Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study reports the correlation of the thrombin generation test and the plasma clot impedance test with clinical evidence of hypercoagulability. Thrombin generation is increased and the rate of change of plasma from a liquid to a gel (clot impedance) is increased in situations where the risk of thrombosis is increased. These situations include increasing clinical signs and/or symptoms of thromboembolism, positive lung scans, postoperative total hip replacement, patients over 40 years old, low serum antithrombin III, thrombocytosis, transient cerebral ischemia, and positive isotope venogram for thrombosis. The two tests failed to indicate a significant effect of antiplatelet drugs on the hypercoagulable state. This study shows that the thrombin generation and plasma clot impedance tests are practical, rapid and useful tests for the detection and monitoring of the hypercoagulable state.
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PMID:Evaluation of the in vitro detection of the hypercoagulable state using the thrombin generation test and plasma clot impedance test. 50 79

In order to investigate some aspects of blood coagulation and of platelet function in cerebral ischemia, 18 healthy subjects, 24 patients with previous cerebral infarction and 12 patients with transient ischemic attacks were studied. All patients were in a non-active state of the illness. In all subjects, platelet count, prothrombin time, activated partial thromboplastin time and determination of the fibrinogen concentration were performed as routine. All subjects were tested for platelet adhesiveness, circulating platelet aggregates, factor VIII coagulant (VIII C), factor VIII-related von Willebrand factor (VII RWF), factor VIII-related antigen (VII RAg), antithrombin III (AT III) concentration and activity and euglobulin clot lysis time. No significant difference between patients and controls was found in routine tests, platelet function, AT III concentration or activity. Plasma levels of VIII C, VIII RWF, VIII RAg were significantly increased in both patient groups. The VIII RAg/VIII C ratio was significantly increased only in patients with previous cerebral infarction. Euglobulin clot lysis time was significantly increased in both patient groups.
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PMID:Evaluation of some coagulation parameters in cerebral ischemia. 685 12

The present study evaluates the hematochemical and hemorheologic effects of mesoglycan, a preparation of natural glycosaminoglycans, administered by the intramuscular route to patients with a recent episode of cerebral ischemia. A total of twenty patients (13 males and 7 females), between the ages of 45 and 75, under observation for a cerebral ischemic episode occurring at least 2 months prior to enrollment, were treated with intramuscular mesoglycan (30 mg, twice daily), for 15 days. Blood samples were taken prior to and at the end of treatment to measure the investigated parameters. Following mesoglycan treatment we observed a statistically significant decrease in fibrinogen plasma concentration, total cholesterol and triglycerides, while HDL cholesterol was found to increase. In addition, erythrocytes filterability improved at the end of treatment. No changes were observed in coagulation parameters such as prothrombin time, partial thromboplastin time, or antithrombin III. The results of the present study demonstrate that a 15-days treatment of intramuscular mesoglycan in patients recovering from a cerebral ischemic episode produces significant changes in fibrinogen and lipid plasma levels with no apparent anticoagulant effect.
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PMID:Mesoglycan in treatment of patients with cerebral ischemia: effects on hemorheologic and hematochemical parameters. 816 May 57

This study was designed to evaluate the clinical value of consecutive measurements of the levels of the anticoagulation factors protein C. protein S and antithrombin III in the plasma of patients with subarachnoid haemorrhage (SAH). Sequential samples of plasma were obtained from 34 patients at days 0 to 3, 5, 8, 14, and 20 days after SAH. Their levels of protein C, protein S and antithrombin III were measured by specific immuno-assays, and the symptomatic vasospasm and clinical states of the patients were monitored. Based on the retrospective comparisons between the measured levels of the three factors and the levels in pooled plasma from normal volunteers, the time course of changes in the levels allowed the classification of the patients into five groups as follows: A, the levels of the three factors decreased suddenly at 5 days after SAH, then increased again (n = 6); B, the three factors increased continuously (n = 13); C, the three factors remained below the normal range (n = 3); D, the three factors remained within the normal range (n = 6); and E, the three factors decreased continuously (n = 6). In group A patients, temporary deficiencies in the three factors occurred that coincided with the occurrence of delayed neurological deficit (DND). Twelve patients (92%) in group B had a favourable outcome (good and moderate disability) without DND. The patients in group C had low levels of anticoagulation factors and mild DND followed by a favourable outcome. Five patients (83%) in group D had a favourable outcome. In group E, five patients (83%) had a poor outcome (severe disability and death) due to DND. When clinical outcomes were compared by patient group, the patients in group E had significantly more unfavourable outcomes than did the other groups (P < 0.01). Although the mechanism responsible for the decrease in anticoagulation factor levels remained unclear, the results suggested that the decrease in anticoagulation factors may indicate hypercoagulability and cerebral ischaemia after SAH.
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PMID:Plasma levels of protein C, protein S, and antithrombin III in patients with subarachnoid haemorrhage. 908 71

A possible association between anticardiolipin antibodies (ACA), which are a marker for increased risk of cerebral ischemia, and deficiency of free Protein S, a naturally occurring anticoagulant, has been suspected in some studies of ischemic stroke, particularly in young adults. In order to investigate this further, we prospectively studied all stroke patients </= 65 years of age admitted to our stroke unit during 1991-1992. A total of 66 patients with acute ischemic stroke or transient ischemic attacks (TIA) (embolic/thrombotic infarction n = 30, embolic infarction n = 13, thrombotic infarction n = 10, and TIA n = 13) were analysed for ACA, protein C and S, free protein S and antithrombin III (AT III). Traditional risk factors were scrutinized in each patient. Eight patients had some previously undetected derangement of the coagulation process; five had elevated ACA levels, four had low, free Protein S levels, and three had low AT III levels. None of the patients showed any decrease in total protein C or S levels. A striking association between the presence of ACA and free protein S deficiency was noted. All patients with free protein S deficiency had concomitant elevated ACA levels. Sixteen patients had had a previous episode of ischemic stroke/TIA or mycocardial infarction, two of them had lowered AT III levels. Thirty-four patients had one or more elevated infectious parameters but with no clear correlation to derangement of the coagulation factors. We conclude that a probable association between ACA and free protein S deficiency exist in ischemic stroke patients, and that it may have a pathogenetic importance. Copyright 1998 Lippincott Williams & Wilkins
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PMID:Association between deficiency of free protein S and anticardiolipin antibodies in patients </= 65 years of age with acute ischemic stroke and TIA. 1021 Aug 79

Protein C (PC), protein S (PS), and antithrombin III (AT-III) are vital thrombin antagonists in circulation. However, the prevalence of these natural inhibitors for cerebral ischemia is barely mentioned in the Chinese population. The prevalence of PC, PS, and AT-III deficiency in Chinese adults with cerebral ischemia is reported. The study subjects were free of antiphospholipid antibody syndrome or systemic lupus erythematosus. Cardiac, liver, and renal function were normal. An overall rate of thrombophilia was 27%. PS deficiency was the most common disorder, followed by PC with PS and PC deficiency. There was only one patient with AT-III deficiency. No gender was specific for thrombophilia. However, PS deficiency was predilected in young adults. A positive correlation between PC and AT-III was achieved in patients with a normal PC activity but not PC deficiency. There was no correlation between AT-III or PS. The odds ratios of PC and PS were 5.29 and 2.86, respectively. Accordingly, an inability for thrombin antagonization by the PC/PS axis may relate to the occurrence of cerebral ischemia in the Chinese population. AT-III seems to display a minor role only.
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PMID:The prevalence of protein C, protein S, and antithrombin III deficiency in non-APS/SLE Chinese adults with noncardiac cerebral ischemia. 1281 86

Vancomycin precipitates fibrinogen. The turbidity induced by this vancomycin-fibrinogen interaction is used to establish a simple standardized antigenic assay for plasmatic fibrinogen, the FIATA. 1 mM vancomycin or 2 mM chloramine-T inactivates 50% of fibrinogen in human plasma. In contrast to chloramine-T, vancomycin does not react in NaJ-based photometric assay for chloramines,vancomycin does not inactivate the singlet oxygen-sensible antithrombin III, and the vancomycin action against fibrinogen is not changed in spite of the presence of the 1O2 quenchers methionine or ascorbic acid. The FIATA is performed as follows: to 25 microL plasma 50 microL PBS are added and the absorbance (A) at 405 nm is read. Then 50 microL FIATA-reagent, consisting of 4.4 mM vancomycin in PBS, are added. After 2 minutes (RT) DeltaA is determined and standardized against a plasma pool of 100% of norm (2.8 g/L) fibrinogen. The FIATA is nearly linear up to a fibrinogen concentration of about 150% of norm (4.2 g/L), resulting in a DeltaA of about 600 mA. The lower detection limit is 4% of norm (0.1 g/L). The intra-assay and interessay CV values are < 4%. The normal range of FIATA is 100% +/-20% (x- +/- 1 SD). In = 321 or 344 unselected patient plasmas the FIATA (x- = 130%; SD = 52% or 43%) correlated with the functional fibrinogen assays a) modified Clauss-Method (x- = 4.1 g/L; SD =1.7 g/L) with r = 0.755 and b) FIFTA (x- = 124%; SD = 40%) with r = 0.813. The vancomycin/fibrinogen interaction (binding of about 16 molecules of vancomycin/molecule of fibrinogen) can be used to purify fibrinogen out of plasma. Vancomycin also clouds dysfunctional fibrinogen (fibrinogen in presence of EDTA or chloramine-T)or soluble fibrin. Vancomycin-reacted fibrinogen stimulates tissue type plasminogen activator (t-PA) up to about 20-fold. The experimental data are analyzed by a new significance test: the two foldYates-corrected chi-square comparison against the mean value ofthe control-collective, called the Chi2x - Test. The P < .05 significance barrier calculated with the Chi2x - Test is equivalent to that calculated with the Fisher's Exact Test. The FIATA might be considered an interesting screening test for inactive fibrinogen forms or soluble fibrin, as eg in disseminated intravascular coagulation. Fibrinogen precipitation by vancomycin within the blood vessel might explain why vancomycin has to be infused slowly (< 10 mg/min) to prevent nephrotoxicity. The FIATA is of such a simplicity that the determination of fibrinogen antigen in plasma can be performed anywhere--even outside a hospital--within seconds. Thus, the presented FIATA might contribute to extra hospital testing of patients for assessing their risk for myocardial or cerebral ischemia/infarction.
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PMID:The fibrinogen antigenic turbidimetric assay (FIATA): the X2x test--the corrected chi-square comparison against the control-mean. 1716 98

The complex picture of inflammation and coagulation alterations comes to life in acute stroke phases. Increasing evidence points to a strong interaction and extensive crosstalk between the inflammation and coagulation systems: the interest towards this relationship has increased since recent experimental research showed that the early administration of antithrombin III (ATIII) decreases the volume of ischemia in mice and might be neuroprotective, playing an antiinflammatory role.We aimed to establish the extent of the relationship among markers of inflammation (S100B and IL-18) and procoagulant and fibrinolytic markers (ATIII, thrombin-antithrombin III complex (TAT), Fibrin Degradation Products (FDP), D-dimer) in 13 comatose patients affected by focal cerebral ischemia.Plasma levels of TAT, D-dimer and FDP, IL18 and S100B were increased. IL-18 and S100B high serum levels in ischemic patients suggest an early activation of the inflammatory cascade in acute ischemic injury.The basic principles of the interaction between inflammatory and coagulation systems are revised, from the perspective that simultaneous modulation of both coagulation and inflammation, rather than specific therapies aimed at one of these systems could be more successful in stroke therapy.
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PMID:Thrombin antithrombin complex and IL-18 serum levels in stroke patients. 2157 33

Thrombin's role in the nervous system is not well understood. Under conditions of blood-brain barrier compromise (e.g., neurosurgery or stroke), thrombin can result in neuroapoptosis and the formation of glial scars. Despite this, preconditioning with thrombin has been found to be neuroprotective in models of cerebral ischemia and intracerebral hemorrhage. We investigated the effects of physiologically relevant concentrations of thrombin on cortical neurons using two culture-based assays. We examined thrombin's effect on neurites by quantitative analysis of fluorescently labeled neurons. To characterize thrombin's effects on neuron survival, we spectrophotometrically measured changes in enzymatic activity. Using receptor agonists and thrombin inhibitors, we separately examined the role of thrombin and its receptor in neuroprotection. We found that low concentrations of thrombin (1 nM) enhances neurite growth and branching, neuron viability, and protects against excitotoxic damage. In contrast, higher concentrations of thrombin (100 nM) are potentially detrimental to neuronal health as evidenced by inhibition of neurite growth. Lower concentrations of thrombin resulted in equivalent neuroprotection as the antifibrinolytic, aprotinin, and the direct thrombin inhibitor, argatroban. Interestingly, exogenous application of the species-specific thrombin inhibitor, antithrombin III, was detrimental to neuronal health; suggesting that some endogenous thrombin is necessary for optimal neuron health in our culture system. Activation of the thrombin receptor, protease-activated receptor-1 (PAR-1), via micromolar concentrations of the thrombin receptor agonist peptide, TRAP, did not adversely affect neuronal viability. An optimal concentration of thrombin exists to enhance neuronal health. Neurotoxic effects of thrombin do not involve activation of PAR receptors and thus separate pharmacologic manipulation of thrombin's receptor in the setting of direct thrombin inhibitors could be a potential neuroprotective strategy.
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PMID:Concentration-Dependent Dual Role of Thrombin in Protection of Cultured Rat Cortical Neurons. 2634 29