Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Replantation of a circularly severed palm, partially severed middle finger and completely severed ring and small fingers was done successfully in one patient. Two palmar arteries, 5 digital arteries, 3 dorsal palmar veins, 9 dorsal digital veins were anastomosed. Vein transplantation was carried out to repair the ulnar digital artery defect of the middle finger. Severe swelling after arterial thrombosis was noted on the 7th day and was eliminated by the use of urokinase. All the replanted parts survived with good functional results. Precise anastomosis, prevention and treatment of thrombosis, early exercises were essential to the survival of fingers and functional recovery of hand.
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PMID:[Successful replantation of circularly severed palm and multiply severed fingers. A case report]. 128 92

The isometric contraction (supramaximal tetanic stimulation) of anterior tibialis muscle was studied in 32 New Zealand white rabbits after 5 hr of ischemia. Reperfusion was achieved after systemic heparinization (100 U/kg) by removal of vascular clamps (normal reperfusion, NR, N = 10); isolated pump perfusion at 15 cc/min for 30 min followed by normal reperfusion (controlled reperfusion, CR, N = 8); CR with a Sepacell 500 filter in the circuit (leukopenic, thrombocytopenic, controlled reperfusion, L/TR, N = 9); or adding 25,000 U of urokinase to the initial reperfusate (UKR, N = 5). Experimental muscle is compared to control nonischemic contralateral muscle in each animal and expressed as percentage of control function. Specimens were studied by light microscopy. No significant difference in mean function at 2 hr was seen between the four groups, with NLR having 53% of control function, CR 55% of control function, L/TR 61% of control function, and UKR 48% of control function. "No reflow," as defined by the absence of Doppler flow signals over the muscle pedicle with no recovery of function during reperfusion and continued incidence of persistent ischemia, was seen in NLR 4/10, CR 5/8, and L/TR 6/9 preparations with arteriolar, capillary, and venule thrombi documented by light microscopy. In contrast, "no reflow" was not seen in UKR (0/5, P less than 0.05). Peak function at any interval (potential maximal recovery) in muscles that adequately reperfused was best in CR (73%) and L/TR (73%). No difference in the degree of injury in adequately reperfused muscles was seen between the four groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Skeletal muscle function after ischemia: "no reflow" versus reperfusion injury. 206 59

Despite the limitations of individual ischemia models, experience with fibrinolytic agents suggests that 1) early intervention with rt-PA may result in rapid thrombolysis, functional recovery, and decreased mortality in small animal stroke thromboembolism models, 2) rt-PA has no general effect on clinical recovery following MCA occlusion and reperfusion in the nonhuman primate at dose rates capable of producing very high circulating rt-PA levels, while u-PA has an apparently salutary effect, and 3) intravenous infusion of rt-PA or u-PA early after ischemia/infarction in several model systems is not associated with significant intracerebral hemorrhage. The true clinical relevance of these general impressions must await the completion of human studies and studies in well-conceived models designed to define the vascular consequences to be expected from reperfusion achievable with thrombolytic agents.
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PMID:Relevance of focal cerebral ischemia models. Experience with fibrinolytic agents. 226 Jan 42

To determine the clinical consequences of reocclusion of an infarct-related artery after reperfusion therapy, we evaluated 810 patients with acute myocardial infarction. Patients were admitted into four sequential studies with similar entry criteria in which patency of the infarct-related artery was assessed by coronary arteriography 90 minutes after onset of thrombolytic therapy. Successful reperfusion was established acutely in 733 patients. Thrombolytic therapy included tissue-type plasminogen activator (t-PA) in 517, urokinase in 87, and a combination of t-PA and urokinase in 129 patients. All patients received aspirin, intravenous heparin and nitroglycerin, and diltiazem during the recovery phase. A repeat coronary arteriogram was performed in 88% of patients at a median of 7 days after the onset of symptoms. Reocclusion of the infarct-related artery occurred in 91 patients (12.4%), and 58% of these were symptomatic. Angiographic characteristics at 90 minutes after thrombolytic therapy that were associated with reocclusion compared with sustained coronary artery patency were right coronary infarct-related artery (65% versus 44%, respectively) and Thrombolysis in Myocardial Infarction (TIMI) flow 0 or 1 (21% versus 10%, respectively) before further intervention. Median (interquartile value) degree of stenosis in the infarct-related artery at 90 minutes was similar between groups: 99% for reoccluded (value, 90/100%) compared with 95% for patent (value, 80/99%). Patients with reocclusion had similar left ventricular ejection fractions compared with patients with sustained patency at follow-up. However, patients with reocclusion at follow-up had worse infarct-zone function at -2.7 (value, -3.2/-1.8) versus -2.4 (SD/chord) (value, -3.1/-1.3) (p = 0.016). The recovery of both global and infarct-zone function was impaired by reocclusion of the infarct-related artery compared with maintained patency; median delta ejection fraction was -2 compared with 1 (p = 0.006) and median delta infarct-zone wall motion was -0.10 compared with 0.34 SD/chord (p = 0.011), respectively. In addition, patients with reocclusion had more complicated hospital courses and higher in-hospital mortality rates (11.0% versus 4.5%, respectively; p = 0.01). We conclude that reocclusion of the infarct-related artery after successful reperfusion is associated with substantial morbidity and mortality rates. Reocclusion is also detrimental to the functional recovery of both global and infarct-zone regional left ventricular function. Thus, new strategies in the postinfarction period need to be developed to prevent reocclusion of the infarct-related artery.
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PMID:Consequences of reocclusion after successful reperfusion therapy in acute myocardial infarction. TAMI Study Group. 188 72

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

A case of successful replantation of multiple digits and circular palm amputation caused by an industrial punch force is reported. The two-level amputation was reconstructed by first replanting the severed fingers to the palmar segment and then connecting the palm segment to the hand stump. An arterial crisis was treated with urokinase, and postoperative functional recovery is described.
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PMID:Replantation of a multiple digit and circular palm amputation: a case report. 847 22

This report describes a neonate with acute renal failure associated with extensive aortic and bilateral renal artery thrombosis attributed to inadequate breastfeeding and severe dehydration. Dialytic and general supportive care, together with concurrent anticoagulation, and continuous aggressive intrathrombic instillation of urokinase for 5 days resulted in near-complete thrombolysis. Renal functional recovery began 11 days after the onset of anuria. Despite ischemic atrophy of the left kidney, renal function and blood pressure were normal on follow-up. Thus, in neonates thrombolytic therapy may positively impact survival and recovery of renal function even in the setting of prolonged ischemic renal injury.
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PMID:Aortic and renal artery thrombosis in a neonate: recovery with thrombolytic therapy. 932 98

Axonal outgrowth during peripheral nerve regeneration relies on the ability of growth cones to traverse through an environment that has been altered structurally and along a basal lamina sheath to reinnervate synaptic targets. To promote migration, growth cones secrete proteases that are thought to dissolve cell-cell and cell-matrix adhesions. These proteases include the plasminogen activators (PAs), tissue PA (tPA) and urokinase PA (uPA), and their substrate, plasminogen. PA expression and secretion are upregulated in regenerating mammalian sensory neurons in culture. After sciatic nerve crush in mice, there was an induction of PA mRNAs in the sensory neurons contributing to the crushed nerve and an upregulation of PA-dependent activity in crushed nerve compared with sham counterparts during nerve regeneration. To further assess the role of the PA system during peripheral nerve regeneration, PA-dependent activity as well as recovery of sensory and motor function in the injured hindlimb were assessed in wild-type, tPA, uPA, and plasminogen knock-out mice. Protease activity visualized by gel zymography showed that after nerve crush, the upregulation of PA activity in the tPA and uPA knock-out mice was delayed compared with wild-type mice. Recovery of sensory function was assessed by toe pinch, footpad prick, and the toe-spreading reflex. All knock-out mice demonstrated a significant delay in hindlimb response to these sensory stimuli compared with wild-type mice. For each modality tested, the uPA knock-out mice were the most dramatically affected, showing the longest delay to initiate a response. These studies clearly showed that PAs were necessary for timely functional recovery by regenerating peripheral nerves.
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PMID:Mice lacking tPA, uPA, or plasminogen genes showed delayed functional recovery after sciatic nerve crush. 1140 20

Life-threatening, complete middle cerebral artery infarction occurs in up to 10% of all stroke patients. The "malignant media occlusion" is an infarction occupying more than 50% of middle cerebral artery territory. The malignant, space-occupying supratentorial ischemic stroke is characterised by a mortality rate of up to 80%. Several reports indicate, that hemicraniectomy in this situation can be life-saving. Hemicraniectomy increases cerebral perfusion pressure and optimises retrograde perfusion via the leptomeningeal collateral vessels. A case of a patient is presented, having progressive neurological deterioration due to massive cerebral infarctions. The patient rehabilitation was successful. Decompressive surgery is life saving and can also give acceptable functional recovery. Hemorrhagic stroke is due to stroke in 15% of cases and in 10%, it is "spontaneous" intracerebral hematoma. The intracerebral and intraventricular hemorrhage represents one of the most devastating types of stroke associated with high morbidity and mortality. The 30-day mortality rate is 35% to 50% and most survivors are left with a neurological disability. The value of surgical therapy is debatable. The aspiration and urokinase therapy of the hematoma of intracerebral hemorrhage could improve final neurological outcome. Spontaneous, nontraumatic intraventricular hemorrhage frequently carries a grave prognosis. A large part of morbidity after intraventricular hemorrhage is related to intracranial hypertension from hydrocephalus. One patient presented had intracerebral hemorrhage and another had intraventricular hemorrhage treated with urokinase. Rapid and extensive reduction in the amount of intracerebral and intraventricular blood occurred. Urokinase lysis is safe and can be a potentially beneficial intervention in intracerebral and intraventricular hemorrhage. By performing decompressive craniectomy, the neurologists of stroke departments and intensive care units with the neurosurgeons will have to play major role in the management of stroke patients.
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PMID:[New methods of intensive therapy in stroke: hemicraniectomy in patients with complete middle cerebral artery infarction and treatment of intracerebral and intraventricular hemorrhage with urokinase]. 1212 81

Human adult bone marrow-derived endothelial progenitors, or angioblasts, induce neovascularization of infarcted myocardium via mechanisms involving both cell surface urokinase-type plasminogen activator, and interactions between beta integrins and tissue vitronectin. Because each of these processes is regulated by plasminogen activator inhibitor (PAI)-1, we selectively down-regulated PAI-1 mRNA in the adult heart to examine the effects on postinfarct neovascularization and myocardial function. Sequence-specific catalytic DNA enzymes inhibited rat PAI-1 mRNA and protein expression in peri-infarct endothelium within 48 h of administration, and maintained down-regulation for at least 2 wk. PAI-1 inhibition enhanced vitronectin-dependent transendothelial migration of human bone marrow-derived CD34+ cells, and resulted in a striking augmentation of angioblast-dependent neovascularization. Development of large, thin-walled vessels at the peri-infarct region was accompanied by induction of proliferation and regeneration of endogenous cardiomyocytes and functional cardiac recovery. These results identify a causal relationship between elevated PAI-1 levels and poor outcome in patients with myocardial infarction through mechanisms that directly inhibit bone marrow-dependent neovascularization. Strategies that reduce myocardial PAI-1 expression appear capable of enhancing cardiac neovascularization, regeneration, and functional recovery after ischemic insult.
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PMID:Down-regulation of plasminogen activator inhibitor 1 expression promotes myocardial neovascularization by bone marrow progenitors. 1559 22


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