Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.73 (urokinase-type plasminogen activator)
 10,685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixteen patients, seven men and nine women (mean age of 66 years), with acute arterial ischemia were treated with operative thromboembolectomy by Fogarty catheterization and urokinase. Seven patients were diabetic, ten were hypertensive and six had prior vascular surgical treatment. The operative arteriograms confirmed vascular occlusive phenomenon. The ankle to brachial ratio was a mean of 0.02. Perioperatively, patients had anticoagulation with heparin systemically. All patients underwent transfemoral embolectomy using a Fogarty catheter. An initial retrieval of clots was accomplished, with documentation by arteriography, instillation of urokinase (50,000 units) and clamping of vessel for 15 minutes. Subsequent passage of the Fogarty catheter and repeat urokinase infusion resulted in further retrieval of clots and improvement by repeat intraoperative arteriography. All interventions resulted in clinical restoration of perfusion to the affected limb. Six patients had amputations of the lower extremities (one transmetatarsal and one below the knee) during the 30 day postoperative period. Improvement in distal run-off was demonstrated by intraoperative arteriography and increases in the ankle to brachial ratio from 0.1 to 1.04, with a mean of 0.54, were noted. No complications from bleeding occurred. One patient died postoperatively because of myocardial infarction. Salvage of the limb may increase with combined embolectomy and thrombolytic therapy.
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PMID:Intraoperative intra-arterial urokinase infusion as an adjunct to Fogarty catheter embolectomy in acute arterial occlusion. 238 12

Thrombotic thrombocytopenic purpura (TTP) is characterized by widespread occluding and persistent microthrombotic lesions. Evidence for both endothelial damage and primary platelet aggregation as possible pathogenetic mechanisms has been produced. Persistence of microthrombi has not been explained satisfactorily. In patients with TTP we studied plasma fibrinolysis and protein C. Tissue plasminogen activator (t-PA) activity levels, measured functionally, were low or unmeasurable in 11 of 12 patients; t-PA antigen levels, measured immunochemically, were normal in all six observed. The level of potent inhibitor of plasminogen activation directed against both t-PA and urokinase was elevated significantly in all 12, whereas the alpha 2-antiplasmin level was elevated in only two. Protein C antigen levels were low in three of six patients observed. Fibrinolysis levels in patients in remission did not differ from those in patients with acute disease. Plasma exchange resulted in temporary reversal of the abnormalities, but achievement of clinical remission was not associated with permanent normalization of fibrinolysis. Inasmuch as all 12 patients had severely depressed fibrinolytic mechanisms it is possible that a defect in the fibrin-clearing system permits thrombus formation to occur and proceed in an unchallenged fashion, thereby contributing to the complex events leading to arterial ischemia in vital organs.
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PMID:Fibrinolysis in health and disease: abnormal levels of plasminogen activator, plasminogen activator inhibitor, and protein C in thrombotic thrombocytopenic purpura. 243 36

Early thrombolytic therapy has been shown to reduce hospital mortality after myocardial infarction by 20-50%. This is achieved through reperfusion of the ischemic myocardium, which leads to limitation of infarct size by 15-30% and preservation of regional and global left ventricular function. Thrombolysis and reperfusion can be achieved by intravenous administration of streptokinase, urokinase, APSAC, or rt-PA, or by intracoronary administration of streptokinase or urokinase. Thrombolytic therapy is most effective in patients with extensive myocardial ischemia (large infarction) treated early after the onset of symptoms, but also patients with smaller infarcts may benefit from the therapy. It is uncertain whether treatment later than six hours after the onset of symptoms is beneficial, and if so, in which patients. Thrombolytic therapy leads to bleeding complications in a minority of patients. The risk of intracranial bleeding is approximately 0.5%. However, in several large trials the rate of cerebrovascular accidents (bleeding plus embolism) was not higher after thrombolytic therapy with streptokinase or rt-PA than after placebo. In order to prevent rethrombosis, additional treatment with acetyl salicylic acid and heparin is recommended. Nitrates and antiarrhythmic drugs are not recommended as routine practice. Immediate PTCA does not improve patient outcome. At present angiography and subsequent angioplasty or bypass surgery is recommended in patients with recurrent ischemia (spontaneous or upon exercise) after the infarct.
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PMID:Thrombolytic therapy in acute myocardial infarction. 252 93

A patient with severe hand ischemia due to Buerger's disease was treated by a rapidly effective modification of percutaneous catheterization. Accelerated mechanical and pharmacologic thrombolysis of an occluded palmar arch with 200,000 U urokinase and subsequent small vessel angioplasty abolished pain and restored digital perfusion within 40 min.
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PMID:Accelerated thrombolysis and angioplasty for hand ischemia in Buerger's disease. 252 19

Two cases of acute leg ischemia from unilateral occlusion of an aorto-bifemoral graft, treated with high-dose urokinase intra-arterial infusion, are reported. This therapy allowed identification of the cause of thrombosis, recanalization of the graft and planning of reoperation. Indications for intra-arterial thrombolytic therapy and advantages of urokinase vs streptokinase are discussed.
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PMID:Thrombolysis of graft occlusion using high dose urokinase. An alternative to surgical treatment? 252 5

Skeletal muscle is unique in its ability to tolerate relatively long periods of ischemia without demonstrable damage following reperfusion. Prolonged ischemia, however, has been associated with muscle necrosis and poor recovery of function. Using a rabbit model of hind limb ischemia, periods of ischemia of 1, 2, 3, and 5 hours were studied. Whereas almost complete recovery was seen after 1 or 2 hours of ischemia, a progressive loss of function is seen with increasing ischemic interval. In addition, within the 5 hour group, up to 40% of preparations did not recover function during reperfusion, with no Doppler signals audible over the pedicle. In these, microscopic thrombi was demonstrated histologically. Thus it appears that the "no reflow" phenomenon plays a major role after prolonged (greater than 4 hrs) ischemia. In order to evaluate the effect of fibrinolytic drugs on the "no reflow" phenomenon, urokinase was infused prior to reperfusion, and after 5 hours of ischemia, in a separate group of animals. All of these reperfused without any evidence of "no reflow". We conclude that reperfusion injury may have two major components: the "no reflow" phenomenon secondary to poor reperfusion, and cellular injury resulting from reperfusion itself. Infusion of fibrinolytic agents during the initial phases of reperfusion may have a salutory effect in preventing the "no reflow" phenomenon. It is likely, however, that attempts at effective and safe retrieval of ischemic tissue will necessarily have to address both mechanisms.
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PMID:The role of fibrinolysis during reperfusion of ischemic skeletal muscle. 263 46

21 patients with acute or subacute severe ischemia at the digits due to occlusions of forearm, hand and/or finger arteries were treated by local thrombolysis with urokinase. The medicament (0.6-1.1 million units per day during 1-3 days) was applied by the intraarterial route after cannulation of the cubital or radial artery. Simultaneously, heparin (20,000 units/24 hours) was infused by the same intraarterial catheter. Complete recanalization was obtained in 5 out of 21 patients, partial recanalization with significant clinical improvement in 9 additional patients. Therapeutic success was best with mean duration of symptoms lasting less than 4 weeks and in patients with embolic occlusions. After one year half of the patients had no remaining symptoms. There were no patients with acral necrosis.
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PMID:[Local thrombolysis of acute and subacute forearm, hand and finger artery occlusions. Early and late results]. 274 34

Authors report the results of the treatment of acute ischemia of the limbs with urokinase in patients included in a polycentric study group called "Bologna". A total of 111 patients affected with acute ischemias of the limbs caused by arterial or graft thromboses were treated with intra-arterial urokinase with a loading dose of 200,000 U.I., followed by 75,000 I.U./hour maintenance dose for 72 hours at the most. With this treatment 83.5% of clinically positive results was obtained. Complications and angiographic results are discussed.
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PMID:Endoarterial treatment of acute ischemia of the limbs with urokinase. Italian Cooperative Study "Bologna". 276 59

Acute arterial embolic or thrombotic occlusion of the runoff vessels is associated with an incomplete operative thromboembolectomy and an unacceptably high rate of amputation. This report presents a six year analysis of the use of intraoperative intra-arterial thrombolytic therapy, evaluating 38 patients who presented with impending loss of limb because of an acute occlusion of the runoff vessels. All of the patients had extensive thrombosis of a distal vessel and a complete distal thromboembolectomy was not possible. Fourteen patients received infusion of streptokinase, maximum dose of 50,000 units; 26 received urokinase (UK), maximum dose of 150,000 units, and two underwent an isolated limb perfusion technique using one million units of UK. Thirty-four lower and four upper extremities were treated. Twenty-eight of 38 patients had successful revascularization procedures that resulted in salvage of the limbs, and ten of the 38 underwent an extensive amputation. In 18 of the 28 who were successfully revascularized, lysis was clearly obtained, which contributed to the ultimate success; in ten of the 28, it was unclear whether or not lysis significantly contributed to salvage of the limbs. Although four of the 38 died within 30 days postoperatively and one patient had a hemorrhagic complication, neither the deaths nor the complication could be attributed to a lytic agent. There was no evidence of systemic thrombolysis in these patients. Intraoperative intra-arterial thrombolytic therapy administered by the slow bolus injection technique is safe. It can be an important adjunct to mechanical thromboembolectomy and bypass procedures in patients with limb-threatening ischemia caused by thrombosis of the distal part of the vessel. The isolated limb perfusion technique using high dose UK is particularly valuable in acute, small vessel, multiarterial occlusion. Intraoperative intra-arterial infusion of thrombolytic agents may make the difference between salvage or amputation of the limb without causing additional risk for the patient.
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PMID:Intraoperative intra-arterial thrombolytic therapy for salvage of limbs in patients with distal arterial thrombosis. 278 47

Between August 1983 and December 1987, 23 patients received a 30-minute intraoperative, intraarterial infusion of streptokinase (seven patients) or urokinase (16 patients) because of residual thrombus or persistent ischemia or both after thromboembolectomy. Ages ranged from 21 to 77 years (mean, 58 years). In 15 patients intraoperative lytic therapy was part of the initial operation, whereas in eight patients intraoperative lytic therapy was performed during a secondary operation to treat thrombosis of a recently placed graft. Seven patients in the latter group had hypercoagulable conditions (five had heparin-induced thrombosis; one had protein C deficiency; one had polycythemia with thrombocytosis). Improvement after intraoperative lytic therapy was seen on angiography performed after infusion in 13 of 17 (76%) patients in whom angiography was performed both before and after intraoperative lytic therapy. Grafts in 12 of these patients remained patent without additional intervention, and in one graft thrombus formed again. In contrast, among four patients without angiographic evidence of improvement, thrombus formed again in four grafts (p less than 0.004). Intraoperative lytic therapy was considered successful in 74% of instances (17/23), including four of seven patients with hypercoagulable states. Three of six patients whose grafts failed had major amputations, whereas there were no amputations after successful infusions. Twelve patients were heparinized after intraoperative lytic therapy. Ten patients in this group were considered treatment successes, and two were considered treatment failures. Three of 11 patients not heparinized after intraoperative lytic therapy were considered treatment failures. Four hematomas occurred in the former group and none in the latter (p less than 0.03). No hematomas occurred in the heparin-induced thrombosis group in spite of anticoagulation with sodium warfarin (Coumadin). Only one hematoma occurred within 6 hours of intraoperative lytic therapy, and thus it was attributable to the infusion. We conclude that intraoperative lytic therapy is an effective adjunct to manage residual thrombus or persistent ischemia or both after lower extremity revascularization. Postinfusion angiography is of prognostic value. Heparinization after intraoperative lytic therapy seems beneficial but significantly increases the risk of bleeding complications.
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PMID:Intraoperative infusion of lytic drugs for thrombotic complications of revascularization. 279 66


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