial infarction treated with intravenous streptokinase had normal concentrations of plasma atrial natriuretic peptide (20.2 (3.6) pg/mg), which were significantly lower than those in patients with myocardial infarction not given streptokinase. These changes could not be explained by factors such as age, pre-existing hypertension, renal dysfunction, or cardiac failure, nor treatment other than streptokinase. Raised plasma concentrations of atrial natriuretic peptide in acute myocardial infarction may be a homoeostatic response acting to reduce atrial pressures by natriuresis, diuresis, and venodilatation. The lower concentrations of atrial natriuretic peptide in patients with acute myocardial infarction treated with streptokinase may reflect a short term beneficial haemodynamic effect of streptokinase.

Angina Pectoris↗

PubMed1993

Aspirin does not improve early arterial patency after streptokinase treatment for acute myocardial infarction.

OBJECTIVE: To investigate the hypothesis that the magnitude of the life saving effect of aspirin in the second international study of infarct survival (ISIS-2) trial cannot be explained solely by prevention of late reocclusion of the infarct related artery. The aim of this study was to discover whether or not aspirin in combination with streptokinase had an adjuvant thrombolytic effect. DESIGN: Aspirin (150 mg) or placebo was given at the start of streptokinase infusion to 200 patients seen within six hours of the start of prolonged ischaemic cardiac pain and ST segment elevation. All patients received active aspirin at three hours. Patency of the infarct related artery was assessed non-invasively by the normalised rise of creatine kinase activity at three hours after starting streptokinase in these 200 patients and in a further 52 patients who had already taken aspirin within one week of the start of infarction. MAIN OUTCOME MEASURE: Rise in creatine kinase activity from baseline to > or = 20% or < 20% of the peak rise of activity in blood taken at three hours after starting infusion of streptokinase. This correlates with patency or occlusion of the infarct related coronary artery at about 2.5 hours after starting streptokinase. RESULTS: Assessed in this way, patency of the infarct related artery was 60% in patients given aspirin, 63% in those given placebo, and 62% in patients who had already taken aspirin within one week of infarction. CONCLUSION: The magnitude of the life saving effect of aspirin remains unexplained. Further investigation is needed into the mechanism of action of antiplatelet treatment in relation to thrombolytic treatment.

Aged↗

PubMed1996

The distribution of antibodies to streptokinase.

To determine the distribution of antibodies to streptokinase that might be anticipated in patients requiring treatment with streptokinase, specific anti-streptokinase antibody titres were determined in a group of subjects from the general population and in a group of patients presenting with acute myocardial infarction. Enzyme-linked immunosorbent assays were developed to measure specific anti-streptokinase IgG and subclass IgG1 in 95 subjects from the general population and in 160 patients presenting with acute myocardial infarction. Low titres of IgG1 were found in both the general population (median = 5; range: 0-490) and in the myocardial infarction group (median = 7; range: 0-2000). A minority of subjects in both groups had high titres. The findings suggest that low titres of antibody are widespread in the population. The minority of subjects in both groups who had high titres may explain the infrequent type III immune reactions encountered with streptokinase.

Adult↗