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: UNIPROT:P00750 (PLA)
16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The etiology of intra-abdominal adhesions is explained by hydrolysis of the peritoneal phospholipid layer caused by phospholipase A2 activity. This view could unify the pre-existing hypotheses that intra-abdominal adhesions are due to ischemia or increased plasminogen activator activity. New therapeutic approaches are suggested.
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PMID:Intra-abdominal adhesion formation is initiated by phospholipase A2. 818 30

Proper understanding of the pathologic process of a ruptured plaque followed by thrombus formation, with acute assessment of the deranged pathophysiology of the coronary circulation as a sequel, remains the basis for rational therapy of cardiac ischemia. With the advent of better thrombolytic regimens, improved direct reperfusion via angioplasty, and streamlined recognition/admission procedures, therapeutic strategies for dealing with acute myocardial infarction have once more turned to the options for early therapy. From recent studies of out-of-hospital thrombolysis or immediate percutaneous transluminal coronary angioplasty, the position is reinforced that "early" means the first 100 minutes. It is hoped that the large Global Utilization of Streptokinase and t-PA for Occluded Arteries (GUSTO) study, which specifically analyses the effect of early reperfusion by optimal alteplase and actilyse (recombinant tissue-type plasminogen activator [rt-PA]) versus streptokinase regimens will confirm this essential concept once and for all. Thus, when appropriate therapy--depending in the local availability of facilities--is promptly given, further reductions in myocardial infarction size and ventricular dysfunction can be achieved, resulting in mortality rates < 5%, at substantial savings in ever more expensive healthcare resources. "Early is < 100 minutes; later may be too late or too costly."
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PMID:Expanding indications for thrombolytic therapy in acute myocardial infarction. How late is too late, and how early is early: the clinician's view of the first 100 minutes. 827 56

Patients with a patent coronary artery after reperfusion therapy show an increased rate of evolution of QRS changes and of resolution of S-T changes as compared to patients with a persistent occlusion. Dynamic vectorcardiography permits multi-lead monitoring of changes in QRS complex and S-T segment over time. We monitored 150 patients randomized to alteplase or streptokinase for 24 h after admission. Alteplase was associated with significantly more rapid evolution of electrocardiographic changes but also with an increased occurrence of recurrent S-T changes. This may indicate a higher rate of early reperfusion with alteplase but due to recurrent ischemia, an electrocardiographic catch-up is seen with similar extent of myocardial damage observed after 24 h of monitoring.
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PMID:Early electrocardiographic changes in acute myocardial infarction treated by streptokinase or alteplase: a randomized study with dynamic, multi-lead, electrocardiographic monitoring. 840 57

Intravenous heparin is routinely given after thrombolytic therapy for patients with acute myocardial infarction in the United States and in some, but by no means all, other countries. Several trials have documented improved infarct-artery patency in patients treated with heparin; however, none was large enough individually to assess the effect of heparin on clinical outcomes. We performed a systematic overview of the 6 randomized controlled trials (1,735 patients) to summarize the available data concerning the risks and benefits of intravenous heparin versus no heparin after thrombolytic therapy. Mortality before hospital discharge was 5.1% for patients allocated to intravenous heparin compared with 5.6% for controls (relative risk reduction of 9%, odds ratio 0.91, 95% confidence interval 0.59 to 1.39). Similar rates of recurrent ischemia and reinfarction were observed among those allocated to heparin therapy or control. The rates of total stroke, intracranial hemorrhage, and severe bleeding were similar in patients allocated to heparin; however, the risk of any severity of bleeding was significantly higher (22.7% vs 16.2%; odds ratio 1.55, 95% confidence interval 1.21 to 1.98). There was no significant difference in the observed effects of heparin between patients receiving tissue-type plasminogen activator and those receiving streptokinase or anisoylated plasminogen streptokinase activator complex, or between patients who did and did not receive aspirin. The findings of this overview demonstrate that insufficient clinical outcome data are available to support or to refute the routine use of intravenous heparin therapy after thrombolysis. It is not known if these findings are due to lack of statistical power, inappropriate levels of anticoagulation, or lack of benefit of intravenous heparin. Large randomized studies of heparin (and of new antithrombotic regimens) are needed to establish the role of such therapy.
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PMID:Overview of randomized trials of intravenous heparin in patients with acute myocardial infarction treated with thrombolytic therapy. 861 Jun 1

This study was designed to evaluate the effects of tissue-type plasminogen activator (tPA) and 21- amino steroid (U74006F) in experimental embolic stroke in rabbits. The size of infarction from embolism was compared to controls with tPA alone, 21-amino steroid alone, and in combination. The middle cerebral artery of the rabbit was embolized by injecting an arterial ('white') thrombus in the right internal carotid artery. The rabbit treatment was 2 mg kg-1 of tissue-type plasminogen activator and/or 3 mg kg-1 of 21 amino steroid started at 2 h post-embolization. The animals were terminated 4 h post-treatment and brains were examined for evidence of ischemia and/or hemorrhage. Administration of tissue-type plasminogen activator and/or 21-amino steroid in the raw data show that there is a tendency for all treatments to reduce the ischemic volume when compared to the control group, also it is evident the standard deviation of these estimates is rather large when compared to the differences between treatments. The results of the analysis of variance shows that the differences expressed are not statistically significant. (No statistical differences were found between the treatment groups and the control group.) The results show that administration of tissue-type plasminogen activator and/or 21 amino steroid at 2 h post-embolization alone or in simultaneous administration does not significantly reduce the volume of infarction. Further studies need to be addressed in regards to the region of viable brain in the peri-infarct area, in reducing the time to treatment.
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PMID:Influence of a 'brain protector' drug 21-amino steroid on the effects of experimental embolic stroke treated by thrombolysis. 862 95

The focus of new research efforts to improve the morbidity and mortality associated with acute myocardial infarction (AMI) has turned to adjuvant agents that show promise of improving outcomes following coronary thrombolysis. We enrolled 162 patients with AMI in a randomized trial comparing front-loaded tissue-plasminogen activator (t-PA) plus weight-adjusted heparin with anisoylated plasminogen streptokinase activator complex (APSAC) without heparin as well as standard-dose (325 mg) and low-dose (81 mg) aspirin. The primary end point was an in-hospital morbidity profile; secondary end points were clinical and angiographic potency and hemorrhagic events. Selected sites performed an electrocardiographic substudy to determine the time to 50% ST-segment recovery and the time to steady state. Although the trial was terminated when the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries-I trial showed that t-PA had a significant mortality advantage over streptokinase, important trends were evident. Patients given t-PA and heparin were better anticoagulated (p = 0.001), yet AP-SAC-treated patients had more bleeding complications. The primary end point favored t-PA (25.4% vs 31.3%), and the secondary end points were similar in both groups. In the electrocardiographic substudy, the t-PA group achieved both 50% ST-segment recovery and steady-state recovery sooner than the APSAC group. Patients taking low-dose aspirin had lower in-hospital mortality and less recurrent ischemia but more strokes than the standard-dose aspirin group. Thus, this trial demonstrated trends favoring front-loaded t-PA with weight-adjusted heparin over APSAC without heparin in the treatment of AMI. The use of low-dose aspirin did not appear to impose a loss of protection from adverse events, nor did standard-dose aspirin increase serious bleeding.
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PMID:A randomized factorial trial of reperfusion strategies and aspirin dosing in acute myocardial infarction. The DUCCS-II Investigators. 862 29

We investigated changes in vascular reactivity to endothelin (ET) and local release of ET-like immunoreactivity (ET-LI) induced by myocardial ischemia and reperfusion in a pig model of coronary thrombosis and thrombolysis and studied the possible mechanisms producing the changed vascular reactivity to ET-1. We induced coronary thrombosis by inserting a copper coil into the left anterior descending coronary artery (LAD) and achieved thrombolysis with tissue plasminogen activator (t-PA). Vascular reactivity to ET-1 in the nonischemic and ischemic/reperfused LAD diagonal branches was evaluated in vitro. ET-LI was analyzed in plasma from the great cardiac vein and aorta for estimation of local release. The vasoconstrictor response to ET-1 was enhanced twofold (p < 0.01) in the ischemic/reperfused arteries as compared with the nonischemic arteries. The vasoconstriction induced by the ETB receptor agonist [Ala 1,3,11,15] ET-1 or serotonin was not significantly affected by ischemia/reperfusion. The ETA receptor antagonist BQ-123 reversed the ET-1-induced vascular contraction to a similar degree in ischemic/reperfused and control arteries. The ET-1-induced vasoconstriction of control arteries was not affected by inhibition of nitric oxide (NO) synthase with NG-nitro-L-arginine (L-NNA) or cyclooxygenase with indomethacin. During reperfusion, the myocardial venoarterial plasma concentration difference of ET-LI and blood flow increased, resulting in an increased overflow of ET-LI. Our results demonstrate that coronary thrombosis and thrombolysis evokes enhanced local release of ET-LI during the reperfusion period and increases the vasoconstrictor effects of ET-1 through a mechanism related to ETA receptor activation but unrelated to altered endothelial function. These changes may play a role in the development of ischemic/reperfusion injury and no-reflow phenomenon.
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PMID:Myocardial release of endothelin (ET) and enhanced ET(A) receptor-mediated coronary vasoconstriction after coronary thrombosis and thrombolysis in pigs. 863 92

We investigated the reversibility of compound action potential (CAP) changes induced after transitory local ischemia induced by rose bengal photochemically induced thrombosis of the rat anterior inferior cerebellar artery (AICA). Cochlear blood flow (CBF) was measured with a laser-Doppler flowmeter positioned on the lateral bony wall of the basal turn of the cochlea, and the CAP to an 8-kHz half-wave of sinusoid sound at 100 dB sound pressure level was monitored. The irradiation was started 5 minutes before the rose bengal administration and continued through the thrombosis formation. Tissue-type plasminogen activator (t-PA, 1 mg/kg) dissolved in saline was injected intravenously 2 minutes after complete photothrombotic blockade of the AICA in the rats presenting complete abolition of CAPs just after the vascular occlusions. Nineteen of the 51 rats presented complete abolition of the CAP just after the AICA occlusion, and the thrombosed AICA was successfully reperfused by t-PA administration in 11 of the 19 rats. The result showed that duration of ischemia was the more important determinant for the reversibility of CAPs during the acute phase (p = .00001), and the residual level of cochlear blood flow during ischemia was also an important factor (p = .066). It appeared that the critical time of ischemia for the complete recovery of CAPs was around 5 minutes, and that the critical limit for the irreversibility of CAPs within the acute phase was between 20 and 25 minutes.
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PMID:Reversibility of compound action potential during the acute phase after transitory local ischemia. 863

Intraarterial thrombolysis is used increasingly for management of arterial and bypass graft occlusions. Current research has been directed at the indications for and methods of catheter-directed thrombolysis. Streptokinase, urokinase, and tissue plasminogen activator (t-PA) are the most commonly used agents. They are administered by a variety of techniques and in various doses involving intrathrombic infusions, thrombus lacing, high-dose bolus therapy, and pulse-spray lysis. The latter methods appear to produce thrombolysis within a few hours, so this chemical therapy has the potential to become the first-line management for all episodes of acute limb ischemia. The role of thrombolysis is to return patients to their prethrombotic or preembolic state, so the underlying condition can be treated by radiologic intervention, surgery, or anticoagulation. Intraarterial thrombolysis is indicated for occlusions of less than 2 weeks' duration where the limb is able to withstand a period of further ischemia. Older occlusions should be treated by surgery, reserving intraoperative lysis for specific situations.
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PMID:Lower limb intraarterial thrombolysis as an adjunct to the management of arterial and graft occlusions. 866 48

Surgical revascularization as the initial therapy in acute lower limb ischemia (ALLI) is associated with a high cumulative mortality and amputation rate. Catheter-directed delivery of low-dose thrombolytic agents (intra-arterial thrombolysis, IAT) offers the possibility for a gentle revascularization with a minimum of stress for the patients. In two randomized studies, the primary rates of revascularization, amputation, and mortality did not differ significantly between IAT and surgical revascularization. However, in one study the 6-month event-free survival rate was 85% in the IAT group, and 63% in the surgical group. Also in the second study the 12-month results were significantly better in the IAT group (event-free survival 75%) than in the surgical group (event free survival 52%). The high-dose urokinase regimen recommended by some authors in IAT is associated with an unacceptable cerebral bleeding rate of up to 2%. Low-dose recombinant tissue-type plasminogen activator (rt-PA) (0.02 to 0.05 mg/h) is the most suitable agent in IAT because of rapid lysis and low bleeding complications. Patients with ALLI, classified as viable or threatened without neurologic deficit, benefit most from the IAT as the initial therapy in ALLI. When IAT is performed as the initial therapy in ALLI, surgical intervention becomes unnecessary in approximately one-third of the patients. In another third the subsequent correction of the cause of the ALLI can be performed electively, which reduces mortality and morbidity rates.
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PMID:Thrombolytic therapy in acute lower limb ischemia. 871 91


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