Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of spa bathing on blood coagulation and fibrinolysis were studied in 20 patients with chronic cerebral infarction. Blood was obtained before and after a 10-minute period of spa bathing at 41 degrees C. Prothrombin time, activated partial thromboplastin time, fibrinogen, factor VIII activity, von Willebrand factor activity, and antithrombin III activity did not show significant changes after bathing, but euglobulin lysis time was significantly reduced (p < 0.01) and fibrin lysis activity was increased (p < 0.05). These findings suggest that spa bathing activates fibrinolysis without markedly changing blood coagulation in patients with chronic cerebral infarction. It is thought that the activation of fibrinolysis without the activation of coagulation has a favorable effect on blood circulation. The results of fibrin-plate assays using C1 inactivator indicated that tissue-type plasminogen activator was the major contributor to the activation of fibrinolysis during spa bathing.
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PMID:Spa bathing activates fibrinolysis in patients with cerebral infarction. 831 58

To examine the fibrinolytic system and platelet factors (PF4 and beta-TG), we conducted a venous occlusion test (V.O. test) on two groups of elderly patients suffering from cerebral infarction, one group being able to walk (A group), the other being bed-ridden for during a long period (B group). Their levels of t-PA, PAI-1 antigen and platelet factors were compared between A or B, A + B and healthy elderly groups. The t-PA antigen level of both group A and B after the V.O. test tended to increase. The t-PA values of A + B groups after the V.O. test were also similar to that of the healthy elderly. The PAI-1 antigen level of both group A and B before the V.O. test was higher than that of the healthy elderly. However, the PAI-1 antigen level of both group A and B tended to decrease after the V.O. test. No remarkable changes were noted in PF4 and beta-TG, which have been thought to reflect platelet function. The above findings suggest that the fibrinolytic activity in A or B groups can recover through stimulation by exercise training and some medical treatment.
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PMID:[Changes of the plasma levels of tissue plasminogen activator and plasminogen activator inhibitor-1 in cerebral infarction induced by the venous occlusion]. 853 2

We have established a novel thrombosis model of the middle cerebral artery (MCA). The thrombotic occlusion of the MCA was induced by the photochemical reaction between Rose Bengal and green light, which causes endothelial injury followed by platelet adhesion, aggregation and formation of a platelet and fibrin-rich thrombus at the site of the photochemical reaction. With this model, we have investigated the effects of anti-thrombotic agents, thrombolytic agents and neuroprotective agents. In our model, ADP, thromboxane A2 (TXA2) and thrombin play a key role in thrombus formation of the MCA. Tissue-type plasminogen activator (tPA) could cause an opening of the thrombotic MCA occlusion and reduced the size of the cerebral infarction. Furthermore, a TXA2 antagonist enhanced the thrombolytic efficacy of tPA. MS-153 ((R)-(-)-5-methyl-1-nicotinoyl-2-pyrazoline), a glutamate release inhibitor and YM90K [6-(1 H-imidazol-1-yl)-7-nitro-2,3(1H, 4H)-qunoxalinedione monohydrochloride, an alpha-amino-3hydroxy-5methyl-4-isoxazole (AMPA) antagonist reduced the cerebral infarction 24 hr after the MCA occlusion. This model is very useful for investigating the mechanisms of anti-thrombotic and neuroprotective agents and evaluating the effects of these agents.
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PMID:[A novel photochemical model of the middle cerebral artery for thrombosis research and evaluation of anti-thrombotic agents]. 916 Mar 47

Since the publication of the NINDS rt-PA trial in 1995, tissue plasminogen activator has been licensed for the treatment of acute cerebral infarction in the U.S. The demonstrated benefit was confirmed to patients presenting within three hours of symptom onset on adhering to study guidelines, which subsequently have formed the basis for a protocol for thrombolysis in acute stroke. The implementation of a thrombolysis programme in Ireland would require a restructuring of hospital facilities to manage acute stroke. We conducted a prospective study of 100 patients admitted to an acute stroke unit to assess the potential for intervention with t-PA under NINDS guidelines. Data was collected on stroke type. CT appearances, time of onset of stroke and laboratory parameters. Only 6% of all strokes assessed were eligible for thrombolysis and time to presentation was the major excluding factor. When time was removed as an exclusion criteria only 1/5 of all strokes were potential candidates in this best case scenario. Thrombolysis does improve outcome in cerebral infarction in a a strictly controlled setting but only 6% of our patients would currently be eligible for treatment. While this may improve with better public education regarding stroke and it's treatment, only a 1/5 of our patients would still be eligible were they all to present within 2 hours of symptoms onset.
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PMID:Potential for treatment with thrombolysis in an Irish stroke unit. 1036 96

We evaluated the efficacy of local intra-arterial fibrinolysis (LIF) used in tissue plasminogen activator (t-PA) and its indication for acute middle cerebral artery (MCA) occlusion on angiographic degree of leptomeningeal collateral flow in a series of 26 patients (mean age: 67.2 years old). The occlusion types were classified into three types: (1) M 1 proximal occlusion (N = 8) involved the lenticulostriate arteries (LSA), (2) M 1 distal occlusion (N = 6) without involvement of the LSA to M 2 bifurcation, (3) M 2-3 occlusion (N = 12). In M 1 proximal and distal type, 100% patients had complete or partial recanalization till 5.3 and 6 hours, and 91.7% recanalized in M 2-3 type within 3.96 hours from attack on the average. Small cerebral infarction post LIF showed in 50%, but had no clinical change for the worse in all types. There was 65% in excellent or good prognosis on 2 months after attack. Within the range of 600,000-2,400,000 units of t-PA (mean = 1,107,000 units), small hemorrhagic transformation were developed in 5 cases (19.2%) without influence on its outcome. It means that below 2,400,000 units t-PA for LIF were safety amounts. In patients with poor collateral flow in angiographic findings, good prognosis could be possible in 75% within 4 hours (M = 3.96 hours) recanalization on the average. We conclude that LIF used in t-PA would be efficatious in M 1 proximal occlusion within 4 hours of onset and in patients with poor collateral flow when recanalized within 4 hours after attack.
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PMID:[Clinical study of therapeutic time window of local fibrinolysis for acute middle cerebral artery occlusion]. 1051 55

This paper aimed to investigate the effect of lumbrokinase on the anticoagulation and fibrinolysis in treating cerebral infarction. Lumbrokinase was used in patients with cerebral infarction. Patients were randomly divided into treatment group (n = 31) and control group (n = 20). Single blind method was used in this investigation. The Chinese stroke score was used to evaluate the results of treatment before and after administration of lumbrokinase. Kaolin partial thromboplastin time (KPTT), prothrombin time (PT), fibrinogen content, vWF content were analyzed, and tissue plasminogen activator (t-PA) activity, plasminogen activator inhibitor (PAI) activity, D-dimer level were assayed. In both groups, the stroke score decreased after administration, but in the treatment group, it was more obvious. In the treatment group, KPTT was prolonged, t-PA activity and D-dimer level increased, while the content of fibrinogen decreased significantly. There were no significant changes of PT and PAI activity in both groups. It is concluded that lumbrokinase is beneficial to the treatment of cerebral infarction. The effect of lumbrokinase is related to the inhibition of intrinsic coagulation pathway and the activation of fibrinolysis via an increase of t-PA activity.
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PMID:Changes in coagulation and tissue plasminogen activator after the treatment of cerebral infarction with lumbrokinase. 1132 42

The possible existence of distinctive, vascular bed specific alterations of coagulation and fibrinolytic parameters associated with three different types of thrombosis was investigated in young women (n = 68, <45 years at onset of the event) following myocardial infarction (MI) (n = 22), lacunar cerebral infarction (LACI) (n = 16), idiopathic deep vein thrombosis (VT) (n = 14) and venous thrombosis due to oral contraceptive use (n = 16) in the stable period after the acute thrombotic event. Coagulation and fibrinolytic parameters, as well as classical metabolic variables, were measured and compared with 52 age-matched, healthy controls. In MI women we observed elevated tissue type plasminogen activator (t-PA) antigen levels, which correlated significantly with parameters of the plurimetabolic syndrome. In LACI women we found elevated fibrinogen, which correlated with D-dimer, systolic blood pressure, smoking, and sedimentation rate. Prolonged euglobulin clot lysis time, elevated t-PA antigen, PAI-1 antigen and activity, which all correlated with parameters of the plurimetabolic syndrome, were found in women with idiopathic VT, who were also clearly obese but not in women in whom oral contraceptives were the triggering factor for VT. Our results showed not parallel, but different profiles of alterations in fibrinolytic and coagulation parameters in line with the prediction of a vascular bed specific thrombosis process.
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PMID:Vascular bed specific alterations in coagulation and fibrinolytic parameters in young women following myocardial infarction, lacunar cerebral infarction and deep vein thrombosis. 1462 51

The role of endogenous tissue-type plasminogen activator (tPA) on focal cerebral ischemic injury (FII) after middle cerebral artery (MCA) occlusion was studied by using tPA gene deficient (KO) mice and wild type (WT) mice. MCA was occluded by thrombosis induced by 3 different intensities of photochemical damage of MCA. FII size in KO mice was smaller than in WT mice in mild damage whereas it was larger in severe damage. These results suggested that endogenous tPA protected FII through its thrombolytic action on transient occlusion with mild damage, but deteriorated on persistent occlusion with severe damage. Cerebral hemorrhage associated with antithrombotic and thrombolytic therapy in acute stroke is a major clinical problem. We investigated the roles of endogenous tPA and MMPs in hemorrhagic cerebral infarction associated with heparin. We demonstrated that heparin administration caused cerebral hemorrhage in WT but not in KO. Heparin administration increased tPA activity and its mRNA expression in WT. We also observed an induction of MMP9 and its mRNA expression by heparin administration in WT but not in KO. Our findings suggest that endogenous tPA plays an important role in heparin-produced cerebral hemorrhage via MMP9 induction and activation.
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PMID:[Role of endogenous tPA in stroke]. 1619 Mar 67

We performed a preliminary feasibility and safety study using intravenous (IV) administration of a platelet glycoprotein IIb/IIIa inhibitor (abciximab) in conjunction with intraarterial (IA) administration of a thrombolytic agent (reteplase) in a primate model of intracranial thrombosis. We introduced thrombus through superselective catheterization of the intracranial segment of the internal carotid artery in 16 primates. The animals were randomly assigned to receive IA reteplase and IV abciximab ( n =4), IA reteplase and IV placebo ( n =4), IA placebo and IV abciximab ( n =4) or IA and IV placebo ( n =4). Recanalization was assessed by serial angiography during the 6-h period after initiation of treatment. Postmortem magnetic resonance (MR) imaging was performed to determine the presence of cerebral infarction or intracranial hemorrhage. Partial or complete recanalization at 6 h after initiation of treatment (decrease of two or more points in pre-treatment angiographic occlusion grade) was observed in two animals treated with IA reteplase and IV abciximab, three animals treated with IA reteplase alone and one animal treated with IV abciximab alone. No improvement in perfusion was observed in animals that received IV and IA placebo. Cerebral infarction was demonstrated on postmortem MR imaging in three animals that received IA and IV placebo and in one animal each from the groups that received IA reteplase and IV abciximab or IV abciximab alone. One animal that received IV abciximab alone had a small intracerebral hemorrhage on MR imaging. IA reteplase with or without abciximab appeared to be the most effective regimen for achieving recanalization in our model of intracranial thrombosis. Further studies are required in experimental models to determine the optimal dose, method of administration and efficacy of these medications in acute ischemic stroke.
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PMID:Intraarterial reteplase and intravenous abciximab for treatment of acute ischemic stroke. A preliminary feasibility and safety study in a non-human primate model. 1620 96

Wasp is an important venomous animal that can induce human fatalities. Aortic thrombosis and cerebral infarction are major clinical symptoms after massive wasp stings but the reason leading to the envenomation manifestation is still not known. In this paper, a toxin protein is purified and characterized by Sephadex G-75 gel filtration, CM-Sephadex C-25 cationic exchange and fast protein liquid chromatography (FPLC) from the venom of the wasp, Vespa magnifica (Smith). This protein, named magnifin, contains phospholipase-like activity and induces platelet aggregation. The cDNA encoding magnifin is cloned from the venom sac cDNA library of the wasp. The predicted protein was deduced from the cDNA with a sequence composed of 337 amino acid residues. Magnifin is very similar to other phospholipase A(1) (PLA(1)), especially to other wasp allergen PLA(1). Magnifin can activate platelet aggregation and induce thrombosis in vivo. The current results proved that PLA(1) in wasp venom could be contributable to aortic thrombosis after massive wasp stings.
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PMID:A phospholipase A1 platelet activator from the wasp venom of Vespa magnifica (Smith). 1802 35


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