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M Gjurasin

Publications and source records attributed to M Gjurasin.

At least 19 recordsLinked to original sources
PubMed2003

Corticosteroid-impairment of healing and gastric pentadecapeptide BPC-157 creams in burned mice.

The amelioration of corticosteroid-impairment of healing by a stable gastric pentadecapeptide BPC-157 (GEPPPGKPADDAGLV, M(w) 1419, currently in early clinical trials for inflammatory bowel disease) was studied in thermally injured mice. Its effects on corticosteroid impaired healing of deep partial skin thickness burns, and burn-gastric lesions were investigated. Male NMRI-Hannover mice (sacrificed at 1-3,7,14 and 21 days following burning 20% of total burn area at the back (open flame for 7s) received intraperitoneally (per kg bw) 6alpha-methylprednisolone (Depo-medrol, 1.0 or 10.0mg), or an equal volume of saline (5.0 ml), once daily, first application 30 min after injury, last 24h before sacrifice. The injury was subsequently treated by topical application of a thin layer of pentadecapeptide BPC-157 cream at three different levels a neutral cream of no treatment. Pentadecapeptide BPC-157 consistently improved given burn healing (both microscopical and tensionmetry assessment), and counteracted corticosteroid-impairment of burn healing. In burn-gastric lesions investigation of the effects of BPC showed an anti-ulcer effect of its own in burned non-corticosteroid-treated mice and potentiated the anti-ulcer effect observed in 6alpha-methylprednisolone-treated mice. Pentadecapeptide BPC-157 inhibited corticosteroid immunosuppression. In vitro, in spleenic cells assessment, animals (sacrificed at day 21) treated with 6alpha-methylprednisolone 1mg showed decreased reactivity to nitrogen in comparison with control, healthy animals, while the addition of BPC-157 (1 microg/g cream) returned cell reactivity to values noted in control healthy animals.

Analysis of Variance↗
PubMed1999

The effect of pentadecapeptide BPC 157, H2-blockers, omeprazole and sucralfate on new vessels and new granulation tissue formation.

A clear protection of the gastrointestinal tract and an evident anti-inflammatory effect were shown for a novel stomach pentadecapeptide BPC 157 (i.p./i.g.) in comparison with several reference standards in various ulcer models along with a protection of endothelium and particular interaction with the NO-system. Thus, we evaluated whether this pentadecapeptide along with other gastroprotective agents could affect angiogenesis and the healing process in vivo using a procedure initially described by Szabo and co-workers. In each rat, two sterile sponges (1 x 1 x 0.25 cm; V = 0.25 mL) with the same quantities of BPC 157 (10 ng x mL(-1), 10 microg x mL(-1), 50 microg x kg(-1)) or reference agents (cimetidine: 10, 100, 500 mg x mL(-1); ranitidine: 2.5, 25, 250 mg x mL(-1); famotidine: 10, 50, 100 mg x mL(-1); omeprazole: 10, 50, 100 mg x mL(-1); sucralfate: 1, 5, 10 mg x mL(-1) were implanted subcutaneously in the lumbar region. The sponges were removed after 3 or 7 d, fixed in formalin, and processed for histologic and histochemical evaluation and morphometry assessment. Compared with the control values, the number of newly formed endothelial spaces inside newly formed granulation tissue was markedly increased in all animals treated with BPC 157, cimetidine, ranitidine, famotidine, sucralfate and omeprazole, a consistent finding noted after either 3 or 7 d. Compared with control values, markedly more granulation tissue was noted in the rats in the groups of animals treated with BPC 157 (50 microg) and in the rats treated with sucralfate in all dosages used, euthanized after 3 d. In all groups treated with H2-blockers however, similar values to those of controls were noted. Thus, it could be concluded that an evident angiogenic property was consistently noted for the novel pentadecapeptide BPC 157, H2-blockers (cimetidine, famotidine and ranitidine) and omeprazole, besides the well known angiogenic effect of sucralfate. Furthermore, unlike H2-blockers and omeprazole, BPC 157 stimulates the formation of granulation tissue, suggesting a particular activity, similar to that previously noted for sucralfate.

Animals↗
PubMed1999

Long-lasting cytoprotection after pentadecapeptide BPC 157, ranitidine, sucralfate or cholestyramine application in reflux oesophagitis in rats.

Recently, the effectiveness of pentadecapeptide BPC 157 and other anti-ulcer agents, called 'direct cytoprotection', was evidenced in totally gastrectomized rats duodenum challenged with cysteamine 24 h after surgery, and sacrificed 24 h after ulcerogen application. The further focus was on the possibility that this effect could be seen over a more prolonged period (1, 2, 4 weeks), and in other parts of the gastrointestinal tract (i.e. oesophagus). After the removal of the stomach, the oesophagus and jejunum were joined by a termino-lateral anastomosis. The animals were euthanized 7, 14 or 28 d after surgery, when oesophagitis was blindly assessed both macroscopically (percentage of ulcerations areas) and microscopically (percentage of areas of ulcers, regeneration and hyperplasia; number of inflammatory cells - polymorphonuclear and mononuclear). Starting 24 h after surgery, the medication was continuously given in the drinking water, in a volume of 12.5 mL/rat daily, until euthanasia at the end of the observation period, i.e. 7, 14, 28 d following surgery. Based on previous experiments, the doses of agents were daily calculated per kg b.w. as follows: BPC 157 125 mg or 125 ng, cholestyramine 2.5 mg, ranitidine 125 mg, sucralfate 725 mg, whereas controls received 72.5 mL x kg(-1) water. In support of these initial findings, and considering gastrectomized acid-free rats as an ideal model for long-term cytoprotective studies as well, pentadecapeptide BPC 157 markedly attenuated termino-lateral oesophagojejunal anastomosis-reflux oesophagitis also over a quite prolonged period. This efficacy was only partly shared by other anti-ulcer agents. After 1-week-old oesophagitis (microscopical assessment), but not after 2 or 4 weeks, less damaged mucosa was noted in rats drinking ranitidine or sucralfate compared to controls. Similar effectiveness was noted for cholestyramine. The obtained results were supported also by inflammatory cell assessment. Compared with control values, BPC 157-treated groups consistently presented less polymorphonuclears and less mononuclears in all assessed periods. Interestingly, the values obtained in other treated groups showed no difference compared with control values. Thus, despite limitations, a generalization supporting a direct importance of a common cytoprotective approach, could be clearly provided. A useful, long-lasting cytoprotective activity (apparently more prominent in BPC 157 rats, than in reference agents, ranitidine, sucralfate, as well as cholestyramine) may be a likely suitable therapy in otherwise resistant reflux oesophagitis conditions.

Animals↗
PubMed1997

The influence of a novel pentadecapeptide, BPC 157, on N(G)-nitro-L-arginine methylester and L-arginine effects on stomach mucosa integrity and blood pressure.

The known effects of a novel stomach pentadecapeptide BPC157 (10 microg or 10 ng/kg), namely its salutary activity against ethanol (96%, i.g.)-induced gastric lesions (simultaneously applied i.p.) and in blood pressure maintenance (given i.v.), were investigated in rats challenged with a combination of N(G)-nitro-L-arginine methylester (L-NAME) (5 mg/kg i.v.), a competitive inhibitor of endothelium nitric oxide (NO)-generation and NO precursor, L-arginine (200 mg/kg i.v.) (D-arginine was ineffective). In the gastric lesions assay, NO agents were given 5 min before ethanol injury and BPC 157 medication. Given alone, BPC157 had an antiulcer effect, as did L-arginine, but L-NAME had no effect. L-NAME completely abolished the effect of L-arginine, whereas it only attenuated the effect of BPC 157. After application of the combination of L-NAME + L-arginine, the BPC157 effect was additionally impaired. In blood pressure studies, compared with L-arginine, pentadecapeptide BPC 157 (without effect on basal normal values) had both a mimicking effect (impaired L-NAME-blood pressure increase, when applied prophylactically and decreased already raised L-NAME values, given at the time of the maximal L-NAME-blood pressure increase (i.e., 10 min after L-NAME)) and preventive activity (L-arginine-induced moderate blood pressure decrease was prevented by BPC 157 pretreatment). When BPC 157 was given 10 min after L-NAME + L-arginine combination, which still led to a blood pressure increase, its previously clear effect (noted in L-NAME treated rats) disappeared. In vitro, in gastric mucosa from rat stomach tissue homogenates, BPC 157, given in the same dose (100 microM) as L-arginine, induced a comparable generation of NO. But, BPC 157 effect could not be inhibited by L-NAME, even when L-NAME was given in a tenfold (100 versus 1000 microM) higher dose than that needed for inhibition of the L-arginine effect. NO synthesis was blunted when the pentadecapeptide BPC 157 and L-arginine were combined. In summary, BPC 157 could interfere with the effects of NO on both gastric mucosal integrity and blood pressure maintenance in a specific way, especially with L-arginine, having a more prominent and/or particularly different effect from that of NO.

Animals↗
PubMed1997

Pentadecapeptide BPC 157 interactions with adrenergic and dopaminergic systems in mucosal protection in stress.

Since superior protection against different gastrointestinal and liver lesions and antiinflammatory and analgesic activities were noted for pentadecapeptide BPC (an essential fragment of an organoprotective gastric juice protein named BPC), the beneficial mechanism of BPC 157 and its likely interactions with other systems were studied. Hence its beneficial effects would be abolished by adrenal gland medullectomy, the influence of different agents affecting alpha, beta, and dopamine receptors on BPC 157 gastroprotection in 48 h restraint stress was further investigated. Animals were pretreated (1 hr before stress) with saline (controls) or BPC 157 (dissolved in saline) (10 microg or 10 ng/kg body wt intraperitoneally or intragastrically) applied either alone to establish basal conditions or, when manipulating the adrenergic or dopaminergic system, a simultaneous administration was carried out with various agents with specific effects on adrenergic or dopaminergic receptors [given in milligrams per kilogram intraperitoneally except for atenolol, which was given subcutaneously] phentolamine (10.0), prazosin (0.5), yohimbine (5.0), clonidine (0.1) (alpha-adrenergic domain), propranolol (1.0), atenolol (20.0) (beta-adrenergic domain), domperidone (5.0), and haloperidol (5.0) (peripheral/central dopamine system). Alternatively, agents stimulating adrenergic or dopaminergic systems--adrenaline (5.0) or bromocriptine (10.0)--were applied. A strong protection, noted following intragastric or intraperitoneal administration of BPC 157, was fully abolished by coadministration of phentolamine, clonidine, and haloperidol, and consistently not affected by prazosin, yohimbine, or domperidone. Atenolol abolished only intraperitoneal BPC 157 protection, whereas propranolol affected specifically intragastric BPC 157 protection. Interestingly, the severe course of lesion development obtained in basal conditions, unlike BPC 157 gastroprotection, was not influenced by the application of these agents. In other experiments, when adrenaline and bromocriptine were given simultaneously, a strong reduction of lesion development was noted. However, when applied separately, only adrenaline, not bromocriptine, has a protective effect. Thus, a complex protective interaction with both alpha-adrenergic (eg, catecholamine release) and dopaminergic (central) systems could be suggested for both intragastric and intraperitoneal BPC 157 administration. The involvement of beta-receptor stimulation in BPC 157 gastroprotection appears to be related to the route of BPC 157 administration. The demonstration that a combined stimulation of adrenergic and dopaminergic systems by simultaneous prophylactic application of adrenaline (alpha- and beta-receptor stimulant) and bromocriptine (dopamine receptor agonist) may significantly reduce restraint stress lesions development provides insight for further research on the beneficial mechanism of BPC 157.

Adrenergic Agents↗
PubMed1997

Pentadecapeptide BPC 157, cimetidine, ranitidine, bromocriptine, and atropine effect in cysteamine lesions in totally gastrectromized rats: a model for cytoprotective studies.

A superior effectiveness in various lesion assays was noted for the novel pentadecapeptide BPC 157, originated from human gastric juice protein (BPC) and claimed to be a cytoprotective agent. From this viewpoint, as a previously untreated experimental improvement to create an acid-free environmental for cytoprotection studies, total gastrectomy was done 24 hr before the ulcerogenic procedure. In the absence of stomach and gastric acid, the damaging effects of cysteamine (400 mg/kg subcutaneously, death 24 hr thereafter), to date thought to be an acid-related duodenal ulcerogen, and the BPC 157 cytoprotective effect (10 microg or 10 ng/kg intraperitoneally) were further challenged. BPC 157 was compared with reference agents [cimetidine (50), ranitidine (10), omeprazole (10), bromocriptine (10) and atropine (10) (mg/kg intraperitoneally, 1 hr before cysteamine] known to be also cytoprotective. In naive rats, with intact stomach, all of them showed a strong beneficial effect. Interestingly, in gastrectomized animals, the application of BPC 157 or the reference agents before cysteamine significantly prevented the otherwise severe duodenal lesion development noted in the control gastrectomized cysteamine rats. In groups without cysteamine, no lesions were noted (laparotomy, gastrectomy only, 24 or 48 hr postsurgical period), nor was lesion potentiation seen in cysteamine-treated laparotomized animals. In summary, these findings--equal damaging effect of cysteamine and equal protection of pentadecapeptide BPC 157 and reference agents in gastrectomized and rats with intact stomach--seem to be particularly relevant for a cytoprotective viewpoint. Without a stomach, the cysteamine damaging effect was convincingly defined as an essential gastric acid-independent injury (analogous to ethanol gastric lesions). Likewise, a high "cytoprotective capacity," apparently acid independent, common for all tested agents (novel pentadecapeptide BPC 157, cimetidine, ranitidine, omeprazole and atropine) could be clearly stressed.

Animals↗
PubMed1996

Beneficial effect of a novel pentadecapeptide BPC 157 on gastric lesions induced by restraint stress, ethanol, indomethacin, and capsaicin neurotoxicity.

Very recently, the integrity of capsaicin somatosensory neurons and their protection were suggested to be related to the activity in nociception of a newly discovered 15-amino acid peptide, BPC 157, shown to have strong beneficial effect on intestinal and liver lesions. Therefore, from this viewpoint, we have studied the gastroprotective effect of the pentadecapeptide BPC 157, on gastric lesions produced in rats by 96% ethanol, restraint stress, and indomethacin. The possible involvement of sensory neurons in the salutary actions of BPC 157 (10 micrograms/kg, 10 ng/kg intraperitoneally) was studied with capsaicin, which has differential effects on sensory neurons: a high dose in adult (125 mg/kg subcutaneously, 3 months old) or administration (50 mg/kg subcutaneously) to neonatal animals (age of the 7 days) destroys sensory fibers, whereas a low dose (500 micrograms/kg intraperitoneally) activates neurotransmitter release and protective effects on the mucosa. In the absence of capsaicin, BPC 157 protected gastric mucosa against ethanol, restraint, and indomethacin application. In the presence of neurotoxic doses of capsaicin, the negative influence of capsaicin on restraint, ethanol, or indomethacin lesions consistently affected salutary activity of BPC 157. However, BPC 157 protection was still evident in the capsaicin-treated rats (either treated as adults or as newborns) in all of these assays. Interestingly, after neonatal capsaicin treatment, a complete abolition of BPC gastroprotection was noted if BPC 157 was applied as a single nanogram-regimen, but the mucosal protection was fully reversed when the same dose was used daily. In line with the excitatory dose of capsaicin the beneficial effectiveness of BPC 157 appears to be increased as well. Taken together, these data provide evidence for complex synergistic interaction between the beneficial effectiveness of BPC 157 and peptidergic sensory afferent neuron activity.

Age Factors↗
PubMed1996

Salutary and prophylactic effect of pentadecapeptide BPC 157 on acute pancreatitis and concomitant gastroduodenal lesions in rats.

The superior effectiveness of a new pentadecapeptide, BPC 157, on gastrointestinal and liver lesions, in conjunction with an antiinflammatory and analgetic activity was recently noted. In the present study, BPC 157 was tested as either a protective or healing agent in bile duct ligation-induced acute pancreatitis in rats. In addition, the positive influence of BPC 157 on concomitantly developed gastric and duodenal lesions was simultaneously investigated. BPC 157 (10 microg, 10 ng/kg body wt, intraperitoneally or intragastrically) was given prophylactically 1 hr before ligation, whereas the therapy was given once daily beginning with the 24 hr following ligation (last application 24 hr before killing). The effect was investigated at daily intervals until the end of the fifth day after ligation. In the pretreatment regimen, a strong pancreas protection was obtained. When applied in the condition of already established severe acute pancreatitis, an obvious salutory effect was consistently noted. Assessing the appearance of the necrosis, edema, neutrophils, and mononuclears, consistently less necrosis, edema, and neutrophils, but more mononuclears, were found in BPC-treated rats. Likewise, in studies of the serum amylase values, relative to control data, a markedly lower rise (BPC pretreatment regimen) as well as a worsening of the already raised values (BPC therapy regimen) was noted. Along with its beneficial effect on pancreatitis, a positive influence of BPC 157 on the gastric and duodenal lesion course in bile duct-ligated rats was noted in both the pre- and posttreatment regimen. Taken together, in further studies of acute pancreatitis therapy, BPC could be an interesting and useful agent with an additional positive impact on concomitant gastroduodenal pathology.

Acute Disease↗
PubMed1995

Incidence and hospital mortality of acute coronary artery disease among civilians in Zagreb during air-raid alarms.

During the period of air-raid alarms in Zagreb (September 1991), the influence of war-induced stress on the incidence and mortality of acute coronary artery disease was investigated. Control periods were September 1989 and September 1990. Among 2903 patients admitted to Emergency Care Units, 369 (13%) were examined for suspect acute coronary artery disease. During the same periods in 1989 and 1990, 10% and 11% of acute coronary artery disease patients were recorded, respectively. The percentage of patients with myocardial infarction or unstable angina, admitted to Coronary Care Units during September 1989, 1990 and 1991, was 49%, 50% and 55%, respectively. The number of Q myocardial patients admitted during September 1991 was significantly higher than that recorded during the same period in 1990. The incidence and mortality patterns in acute coronary artery disease patients were also examined during August, September and October 1991. The peak incidence of acute coronary artery disease was found in the first half of September, while the peak mortality in these patients was found during the second half of September. During the second half of September of 1989, 1990 and 1991, the mortality in Q myocardial patients in Coronary Care Units, was 16.7%, 15.2% and 23.8%, respectively. Besides the war-induced stress, transportation of our patients to shelters or inner parts of the hospital caused additional stress, probably contributing to the development of refractory malignant arrhythmia or heart failure.

Angina, Unstable↗
PubMed1995

[Causes of disorders of consciousness in internal medicine intensive care units].

The present study on 5330 patients admitted to the internal intensive care unit over the five year period (1990-1994) indicated that consciousness disorders are most frequently associated with poisoning. On admission, the state of consciousness of 665 of these 5330 patients was retrospectively evaluated. Poisoning by drugs was most common among intoxications (93 patients of 154 cases of poisoning). Coma, which is the most severe manifestation of consciousness disorder, occurred very often in these patients. Poisoning caused by other agents was connected with other forms of consciousness disorders. Low Glasgow Coma Score (GCS) was a severe predictor, while the number of deaths among patients with GCS > 10 was low. Sepsis was the next most common cause of consciousness disorder among our patients (88 patients). Death rate in these patients was high, amounting to almost 50%, regardless of GCS on admission, suggesting that the severity of main event determines the outcome. Glycemia disorders, including hypoglycemia, hyperglycemia as well as hyperosmotic state, did not result in lethal outcome, regardless of GCS on admission. The highest death rate was registered in patients with cardiopulmonary arrest and lowest GCS on admission. Patients with cardiogenic shock, despite high GCS on admission, had high death rate.

Coma↗
PubMed1995

[Disorders of consciousness due to disorders of body fluid composition--case report of a female patient].

We report a female patient presenting with sepsis and multi-organ failure following eclampsia and intrauterine childdeath. In the phase of recovery, the patient developed consciousness disorder and coma characterized by fasciculation, generalized myoclonia and respiratory insufficiency. The clinical picture corresponded to that of Lance Adam's syndrome. A quick change in the composition of body fluids in the polyuric phase of renal insufficiency associated with an antidiuretic hormone deficit was a cause of that disorder. Metabolic dysfunction and hyperexcitability of neurons developed as a result. Hyperexcitability of the caudal part of the medulla oblongata was responsible for the development of myoclonia. Following the correction of that disorder, the patient completely improved.

Acute Kidney Injury↗
PubMed1995

[Immunotherapy of sepsis and septic shock].

An extraordinary advance in basic sciences and technology did not reduce high lethality rate of the septic shock patients. The lethality rate of those patients was and still is around 50%. A new knowledge about a role of an inflammatory response on the infection in the later fatal course of the septic patients, led to the new approach in the treatment. A trial to block an endotoxin, cytokines, especially TNF and IL-1, as well as some other substances, in experimental models of sepsis, in spite of inconsistent results, is promising. A clinical experiences are disappointing, at first because of our still poor knowledge about various cytokines cascade, feedback mechanisms, cellular protective mechanisms, etc. The new chapter on the treatment of that highly lethal syndrome is open, though a final achievement of that approach is not clear till now.

Animals↗
PubMed1993

The significance of immunocompromised condition in the prophylaxis of hepatitis B in chronic renal insufficiency.

The paper presents the immunogenicity of hepatitis vaccine (obtained by genetic engineering) in immunocompromised patients with preterminal renal insufficiency defined by depression of creatinine clearance of 10 to 25 ml/min. The study consisted of 28 randomized patients with impaired renal function. Sixteen patients received a single dose and, twelve a double dose of vaccine. Revaccination following 3 intramuscular doses of vaccine had been undertaken after 24 weeks if antibodies were not detected or their titer was 10 i. u. or less. All patients obtained a booster dose following 52 weeks. There was no statistically significant difference in titer values between immunocompromised patients regardless of whether they were vaccinated with a single or double dose. The antibody titer in patients with chronic renal insufficiency was significantly lower as compared with the results of vaccination in healthy population. It may be concluded that it is more beneficial and less expensive to use a single dose vaccine and revaccination if the titer is negative or insufficiently high.

Hepatitis B↗
PubMed1990

[Use of recombinant erythropoietin on secondary anemia in patients in the terminal phase of renal insufficiency on hemodialysis].

A group of 6 patients with a history of end-stage renal insufficiency on hemodialysis was receiving erythropoietin (EPO) in a dosage of 50 IU/kg body weight i. v. The hemogram values were followed regularly every week and the patients underwent other laboratory evaluations every month. At the beginning of the study, the number of erythrocytes amounted to 2.2 +/- 0.3 x 10(12)/l. After 4 weeks it was 2.3 +/- 0.4 (NS) (p = 0.001), after 8 weeks 2.8 +/- 0.4 (p = 0.007), and after 12 weeks 3.2 +/- 0.3. At the beginning, hemoglobin was 70 +/- 8 g/l, after 4 weeks 76.3 +/- 13.7 (NS), after 8 weeks 95.7 +/- 14.3 (p = 0.008), and after 12 weeks 102.2 +/- 12 (p = 0.001). The hematocrit value rose from 21.4 +/- 3.4 at the beginning of the study to 32.1 +/- 3.6 (p = 0.001) after 12 weeks. The trial showed no significant effect of EPO on serum potassium which amounted to 5.3 +/- 0.4 mmol/l at the beginning of the trial and 5.6 +/- 0.8 (NS) after 12 weeks; the rate of the rise of platelets from 132.8 +/- 2.4 x 10(9)/l to 155.2 +/- 42.2 was not significant either. The results demonstrate a marked improvement in the red blood cells of patients receiving EPO in the end-stage of renal insufficiency and its influence on their general condition. One female patient was excluded from the study participation because of a severe bone pain.

Adult↗
PubMed1990

[Evaluation of the effectiveness of streptokinase in acute myocardial infarct with respect to the pump function of the heart].

During 2 years and 3 months 230 patients suffering from acute myocardial infarction were treated at an Intensive Care Unit and a Department of Cardiology. Streptokinase was given intravenously to 54 of them. Out of 54 patients, in 52% the localisation of the myocardial infarction was in the anterior and in 48% in the posterior wall. The patients were divided in the three categories according to the onset of symptoms: up to 2 hours, 2-4 hours and 4-6 hours. The dose of streptokinase was 1,500,000 i.u. during 1.5 hours. The CPK and MBCPK level reached the maximum values up to 12 hours and was to lowest in the first group. In 74% of the patients the serum enzyme level showed successful reperfusion of a coronary artery. Electrocardiographic findings of a successful myocardial reperfusion amounted to 36% in the first, 40% in the second, and 17% in the third group. Malignant ventricular arrhythmias appeared in the first group in 3.6%, in the second in 12.5% and in the third group in 14.2%. The criteria for successful myocardial reperfusion by echocardiography (analysed regional wall motion) were present in 52% in the first, in 50% in the second, and in 17% in the third group. Coronarography and ventriculography were performed in 17 patients after 21 days of treatment, with successful results in 88% (15 out of 17 patients). In a group of 176 patients unable to be treated with streptokinase because of the onset of symptoms of myocardial infarction (more than 6 hours) or because of contraindications for that treatment, the lethality rate reached 17.6%. The lethality rate in the group of 54 patients treated with streptokinase was 5.5%. Local complication (hemorrhage) during the treatment was observed in one patient (2%).

Heart↗