Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.68 (tissue plasminogen activator)
 11,311 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It was the aim of this study to investigate possible effects of biomaterials used to produce vascular grafts on the fibrinolytic system of endothelial cells. Therefore growth conditions for human umbilical vein endothelial cells on polytetrafluoroethylene and on polyurethane were optimized. Tissue culture polystyrene was used as a control material. We could demonstrate that precoating of the materials with fibronectin significantly increased the growth rate of human umbilical vein endothelial cells on these materials. Furthermore, we showed that human umbilical vein endothelial cells grown on polytetrafluoroethylene or polyurethane released more plasminogen activator inhibitor-1 and tissue type-plasminogen activator into the conditioned media than did human umbilical vein endothelial cells grown on tissue culture polystyrene. Human umbilical vein endothelial cells cultured on polytetrafluoroethylene also deposited more plasminogen activator inhibitor-1 into the extracellular matrix than did control cells grown on tissue culture polystyrene. Our results give evidence that human umbilical vein endothelial cells grown on two biomaterials used to construct vascular grafts, namely polytetrafluoroethylene and polyurethane, produce tissue-type plasminogen activator as well as plasminogen activator inhibitor-1, two major components of the fibrinolytic system also expressed by endothelial cells in vivo. In conclusion, our data suggest that endothelial cells grown on vascular grafts show functional integrity concerning their fibrinolytic system, which in turn might contribute to reduce the thrombogenic properties of the graft material.
J Thorac Cardiovasc Surg 1995 Jun
PMID:Growth and fibrinolytic parameters of human umbilical vein endothelial cells seeded onto cardiovascular grafts. 777 69

Recent studies have strengthened the arguments for the use of angiotensin-converting enzyme (ACE) inhibitors in the early postinfarct period. Those with clinically detectable heart failure, and hence at highest risk, will benefit most, as shown in the AIRE study, but those at lower risk with left ventricular dysfunction still have some benefit, theoretically through ventricular remodeling. In patients in the very early stages of acute myocardial infarction, three trials have shown discordant results. In CONSENSUS-II, intravenous enalaprilat followed by oral enalapril gave no benefit, rather causing excess hypotension and a possible increase in mortality. In ISIS-4 and GISSI-3, mortality improved by 0.46% and 0.8%, respectively, with risk reductions of 9% and 11%. Added transdermal nitrate in GISSI-3 gave a total reduction of 17%. In view of the risk of hypotension (20% in ISIS-4, compared with placebo 10%), very early ACE inhibition will probably only be used for selected patients. Logically, one target group would be those seen 7-24 hours after the onset of symptoms, particularly 7-12 hours, at which time captopril alone gave a reduction of 14.5% in risk. These mortality differences compare favorably with those recently found when comparing tPA and streptokinase in the GUSTO study.
Cardiovasc Drugs Ther 1994 Jun
PMID:The new trials: AIRE, ISIS-4, and GISSI-3. Is the dossier on ACE inhibitors and myocardial infarction now complete? 794 63

A 66-year-old man with atrial fibrillation was referred soon after developing left lower limb and abdominal pain with rectal bleeding. An immediate flush aortogram showed embolic occlusion of the left distal superficial femoral artery and superior mesenteric artery (SMA), 3 cm from its ostium. Recombinant tissue plasminogen activator (rtPA) 40 mg was selectively instilled in the SMA in two boluses. Abdominal symptoms resolved within 48 h, and complete recanalization of the SMA was shown on angiography. Exploratory laparotomy after 72 h showed a normal small bowel and right colon, and was completed by femoropopliteal embolectomy. Six months later, the patient remained asymptomatic.
Cardiovasc Intervent Radiol
PMID:Local fibrinolysis for superior mesenteric artery thromboembolism. 795 77

Arterial embolization from thrombolytic therapy for acute myocardial infarction is rare. We report two cases of spontaneous arterial embolization following the use of tissue plasminogen activator for acute myocardial infarction. Transesophageal echocardiography was able to identify the source of embolism as mobile atherosclerotic debris within the thoracic aorta. This information was of value in the management of these patients, in that femoral catheterization which could have precipitated further embolization was avoided.
Cathet Cardiovasc Diagn 1994 Mar
PMID:Spontaneous arterial embolization after thrombolytic therapy for acute myocardial infarction: the role of transesophageal echocardiography. 802 36

The clotting and fibrinolytic systems are activated by tissue factor and by tissue-type plasminogen activator in the pericardial cavity, where the thrombogenicity is greater than that of the surface of modern extracorporeal circuits. This local activation may have consequences for the systemic activation processes during cardiopulmonary bypass. To test this hypothesis, we investigated blood activation by interrupting the blood suction from the pericardial cavity during cardiopulmonary bypass in clinical coronary artery bypass operations. In blood collected in the pericardial cavity, thrombin-antithrombin III complex (p < 0.01), tissue-type plasminogen activator antigen (p < 0.05), fibrinogen degradation products (p < 0.01), and fibrin degradation products (p < 0.01) were significantly higher than in the systemic blood. Plasma heparin was significantly consumed in the pericardial cavity (p < 0.01). Once the pericardial blood was returned to the systemic circulation after resumed suction during cardiopulmonary bypass, thrombin-antithrombin III complex (p < 0.05), fibrinogen degradation products (p < 0.05), and fibrin degradation product (p < 0.05) concentrations increased significantly in the systemic blood. The effects of pericardial tissue on activation of clotting and fibrinolysis were also studied in vitro. When human plasma was incubated for 5 minutes with rabbit pericardium at reduced heparin concentrations, we found significant generation of thrombin (p < 0.05) and plasmin (p < 0.05). If the thrombin inhibitor hirudin was added, plasmin generation was also inhibited (p < 0.05). The results of the clinical and experimental study are in agreement with our hypothesis that tissue factor and tissue-type plasminogen activator accelerate the activation of clotting and sequentially of fibrinolysis under conditions of low heparin concentrations in the pericardial cavity and that this local activation contributes highly to the systemic activation, affecting hemostasis during cardiopulmonary bypass. Topical use of heparin in the pericardial cavity therefore seems indicated to reduce blood activation during cardiopulmonary bypass.
J Thorac Cardiovasc Surg 1993 Nov
PMID:Activation of fibrinolysis in the pericardial cavity during cardiopulmonary bypass. 823 Dec 4

Reduced hemostasis and bleeding tendency after cardiopulmonary bypass results from platelet dysfunction induced by the bypass procedure. The causes of this acquired platelet dysfunction are still subject to discussion, although, recently, greater emphasis has been placed on an overstimulated fibrinolytic system as a probable cause. In the first part of this study we assessed the effects of postoperative retransfusion of shed blood on blood loss to patients undergoing cardiopulmonary bypass. We observed that increasing concentrations of fibrinogen degradation products and tissue-type plasminogen activator stimulating activity in shed blood correlated significantly with a higher postoperative bleeding tendency (p < 0.05 for both). We further noted that retransfusion of shed blood increased the total postoperative blood loss by 43% (925 versus 1320 ml, p < 0.05). On the basis of these clinical observations, we hypothesized that the increased bleeding tendency was caused by fibrinolysis. In the second part of this study we collected evidence in support of this hypothesis by an in vitro study, in which we introduced similar (pro)fibrinolytic activity to platelet-rich plasma and measured the influence of this treatment on platelet function indicated by ristocetin agglutination. Tissue-type plasminogen activator and fibrin monomers (tissue-type plasminogen activator stimulator) together induced severe platelet damage, resulting in a decreased ristocetin agglutination response. Therefore, we propose a fibrinolysis-related mechanism for platelet dysfunction during cardiopulmonary bypass, dependent on fibrinolytic factors such as fibrin monomers, D-dimers, and tissue-type plasminogen activator.
J Thorac Cardiovasc Surg 1993 Dec
PMID:Tissue-type plasminogen activator and fibrin monomers synergistically cause platelet dysfunction during retransfusion of shed blood after cardiopulmonary bypass. 824 33

A 43-year-old female received tissue plasminogen activator for an acute antero-apical myocardial infarction. Cardiac catheterization demonstrated three focal dissections involving the left anterior descending and circumflex arteries. She expired unexpectantly after undergoing emergency coronary artery bypass grafting for therapy of an extension of her infarct. To our knowledge, this is the fourth report of multiple spontaneous coronary artery dissections and the second in which tissue plasminogen activator was administered. The histologic findings and their implications are reviewed.
Cathet Cardiovasc Diagn 1993 Dec
PMID:Multiple spontaneous coronary artery dissections in a middle aged woman: support for an underlying eosinophilic arteritis predisposing to intimal disruption. 828 55

The presence of pericardial adhesions at resternotomy not only increases the operation time but also increases the risk of serious damage to the heart, great vessels, and extracardiac grafts. The reported prevalence of damage is 2% to 6%. The fibrinolytic activity of pericardial tissue may be a crucial factor in determining the extent of adhesion formation following primary operation. Ten patients undergoing cardiac operations were studied to assess the plasminogen activating activity of homogenates of pericardial tissue samples. Samples were taken at three times during the operation and the plasminogen activating activity was measured by means of a standard fibrin plate technique. Tissue-type plasminogen activator, urokinase-type plasminogen activator, plasminogen activator inhibitor-1, and plasminogen activator inhibitor-2 were also measured by means of enzyme-linked immunosorbent assays. Compared with its initial levels (median 2.06 IU/cm2, range 1.28 to 6.48 IU/cm2), the plasminogen activating activity of pericardial biopsy tissue was significantly reduced at 75 minutes (median 0.64 IU/cm2, range 0.12 to 2.44 IU/cm2, p < 0.01) and at 135 minutes (median 1.45 IU/cm2, range 0.12 to 4.39 IU/cm2, p < 0.05). The major plasminogen activator present was tissue-type plasminogen activator. Compared with its initial levels (median 2.34 ng/ml, range 1.03 to 6.42 ng/ml), subsequent tissue-type plasminogen activator values were also significantly reduced at 75 minutes (median 0.83 ng/ml, range 0.75 to 5.13 ng/ml, p < 0.005) and at 135 minutes (median 1.24 ng/ml, range 0.75 to 6.67 ng/ml, p < 0.05). Low levels of urokinase-type plasminogen activator were found in 5 of 10 patients. However, neither plasminogen activator inhibitor-1 nor plasminogen activator inhibitor-2 was detected. Examination with a light microscope showed both increasing pericardial mesothelial damage and increasing features of acute inflammatory changes with time. This study shows that plasminogen activating activity is present in pericardial tissue and that tissue-type plasminogen activator is the major plasminogen activator. The observed inflammatory changes and concomitant damage to the pericardial mesothelium, and the significant reductions in pericardial tissue-type plasminogen activator and plasminogen activating activity seen during cardiac operations, may be important factors contributing to the early development of pericardial adhesions.
J Thorac Cardiovasc Surg 1993 Aug
PMID:Changes in pericardial morphology and fibrinolytic activity during cardiopulmonary bypass. 834 Oct 74

Valve thrombosis is one of the most serious complications after prosthetic valve replacement. We report the use of tissue-type plasminogen activator (t-PA) in the treatment of a patient with thrombosed aortic and mitral valves. Thrombolysis resulted in immediate hemodynamic improvement and resolution of congestive heart failure, thereby avoiding surgical intervention. Based on our experience, thrombolysis with t-PA is an effective alternative in the treatment of thrombosed prosthetic valves.
J Cardiovasc Surg (Torino) 1993 Jun
PMID:Tissue-type plasminogen activator (t-PA) lysis of aortic and mitral valve thrombosis. 834 79

The purpose of this study was to investigate the effects of beraprost sodium, a stable prostacyclin analog, on the parameters of hemostasis, fibrinolysis, and myocardial ischemia in patients with exertional angina. Thirty-one patients with exertional angina who had significant organic coronary artery stenosis in at least one of the three major coronary arteries were selected. All patients underwent quantitative exercise thallium-201 emission computed tomography before and 1 month after 120 micrograms per day of beraprost sodium administration. Before exercise, blood samples were collected from 8:30 a.m. to 9:30 a.m. after the patients had been lying in bed undisturbed for at least 10 minutes. Plasma platelet factor 4 (PF4), fibrinopeptide A (FPA), tissue plasminogen activator antigen (t-PA), and plasminogen activator inhibitor-1 activity (PAI-1) were measured. There were no significant differences in exercise parameters on both exercise tests. However, both the extent and severity scores of ischemia were significantly aggravated (p < 0.05 for both) during beraprost sodium administration. Plasma FPA levels decreased significantly during beraprost sodium administration (p < 0.01). Likewise, plasma PF4 levels decreased significantly during beraprost sodium administration (p < 0.05). As for plasma t-PA antigen levels, there was no significant difference before versus during beraprost sodium administration. Plasma PAI-1 activity levels decreased significantly during beraprost sodium administration (p < 0.05). The results indicate that beraprost sodium has strong antithrombogenic properties. However, its aggravation of myocardial ischemia may limit clinical usage.
Cardiovasc Drugs Ther 1995 Aug
PMID:Effects of beraprost sodium, a new prostaglandin I2 analog, on parameters of hemostasis, fibrinolysis, and myocardial ischemia in patients with exertional angina. 854 11


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