thromboxane-b2 and Ischemic-Attack--Transient

thromboxane-b2 has been researched along with Ischemic-Attack--Transient* in 30 studies

Trials

1 trial(s) available for thromboxane-b2 and Ischemic-Attack--Transient

ArticleYear
What is the lowest dose of aspirin for maximum suppression of in vivo thromboxane production after a transient ischemic attack or ischemic stroke?
    Cerebrovascular diseases (Basel, Switzerland), 2004, Volume: 17, Issue:4

    There is still worldwide disagreement about the optimal lowest dose of aspirin to be used in patients after a transient ischemic attack (TIA) or nondisabling stroke. We measured the urinary 11-dehydro-thromboxane-B(2) (uTXB(2)) excretion to compare the degree of suppression of in vivo platelet activation by various low doses of aspirin.. 60 patients were randomly allocated to treatment with either 30, 50, 75 or 325 mg of aspirin. All patients received a 413-mg loading dose of carbasalate calcium (equivalent to 325 mg of aspirin) on day 0. The study population was stratified into a subgroup with acute ischemic stroke (AIS; n = 20; onset of symptoms <48 h) and a subgroup with a recent TIA or minor stroke (TIA/mS; n = 40) with onset of symptoms beyond 30 days, but less than a year previously. Urine samples were collected on day 0, 1, 5, 11 and 28 in patients with AIS, and on day 0, 11 and 28 in the patients with a TIA/mS.. On day 28, mean uTXB(2) levels were 241, 130, 217 and 187 pmol/mmol creatinine in the four treatment groups (ANOVA, p = 0.43). In the AIS subgroup, uTXB(2) remained suppressed on days 5 and 11 in all except the patients with the lowest dose (mean uTXB(2) on days 5 and 11: 475 and 392 pmol/mmol creatinine; log-transformed ANOVA, p = 0.05).. In patients with a TIA or nondisabling stroke, a daily dose of 30 mg of aspirin provides sufficient suppression of thromboxane synthesis. No indication of a dose-effect relationship was found. However, whether such a low dose adequately suppresses thromboxane synthesis in patients with acute stroke is uncertain.

    Topics: Adult; Aged; Aspirin; Dose-Response Relationship, Drug; Double-Blind Method; Female; Humans; Ischemic Attack, Transient; Male; Middle Aged; Patient Compliance; Platelet Aggregation Inhibitors; Risk Factors; Stroke; Thromboxane B2; Thromboxanes; Treatment Outcome

2004

Other Studies

29 other study(ies) available for thromboxane-b2 and Ischemic-Attack--Transient

ArticleYear
Aging-Related Decline of Glutathione Peroxidase 3 and Risk of Cardiovascular Events in Patients With Atrial Fibrillation.
    Journal of the American Heart Association, 2016, 09-08, Volume: 5, Issue:9

    Experimental studies demonstrated that glutathione peroxidase 3 (GPx3), an antioxidant enzyme that catabolizes hydrogen peroxide, protects against thrombosis. Little is known about its role in cardiovascular disease.. A prospective cohort study was conducted in 909 atrial fibrillation patients. Serum activities of GPx3, superoxide dismutase (SOD), and catalase were measured at baseline to assess the risk of cardiovascular events during a mean follow-up of 43.4 months (3291 person-years). Serum Nox2 and urinary excretion of 11-deydro-thromboxane B2 were also measured. During follow-up 160 cardiovascular events occurred (4.9%/year). Significantly lower values of GPx3 (P<0.001) and SOD (P=0.037) were detected in patients with, compared to those without, cardiovascular events. A lower survival rate was observed in patients with GPx3 (P<0.001) and SOD (P=0.010) activities below the median, as compared to those above. In a fully adjusted Cox regression model, GPx3 was the only antioxidant enzyme predictor of cardiovascular events (hazard ratio 0.647, 95% confidence interval 0.524-0.798, P<0.001). GPx3 was inversely associated with urinary 11-dehydro-thromboxane B2 (B -0.337, P<0.001) and serum Nox2 (B: -0.423, P<0.001). GPx3 activity progressively decreased with decades of age (P<0.001), with a progressive reduction in people aged ≥70 years.. This study provides evidence that a low antioxidant status, as depicted by reduced levels of GPx3, increases the risk of cardiovascular events in patients with atrial fibrillation. The age-related decline of GPx3 may represent a mechanism for the enhanced cardiovascular risk in the elderly population.

    Topics: Aged; Aged, 80 and over; Aging; Atrial Fibrillation; Cardiovascular Diseases; Catalase; Cohort Studies; Female; Follow-Up Studies; Glutathione Peroxidase; Humans; Ischemic Attack, Transient; Male; Middle Aged; Myocardial Infarction; Myocardial Revascularization; NADPH Oxidase 2; Prognosis; Proportional Hazards Models; Prospective Studies; Stroke; Superoxide Dismutase; Thromboxane B2

2016
Chronic administration of ethyl docosahexaenoate decreases mortality and cerebral edema in ischemic gerbils.
    Life sciences, 2005, Nov-19, Volume: 78, Issue:1

    Dietary docosahexaenoic acid (DHA) intake can decrease the level of membrane arachidonic acid (AA), which is liberated during cerebral ischemia and implicated in the pathogenesis of brain damage. Therefore, in the present study, we investigated the effects of chronic ethyl docosahexaenoate (E-DHA) administration on mortality and cerebral edema induced by transient forebrain ischemia in gerbils. Male Mongolian gerbils were orally pretreated with either E-DHA (100, 150 mg/kg) or vehicle, once a day, for 4 weeks and were subjected to transient forebrain ischemia by bilateral common carotid occlusion for 30 min. The content of brain lipid AA at the termination of treatment, the survival ratio, change of regional cerebral blood flow (rCBF), brain free AA level, thromboxane B(2) (TXB(2)) production and cerebral edema formation following ischemia and reperfusion were evaluated. E-DHA (150 mg/kg) pretreatment significantly increased survival ratio, prevented post-ischemic hypoperfusion and attenuated cerebral edema after reperfusion compared with vehicle, which was well associated with the reduced levels of AA and TXB(2) in the E-DHA treated brain. These data suggest that the effects of E-DHA pretreatment on ischemic mortality and cerebral edema could be due to reduction of free AA liberation and accumulation, and its metabolite synthesis after ischemia and reperfusion by decreasing the content of membrane AA.

    Topics: Animals; Arachidonic Acid; Body Water; Brain; Brain Chemistry; Brain Edema; Cerebrovascular Circulation; Docosahexaenoic Acids; Fatty Acids; Gerbillinae; Ischemic Attack, Transient; Male; Survival Analysis; Thromboxane B2

2005
Effects of dl-3-n-butylphthalide on production of TXB2 and 6-keto-PGF1 alpha in rat brain during focal cerebral ischemia and reperfusion.
    Zhongguo yao li xue bao = Acta pharmacologica Sinica, 1997, Volume: 18, Issue:6

    To study the effects of dl-3-n-butylphthalide (NBP) on the changes of thromboxane B2 (TXB2) and 6-keto-PGF1 alpha (6-keto-PGF1 alpha) contents in hippocampus, striatum, and cerebral cortex of rats subjected to focal cerebral ischemia followed by reperfusion.. Focal cerebral ischemia was induced by inserting a nylon suture into intracranial segment of internal carotid artery from external carotid artery and blockade of the origin of middle cerebral artery. For reperfusion, the suture was pulled out to restore the blood flow to the ischemic brain. Determination of TXB2 and 6-keto-PGF1 alpha was performed by RIA method.. Reperfusion following focal cerebral ischemia resulted in increases in TXB2 at 5 min and 6-keto-PGF1 alpha at 30 min and a decrease in the ratio of epoprostenol (PGI2)/thromboxane A2 (TXA2) (6-keto-PGF1 alpha/TXB2) at 5 min in hippocampus, striatum, and cerebral cortex. NBP 10 mg.kg-1 reduced the content of TXB2 without decreasing effect on 6-keto-PGF1 alpha. NBP 20 mg.kg-1 reduced both TXB2 and 6-keto-PGF1 alpha in lesser extent than aspirin (Asp, 20 mg.kg-1). NBP 20 or 10 mg.kg-1 elevated the ratio of PGI2/TXA2 after reperfusion, but Asp 20 mg.kg-1 did not increase the ratio except in striatum at 5 min after reperfusion.. NBP increases the ratio of PGI2/TXA2 which may have beneficial effects on the impaired microcirculation in postischemic brain tissues.

    Topics: 6-Ketoprostaglandin F1 alpha; Animals; Aspirin; Benzofurans; Brain; Ischemic Attack, Transient; Neuroprotective Agents; Rats; Reperfusion Injury; Thromboxane B2

1997
Prevention of cerebrovasospasm following subarachnoid hemorrhage in rabbits by the platelet-activating factor antagonist, E5880.
    Journal of neurosurgery, 1996, Volume: 84, Issue:5

    Recently, an important role of platelet-activating factor (PAF), an inflammation mediator, has been demonstrated in the genesis of cerebral vasospasm following subarachnoid hemorrhage (SAH). In the current study, the authors examined whether intravenous administration of the novel PAF antagonist, E5880, can prevent vasospasm following SAH in rabbits. A vasospasm model was produced in three groups of rabbits using two subarachnoid injections of autologous arterial blood, followed by intravenous administration of distilled water (control), a low dose of E5880 (0.1 mg/kg in distilled water), or a high dose of E5880 (0.5 mg/kg in distilled water). Neurological deterioration was largely prevented in the rabbits that received E5880. Basilar artery constriction was also reduced by both doses of E5880. Histological examination at autopsy predominantly showed ischemic changes in the brain. Animals in each E5880-treated group exhibited ischemic changes less frequently than those in the control group. Plasma thromboxane B2 concentrations were reduced in rabbits treated with E5880. Platelet-activating factor was immunolocalized in the intima and media of the basilar artery in the control group. The PAF immunoreactivity demonstrated in the basilar artery was decreased in the E5880 groups in a dose-dependent manner. Thus, this study provides evidence that PAF may play a role in the pathogenesis of vasospasm after SAH and that intravenous administration of E5880 is a promising approach in preventing vasospasm.

    Topics: Animals; Female; Ischemic Attack, Transient; Piperidines; Pyridinium Compounds; Rabbits; Subarachnoid Hemorrhage; Thromboxane B2

1996
Delayed elevation of platelet activating factor in ischemic hippocampus.
    Brain research, 1995, Sep-11, Volume: 691, Issue:1-2

    We used in vivo microdialysis to define the chronological relationship between release of thromboxane and platelet activating factor (PAF) into the extracellular space of ischemic hippocampus. The thromboxane level peaked after 20 min of postischemic reperfusion, followed by a delayed PAF response 120 min later. We conclude that cerebral ischemia causes delayed elevation of PAF in the extracellular space, long after the immediate synthesis and release of thromboxane metabolites.

    Topics: Analysis of Variance; Animals; Hippocampus; Ischemic Attack, Transient; Male; Microdialysis; Pilot Projects; Platelet Activating Factor; Rats; Rats, Wistar; Reaction Time; Reperfusion; Thromboxane B2

1995
Effect of a novel thromboxane A2 receptor antagonist, S-1452, on postischemic brain injury in rats.
    Stroke, 1993, Volume: 24, Issue:12

    Arachidonate metabolites have been implicated in the development of cerebral injury after ischemia. Particular importance has been placed on the balance of thromboxane A2 and prostaglandin I2 because of its regulative activity on platelet functions and arterial tone. The purpose of the present study was to shed light on the role of thromboxane A2 in postischemic brain injury.. We evaluated the effects of S-1452, a novel thromboxane A2 receptor antagonist, on brain edema, infarct areas, and survival rate in rats with middle cerebral artery occlusion. A transient middle cerebral artery occlusion model was produced by inserting a piece of silicon-coated nylon thread into the internal carotid artery.. The ratio of plasma thromboxane B2 to 6-keto-prostaglandin F1 alpha significantly rose at 0 hour (P < .05), 1 hour (P < .01), 3 hours (P < .05), and 12 hours (P < .05) and then nearly returned to the normal level at 24 hours after reperfusion following 1-hour occlusion. Pretreatment with S-1452 (5, 10, or 50 mg/kg PO) significantly attenuated the increase in postischemic water content in the cerebral cortex perfused by the anterior cerebral artery and the cerebral cortex perfused by the middle cerebral artery in a dose-dependent manner but slightly attenuated it in the caudate putamen 24 hours after reperfusion following 1-hour occlusion. Pretreatment with S-1452 (10 mg/kg PO) also significantly decreased the areas of infarction in the front parts of the cerebrum. The survival rate of animals after 2 hours of occlusion tended to be improved by treatment with S-1452 (10 mg.kg-1.d-1 PO), although there was no statistical significance.. Our results suggest that thromboxane A2 is closely related to postischemic brain injury in the early phase of recirculation and that S-1452 may have a protective effect on postischemic brain injury.

    Topics: 6-Ketoprostaglandin F1 alpha; Animals; Body Water; Brain; Bridged Bicyclo Compounds; Cerebral Infarction; Fatty Acids, Monounsaturated; Ischemic Attack, Transient; Male; Rats; Rats, Wistar; Receptors, Thromboxane; Reperfusion Injury; Survival Analysis; Thromboxane A2; Thromboxane B2; Time Factors

1993
Increased thromboxane biosynthesis in patients with acute cerebral ischemia.
    Stroke, 1993, Volume: 24, Issue:2

    Clinical and experimental studies suggest that platelets have a major role in the pathogenesis of cerebral ischemia. However, ex vivo both platelet aggregation studies and measurements of platelet-derived products in patients with cerebral ischemia have shown inconsistent results. The present study was designed to resolve this inconsistency.. We have measured the urinary excretion of a thromboxane metabolite, 11-dehydro-thromboxane B2, by a previously validated radioimmunoassay technique in 51 patients with acute cerebral ischemia who had experienced either a transient ischemic attack (14 patients) or an ischemic stroke (37 patients) and in 20 control patients with nonvascular neurological disorders. The median time between the onset of symptoms and urine sampling was 24 hours (range, from 2 hours to 8 days).. The excretion rate of immunoreactive 11-dehydro-thromboxane B2 ranged between 39 and 478 pmol/mmol creatinine in patients with a transient ischemic attack and between 23 and 5,916 pmol/mmol creatinine in stroke patients, with 29% (p = 0.18) and 51% (p = 0.004) of the urine samples, respectively, exceeding the upper limit of the control samples (251 pmol/mmol creatinine [mean +/- 2 SD]) (p = 0.01). In stroke patients, metabolite excretion was not related to the type (cortical or "lacunar") or site of cerebral infarction. Low-dose aspirin (50 mg per day for 7 days) reduced the urinary excretion by approximately 85% in 11 consecutive stroke patients.. We conclude that 1) episodes of enhanced thromboxane biosynthesis are detected infrequently in patients with a transient ischemic attack, 2) aspirin-suppressible episodes of increased thromboxane formation can be detected during the early phase of acute ischemic stroke, and 3) this finding may provide a rationale for testing the efficacy and safety of this drug in this setting.

    Topics: Acute Disease; Aged; Aged, 80 and over; Blood Platelets; Brain Ischemia; Cerebrovascular Disorders; Female; Humans; Ischemic Attack, Transient; Male; Middle Aged; Prospective Studies; Thromboxane B2

1993
Microdialysis measurements of PGD2, TXB2 and 6-KETO-PGF1 alpha in rat CA1 hippocampus during transient cerebral ischemia.
    Prostaglandins, 1993, Volume: 45, Issue:2

    We measured hippocampal CA1 concentrations of PGD2, TxB2 and 6-keto-PGF1 alpha in 18 anesthetized rats with stereotaxically implanted microdialysis probes before, during and after 20 min of global cerebral ischemia. The insertion of the microdialysis probe did not appear to cause a continuous major disturbance of arachidonic acid (AA) metabolism because stable eicosanoid concentrations were obtained prior to ischemia. During reperfusion all three eicosanoids increased significantly reaching a peak after 30-60 min and then gradually declined to baseline levels over the next 2-3 h. The ratio of average peak concentrations for PGD2, TxB2 and 6-keto-PGF1 alpha were approximately 80:2:1, respectively. The results extend previous work by demonstrating the time course of eicosanoid release in a distinct brain region and confirm the role of PGD2 as the major PG metabolite in brain. We conclude that future studies employing microdialysis may be able to provide a more detailed understanding of the role of AA metabolites in ischemic brain.

    Topics: 6-Ketoprostaglandin F1 alpha; Animals; Arachidonic Acid; Dialysis; Hippocampus; Ischemic Attack, Transient; Kinetics; Male; Prostaglandin D2; Rats; Rats, Sprague-Dawley; Thromboxane B2

1993
Brain eicosanoid levels during temporary focal cerebral ischemia in rats: a microdialysis study.
    Journal of neurosurgical anesthesiology, 1993, Volume: 5, Issue:1

    After transient cerebral ischemia, the brain is vulnerable to additional injury via hypoperfusion deficits. Eicosanoids with vasoconstrictor properties, such as thromboxane A2 (TxA2), may worsen postischemic hypoperfusion. The effect of temporary middle cerebral artery occlusion (MCAo) on brain TxB2 (the stable metabolite of TxA2) was evaluated in isoflurane-anesthetized rats. Microdialysis probes were placed in the caudate nucleus and temporal cortex. Each rat underwent one of the following ischemic regimens: groups I, II, and III--MCAo was maintained for 60, 120, and 180 min, respectively, followed by 120 min of reperfusion; group IV--a sham group in which MCAo and reperfusion were simulated; group V--7 h of MCAo only. Dialysate was measured for TxB2 by radioimmunoassay. Brain levels of TxB2 did not deviate from baseline during MCAo (or in the sham group). In contrast, during reperfusion, there was a significant increase in TxB2 following 180 min of MCAo but not after 60 or 120 min or MCAo (p < 0.05). These data indicate that, in this model of cerebral ischemia, TxB2 does not increase during MCAo. However, following a threshold duration of MCAo (180 min), the vasoconstrictor TxB2 may modulate postischemic hypoperfusion. These findings may have implications in the pharmacologic treatment of postischemic hypoperfusion and reperfusion brain injury.

    Topics: Animals; Brain Chemistry; Dialysis; Ischemic Attack, Transient; Male; Rats; Rats, Inbred SHR; Thromboxane B2; Time Factors

1993
[The study of occurrence mechanism in acute and chronic cerebral vasospasm].
    Zhonghua shen jing jing shen ke za zhi = Chinese journal of neurology and psychiatry, 1992, Volume: 25, Issue:6

    Using radioimmunoassay, fluorescence and transmittal++ electronmicroscopy, we studied the of prostaglandin(PG), lipid peroxidation(LPO) and ultrastructure. Fresh arterial blood (imaging acute spasm) produced basilar arterial spasm strongly(+ + +) and vacuole deterioration in vascular walls but there were no changes in 6-keto-PGF1 alpha and TXB2 and PGE2 and LPO. Incubated arterial blood (imaging chronic spasm) produced basilar arterial spasm markedly (+ + +) also. Vacuole deterioration in vascular walls either, and decreased the level of 6-keto-PGF1 alpha apparently (P < 0.01) and elevated the content of LPO significantly (P < 0.01) and there were no changes in the level of TXB2 and PGE alpha. This experiment suggests that the mechanism of acute spasm and chronic spasm is different.

    Topics: 6-Ketoprostaglandin F1 alpha; Animals; Basilar Artery; Female; Ischemic Attack, Transient; Lipid Peroxides; Male; Rabbits; Subarachnoid Hemorrhage; Thromboxane B2

1992
Effects of ischemia/reperfusion on brain tissue prostanoids and leukotrienes in newborn pigs.
    Prostaglandins, 1991, Volume: 42, Issue:6

    We investigated the hypothesis that cerebral prostanoid and peptidoleukotriene (LTs) (LTC4/D4/E4/F4) synthesis are increased during postischemic reperfusion of newborn pig brains. Prostanoids and LTs extracted from brain tissue were determined by RIA in sham-control piglets and at 1h, 3h, or 12h after a 20-min period of total cerebral ischemia. During reperfusion following ischemia, all regional brain tissue (cerebrum, brain stem and cerebellum) prostanoids (6-keto-PGF1 alpha, TXB2, PGE2 and PGF2 alpha) were increased at 1h compared with those in sham-control piglets. Only cerebral and brain stem 6-keto-PGF1 alpha and cerebral TXB2 remained elevated at 3h postischemia and all prostanoids returned to control levels by 12h postischemia. Brain tissue LTs were lower than prostanoids and were not altered 1, 3, or 12h following ischemia. These data indicate that 1) newborn pig brain tissue prostanoids are increased initially, and then returned to control levels at later stages of reperfusion following ischemia; 2) LTs are present in newborn pig brain tissue, but are not increased by ischemia/reperfusion injury and therefore probably do not play a significant role in cerebral ischemia-reperfusion injury.

    Topics: 6-Ketoprostaglandin F1 alpha; Animals; Animals, Newborn; Brain; Brain Stem; Cerebellum; Dinoprost; Dinoprostone; Female; Ischemic Attack, Transient; Leukotriene E4; Male; Prostaglandins; Reperfusion; SRS-A; Swine; Thromboxane B2

1991
Changes of plasma thromboxane level in subarachnoid haemorrhage. A study with 11-dehydro-TXB2 as measuring index.
    Acta neurochirurgica, 1991, Volume: 113, Issue:3-4

    Changes of plasma thromboxane level in subarachnoid haemorrhage (SAH) were studied clinically and experimentally using 11-dehydro-thromboxane B2 (11 DTX) as a measuring index. 11 DTX is a major long-lived metabolite formed from thromboxane (TX) B2, and is said to be a more reliable parameter for detecting TXA2 production in biological systems. In this clinical study, blood was sampled from the cubital vein of 10 SAH patients on the earliest possible day (day 0 or 1), during the vasospasm predilection period (day 7 approximately 11) and in the chronic stage (day 16 approximately 32). Plasma concentrations of 11 DTX and 6-keto-PGF 1 alpha were measured in clinical cases. A canine SAH model was produced by the two haemorrhage methods and blood was sampled from the superior sagittal sinus before and on day 4 of the first cisternal blood injection. 11 DTX, TXB2 and platelet function were examined in each sample. In the clinical studies, plasma 11 DTX levels tended to be higher in the early stage of SAH but decreased thereafter to the normal or lower level. Plasma concentrations of 6-keto-PGF1 alpha tended to decrease mildly during the vasospasm predilection period. In the experimental study, neither definite change of plasma 11 DTX level nor neurological deficit could be induced by the mimic SAH, while an increase in platelet aggregability and narrowing of the basilar artery were observed. 11 DTX was inferred to be a more reliable parameter of TX biosynthesis than TXB2.

    Topics: Adult; Aged; Animals; Disease Models, Animal; Dogs; Female; Humans; Ischemic Attack, Transient; Male; Middle Aged; Platelet Aggregation; Subarachnoid Hemorrhage; Thromboxane B2

1991
Role of platelet function in symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage.
    Stroke, 1991, Volume: 22, Issue:7

    To evaluate the role of platelet function in the pathogenesis of cerebral vasospasm, we compared sequential changes of platelet aggregability and beta-thromboglobulin and thromboxane B2 concentrations in blood samples from the internal jugular and peripheral vein of 13 patients with aneurysmal subarachnoid hemorrhage. Platelet function in blood from the internal jugular vein tended to be enhanced during days 0-1 but recovered to the normal range during days 2-4. After day 5, platelet function showed various patterns depending on the presence of symptomatic vasospasm. In patients without symptomatic vasospasm, sequential changes were relatively minor, with normal or slightly high values. Patients with symptomatic vasospasm already showed high platelet aggregability during the early stage of vasospasm. The concentration of beta-thromboglobulin increased several days after the onset of vasospasm, reaching 80 ng/ml or more in patients with a poor prognosis. Two of the five patients with symptomatic vasospasm showed markedly high concentrations of thromboxane B2 after day 8. These results suggest that vasospasm activates platelets and promotes aggregability and that the resulting increased tendency for thrombus formation may affect the patient's prognosis during the advanced stage.

    Topics: Adult; beta-Thromboglobulin; Blood Platelets; Humans; Intracranial Aneurysm; Ischemic Attack, Transient; Middle Aged; Osmolar Concentration; Platelet Aggregation; Subarachnoid Hemorrhage; Thromboxane B2; Veins

1991
Angiographic vasospasm and release of platelet thromboxane after subarachnoid hemorrhage.
    Stroke, 1991, Volume: 22, Issue:4

    We studied adenosine diphosphate-induced platelet aggregation and the associated release of thromboxane B2 in 49 patients with subarachnoid hemorrhage in relation to angiographic vasospasm. Postoperative cerebral angiography was performed less than or equal to 3 (median 1) days after surgery for an aneurysm 5-14 days after subarachnoid hemorrhage. Correspondingly, one sample from each patient was taken within 24 hours either before or after angiography. The occurrence of severe as well as diffuse, moderate, or severe angiographic vasospasm was associated with the presence of delayed cerebral ischemia (p less than 0.05). Patients with diffuse angiographic vasospasm had significantly higher (p less than 0.05) values for thromboxane B2 release than the others, even after adjustment by the clinical grades on admission and before surgery, the timing of surgery, the time from subarachnoid hemorrhage to angiography and blood sampling, and nimodipine therapy. Severe and diffuse angiographic vasospasm were also associated with poor outcome at 1 year (p less than 0.05). Our results suggest that augmented release of platelet thromboxane may be involved in the pathogenesis of vasospasm in large cerebral arteries.

    Topics: Adenosine Diphosphate; Adult; Blood Platelets; Cerebral Angiography; Female; Humans; Intracranial Aneurysm; Ischemic Attack, Transient; Male; Nimodipine; Platelet Aggregation; Subarachnoid Hemorrhage; Thromboxane B2; Tomography, X-Ray Computed

1991
Anti-lipid peroxidation and protection of ginsenosides against cerebral ischemia-reperfusion injuries in rats.
    Zhongguo yao li xue bao = Acta pharmacologica Sinica, 1990, Volume: 11, Issue:2

    The correlation between protective effect of ginsenosides Rb + R0 and brain endogenously-derived prostacyclin synthesis, thromboxane A2 formation and lipid peroxidation were estimated in rats. Ginsenosides Rb + R0 100 mg/kg iv 30 min before 4-vessel occlusion elevated 6-keto-PGF1 alpha level, declined thromboxane B2 and brain edema formation, reduced the rise of lipid peroxides and suppressed the reduction in both creatine phosphokinase (CK) and superoxide dismutase (SOD) activities in brain tissue after 40-min ischemia followed by 1-h reperfusion. Furthermore, these improvements were partially abolished by pretreating with iv indomethacin. It is concluded that ginsenosides possess protective effect on cerebral ischemia-reperfusion injury of rats and ginsenosides Rb + R0 are the active principles. The underlying mechanism of protection is ascribed partially or mainly to the facilitated synthesis and release of prostacyclin, reduced formation of thromboxane A2 and inhibited generation of free radicals and subsequent lipid peroxidation.

    Topics: 6-Ketoprostaglandin F1 alpha; Animals; Creatine Kinase; Female; Ginsenosides; Ischemic Attack, Transient; Lipid Peroxidation; Male; Malondialdehyde; Panax; Plants, Medicinal; Rats; Rats, Inbred Strains; Reperfusion Injury; Saponins; Superoxide Dismutase; Thromboxane B2

1990
Accumulation of arachidonic acid cyclo- and lipoxygenase products in rat brain during ischemia and reperfusion: effects of treatment with GM1-lactone.
    Journal of neurochemistry, 1989, Volume: 53, Issue:3

    The aim of our study was to investigate the changes of various biochemical parameters (concentrations of lactate, free arachidonate, cyclo- and lipoxygenase products) in rat brain after ischemia and reperfusion and the effects of pretreatment with the ganglioside derivative GM1-lactone on the same parameters. Ischemia was induced by reversible occlusion of common carotid arteries for 20 min, which included a final 5 min of respiration of 5% oxygen in nitrogen. Reperfusion was obtained by removing the occlusion. Pre-ischemic conditions were obtained on sham-operated animals. Animals were killed by microwave irradiation of their heads. Brain levels of lactate and of free arachidonate were markedly increased after ischemia and returned to normal values at 5 min of reperfusion. Levels of the cyclooxygenase metabolites prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, and thromboxane B2 were increased after ischemia, whereas levels of the lipoxygenase metabolite leukotriene C4 (LTC4) did not change. After reperfusion, a very marked increase of the cyclooxygenase products occurred but not of LTC4. Treatment with GM1-lactone prevented the elevation of cyclo- and lipoxygenase metabolites especially during reperfusion, with limited effects on lactate and free arachidonate levels.

    Topics: 6-Ketoprostaglandin F1 alpha; Animals; Arachidonic Acid; Arachidonic Acids; Brain; Dinoprost; G(M1) Ganglioside; Ischemic Attack, Transient; Lactates; Lactic Acid; Lipoxygenase; Male; Prostaglandin-Endoperoxide Synthases; Rats; Rats, Inbred Strains; SRS-A; Thromboxane B2

1989
Microvascular spasm is mediated by vasopressin fibers in the rat hippocampal slice.
    Brain research, 1989, Apr-03, Volume: 483, Issue:2

    Microvessels in the rat hippocampal slice can be used as an in vitro model for the study of cerebral vasospasm. Serum from coagulated blood causes prompt and long-lasting microvascular constriction that is neurogenic in nature. Here we show that a candidate spasmogen, thromboxane B2, has excitatory action on neural elements in the slice. However, spasmogenic serum lacks this excitatory effect. Instead, it is inhibitory for a major population of slice neurons. Thus, neurogenic microvascular spasm is produced by a subpopulation of slice neurons or projection fibers, not all neurons acting in concert. Arginine vasopressin (AVP) is contained in fibers that project to the hippocampus, and hippocampal microvessels contain pressor (V1) receptors for the peptide. AVP causes vasoconstriction in the slice, and a specific V1 antagonist for the peptide blocks the microvascular spasm induced by blood serum. The results are interpreted to mean that neurogenic microvascular spasm is mediated by locally released AVP.

    Topics: Animals; Arginine Vasopressin; Cerebrovascular Circulation; Hippocampus; In Vitro Techniques; Ischemic Attack, Transient; Rats; Thromboxane B2

1989
Prevention of chronic cerebral vasospasm in dogs with ibuprofen and high-dose methylprednisolone.
    Stroke, 1989, Volume: 20, Issue:8

    Severe chronic cerebral vasospasm was produced in dog basilar arteries by two injections, 2 days apart, of autologous blood into the cisterna magna of 25 dogs. Treatment with ibuprofen (n = 8) or high-dose methylprednisolone (n = 8) after the first injection of blood prevented or reduced angiographic vasospasm. Cerebrospinal fluid concentrations of prostaglandin E2, prostaglandin F2 alpha, 6-ketoprostaglandin F1 alpha (a metabolite of prostacyclin), and thromboxane B2 (a metabolite of thromboxane A2) were measured in both treated and untreated (n = 7) dogs. In untreated dogs, the level of prostaglandin E2 increased 94-fold by Day 8 after the first injection of blood and was strongly and positively correlated with the degree of angiographic vasospasm. Treatment with ibuprofen and high-dose methylprednisolone prevented or significantly reduced this increase in prostaglandin E2 concentration. Smaller increases in cerebrospinal fluid concentrations of thromboxane B2 and 6-ketoprostaglandin F1 alpha occurred after experimental subarachnoid hemorrhage; the magnitude of these increases was also reduced by ibuprofen or high-dose methylprednisolone treatment. In contrast, prostaglandin F2 alpha levels were not significantly altered during the study. These data show that enhanced prostaglandin E2 synthesis occurs during experimental subarachnoid hemorrhage, and the by-products generated in its synthesis may play a role in the pathogenesis of cerebral vasospasm.

    Topics: 6-Ketoprostaglandin F1 alpha; Animals; Dinoprost; Dinoprostone; Dogs; Ibuprofen; Ischemic Attack, Transient; Methylprednisolone; Subarachnoid Hemorrhage; Thromboxane B2

1989
Thromboxane synthetase inhibition with imidazole increases blood flow in ischemic penumbra.
    Neurosurgery, 1988, Volume: 22, Issue:2

    Previous studies have indicated that the regional distribution of the arachidonic acid metabolites around a focal ischemic lesion may be important in the pathogenesis of cerebral ischemia. To determine the functional significance of this regionalization, we examined the effect of imidazole (a thromboxane synthetase inhibitor) on the distribution of the vasoconstrictor thromboxane and the vasodilators prostacyclin and prostaglandin E2 (PGE2) and on the distribution of cerebral blood flow (CBF) around a focal ischemic lesion, middle cerebral artery (MCA) occlusion in the cat. The study was conducted in two phases. The first phase examined regional distribution of tissue arachidonic acid metabolites and the effect of imidazole treatment on that distribution. The second phase examined the effect of imidazole treatment on the distribution of blood flow about the focal ischemic lesion as well as on electrocortical function and edema production. MCA occlusion resulted in increased thromboxane, prostacyclin, and PGE2 levels in the ipsilateral hemisphere. These increases were greatest in the region of marginal ischemia and were present both 3 and 6 hours after occlusion. Imidazole pretreatment (50 mg/kg i.p.) significantly inhibited thromboxane production, but augmented production of prostacyclin and PGE2. In the blood flow studies, imidazole was without effect on regions of dense cerebral ischemia (CBF less than 20 ml/minute/100 g for more than 12 of 24 postocclusion hours). In regions of marginal ischemia (20 less than CBF less than 30 ml/minute/100 g for more than 12 of 24 postocclusion hours), imidazole pretreatment significantly increased blood flow in both gray and white matter compared with saline-treated controls.(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: 6-Ketoprostaglandin F1 alpha; Animals; Brain; Brain Edema; Cats; Cerebrovascular Circulation; Dinoprostone; Evoked Potentials, Somatosensory; Imidazoles; Ischemic Attack, Transient; Prostaglandins E; Thromboxane B2; Thromboxane-A Synthase

1988
Association of transient ischaemic attack in alcohol withdrawal with changes in haemostasis.
    British journal of addiction, 1988, Volume: 83, Issue:12

    Topics: Alcohol Withdrawal Delirium; Alcoholism; Humans; Ischemic Attack, Transient; Male; Middle Aged; Platelet Aggregation; Psychoses, Alcoholic; Thromboxane B2

1988
Effects of vasospasm on levels of prostacyclin and thromboxane A2 in cerebral arteries of the monkey.
    Neurosurgery, 1988, Volume: 22, Issue:1 Pt 1

    To determine whether cerebral arteries in spasm have an altered capacity to synthesize the vasoactive substances prostacyclin and thromboxane A2, we measured levels of these arachidonic acid metabolites using a primate model of vasospasm. Twenty-four cynomolgus monkeys were assigned at random to one of three groups designated sham, clot, or clot-removal. All animals underwent base line cerebral angiography and bilateral dissection of the major cerebral arteries from the arachnoid. The clot and clot-removal groups had autologous hematomas placed around the vessels to simulate subarachnoid hemorrhages. The sham group had a similar volume of saline instilled into the subarachnoid space. Twenty-four hours later, the clot-removal group underwent a second craniotomy to remove the hematomas. Seven days after the initial operation, angiography was repeated on all animals. The animals were then killed, and the cerebral arteries were removed. Basal levels of prostacyclin and thromboxane in the cerebral vessels were measured after incubation in vitro by radioimmunoassay. No detectable leukotriene C4 release by these arteries was measurable using radioimmunoassay. Angiography revealed severe cerebral vasospasm in the clot group, but not in the clot-removal or sham groups. There were no statistical differences among the groups in thromboxane release, but prostacyclin levels were significantly lower in the clot group than in the clot-removal group (P less than 0.05). It thus seems that, if an imbalance in constrictor and dilator eicosanoids occurs in association with vasospasm, this is more likely to arise from a relative lack of the vasodilator component prostacyclin than from a surplus of the vasoconstrictor thromboxane.(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: 6-Ketoprostaglandin F1 alpha; Animals; Cerebral Angiography; Cerebral Arteries; Epoprostenol; Female; Ischemic Attack, Transient; Macaca fascicularis; Osmolar Concentration; Radioimmunoassay; Thromboxane A2; Thromboxane B2

1988
Inhibitory effect of acetylsalicylic acid on platelet function in patients with completed stroke or reversible ischemic neurologic deficit.
    Stroke, 1988, Volume: 19, Issue:5

    The purpose of our study was to investigate the effects of different doses of acetylsalicylic acid on platelet aggregation. Among inpatients of the National Taiwan University Hospital, 236 cases of completed stroke and seven cases of reversible ischemic neurologic deficit that were diagnosed by computed tomography of the brain and that had not ingested acetylsalicylic acid or acetylsalicylic acidlike drugs for greater than 2 weeks before admission were selected for this study. Thromboxane B2 and 6-keto-PGF1 alpha were measured by radioimmunoassay, threshold concentration of adenosine diphosphate was measured by Born's method, and circulating platelet aggregates were measured by the method of Wu and Hoak. Various single doses of acetylsalicylic acid (75, 300, or 600 mg) or 300 mg acetylsalicylic acid every 6 hours for four doses or one dose of 300 mg acetylsalicylic acid with 75 mg dipyridamole significantly suppressed the mean plasma thromboxane B2 concentrations and elevated the mean adenosine diphosphate threshold concentrations. Abnormal plasma thromboxane B2 concentrations, adenosine diphosphate threshold concentrations, or circulating platelet aggregate ratios were significantly normalized after administration of these regimens. The effects were not significantly different among treatment groups. Forty milligrams of acetylsalicylic acid seemed to have less platelet-inhibitory effect. A single dose of 75 mg acetylsalicylic acid significantly inhibited platelet hyperfunction and effectively corrected the abnormal plasma thromboxane B2 concentrations, adenosine diphosphate threshold concentrations, and circulating platelet aggregate ratios. Higher doses did not enhance the inhibitory effect. In addition, this single dose of acetylsalicylic acid did not significantly suppress plasma 6-keto-PGF1 alpha. We conclude that 75 mg acetylsalicylic acid per day is adequate to inhibit platelet hyperfunction.

    Topics: Adenosine Diphosphate; Aged; Aged, 80 and over; Aspirin; Blood Platelets; Cerebrovascular Disorders; Female; Humans; Ischemic Attack, Transient; Male; Middle Aged; Platelet Aggregation; Thromboxane B2

1988
Role of arachidonate metabolites in the genesis of cerebral vasospasm.
    Advances in prostaglandin, thromboxane, and leukotriene research, 1987, Volume: 17B

    Topics: 6-Ketoprostaglandin F1 alpha; Arachidonic Acid; Arachidonic Acids; Humans; Ischemic Attack, Transient; Prostaglandin D2; Prostaglandins D; SRS-A; Subarachnoid Hemorrhage; Thromboxane B2

1987
Arachidonic acid metabolism following aneurysm rupture. Evaluation of cerebrospinal fluid and serum concentration of 6-keto-prostaglandin F1 alpha and thromboxane B2 in patients with subarachnoid hemorrhage.
    Surgical neurology, 1987, Volume: 27, Issue:3

    Experimental investigations have suggested an important role of arachidonic acid metabolites in the genesis of cerebral vasospasm following subarachnoid hemorrhage. In this clinical study the cerebrospinal fluid (CSF) and serum levels of the two main arachidonic acid metabolites prostacyclin and thromboxane A2 are evaluated by measuring their stable degradation products 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2) using radioimmunoassay methods during the pre- and postoperative course in patients after aneurysm rupture. Although the serum levels of both substances do not seem to be important for the clinical course of the patients, the CSF concentrations of 6-keto-PGF1 alpha and TXB2 provide important data. A close correlation between the initial TXB2 level of the individual patient and the amount of blood in the basal cisterns as detected by computed tomography scan can be demonstrated. The predictive value of this additional information for the occurrence of cerebral angiospasm is discussed. Comparing the CSF levels of both metabolites the slight preoperative elevation of 6-keto-PGF1 alpha is significantly surmounted by an extraordinary rise in TXB2 concentration. Postoperatively, after cleavage of the basal cisterns there is a decline in the CSF levels of both substances. The pre- and postoperative clinical course in comparison to the CSF levels of 6-keto-PGF1 alpha and TXB2 is demonstrated in four patients. A nearly normal course of TXB2 and 6-keto-PGF1 alpha seems to be associated with an uneventful clinical course, whereas a high TXB2 level--whether occurring preoperatively or, even more important, as a secondary postoperative rise--seems to be associated with ischemic complications and neurological deterioration. It is suggested that pre- and postoperative monitoring of CSF levels of 6-keto-PGF1 alpha and especially TXB2 may serve as a possible indicator for the detection of patients at risk of developing cerebral vasospasm.

    Topics: 6-Ketoprostaglandin F1 alpha; Adult; Arachidonic Acids; Female; Humans; Intracranial Aneurysm; Ischemic Attack, Transient; Male; Middle Aged; Risk; Rupture, Spontaneous; Subarachnoid Hemorrhage; Thromboxane B2

1987
[Sequential measurements of TxB2 and 6-keto PGF1 alpha in cerebrospinal fluid and serum in patients with subarachnoid hemorrhage].
    Neurologia medico-chirurgica, 1986, Volume: 26, Issue:4

    Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Female; Humans; Ischemic Attack, Transient; Male; Middle Aged; Subarachnoid Hemorrhage; Thromboxane B2

1986
[Arachidonic acid metabolism following aneurysm rupture].
    European archives of psychiatry and neurological sciences, 1986, Volume: 236, Issue:2

    Imbalance between the two arachidonic acid metabolites, prostacyclin (PGI2) and thromboxane A2 (TXA2), is thought to be at least in part responsible for the development of cerebral vasospasm following aneurysm rupture. In 12 patients with subarachnoid hemorrhage the pre- and postoperative serum and CSF levels of PGI2 and TXA2 were measured as a function of their stable hydrolysis products, 6-Keto-PGF1 alpha (PGI2) and thromboxane B2 (TXA2), with a highly specific radioimmunoassay. Serum levels of both metabolites were elevated in half of the patients, but no correlation to the clinical course could be found. However, TXB2 concentration in the CSF was significantly increased preoperatively with close correlation to the amount of intracisternal blood, as detected by CT scan. Furthermore, it could be demonstrated that the postoperative course of the TXB2 concentrations in the CSF reflects the clinical course in such a way that a characteristic secondary rise of TXB2, concentration postoperatively is closely related to the occurrence of cerebral vasospasm and clinical deterioration. The conclusion is drawn that measurement of arachidonic acid metabolites in the CSF may provide important information concerning the pathophysiological events following subarachnoid hemorrhage, especially with regard to incipient cerebral vasospasm.

    Topics: 6-Ketoprostaglandin F1 alpha; Adult; Arachidonic Acid; Arachidonic Acids; Blood-Brain Barrier; Carotid Artery Diseases; Carotid Artery, Internal; Epoprostenol; Female; Humans; Intracranial Aneurysm; Ischemic Attack, Transient; Male; Middle Aged; Rupture, Spontaneous; Subarachnoid Hemorrhage; Thromboxane A2; Thromboxane B2

1986
Beneficial effect of OKY-046, a selective thromboxane A2 synthetase inhibitor, on experimental cerebral vasospasm.
    Japanese journal of pharmacology, 1986, Volume: 41, Issue:3

    Effects of OKY-046, a selective inhibitor of thromboxane (TX)A2 synthetase and a platelet aggregation inhibitor, on in vitro and in vivo models of cerebral vasospasm were studied. The contraction of the isolated rabbit basilar artery by an exposure to 1.0 ml of whole rabbit blood plus 0.05 or 0.1 units/ml of thrombin was diminished by the treatment with 10(-4) M of OKY-046 and/or 10(-6) M of cinanserin. When the whole blood of rabbits treated intravenously with 1 mg/kg/min of OKY-046 was used, the contraction of the basilar artery was decreased to about half of the control contraction. Angiographically recognized cerebral vasospasm in vivo, by a transorbital injection of 5.0 to 7.0 ml of autologous arterial blood into the cisterna magna of dogs, was suppressed by 0.05 and 0.5 microgram of OKY-046. Moreover, the decrease in the regional cerebral blood flow in autologous blood infused-dogs was inhibited by 0.5 microgram of OKY-046. The increase in TXB2 in the cerebrospinal fluid of dogs was significantly inhibited, and the level of 6-keto-PGF1 alpha was slightly increased by the treatment of OKY-046. The ratio of 6-keto-PGF1 alpha/TXB2 was increased from 1.5 to 5.2 in OKY-046-treated dogs. No effect on the basal tone and response to vasoactive agonists such as norepinephrine, KCl and PGE1 was observed in the isolated spiral thoracic aorta of guinea pigs or rabbits. Taken together with our previous findings, we conclude that the inhibition of cerebral vasospasm in the in vitro and in vivo models by the treatment of OKY-046 might be due to an inhibition of platelet aggregation, an inhibition of TXA2 generation and an increase in the ratio of PGl2/TXA2.

    Topics: 6-Ketoprostaglandin F1 alpha; Acrylates; Animals; Aorta; Basilar Artery; Brain; In Vitro Techniques; Ischemic Attack, Transient; Methacrylates; Rabbits; Regional Blood Flow; Thromboxane B2

1986
Radioimmunoassay of thromboxane B2 in the prevention and treatment of the ischemic cerebrovascular diseases.
    Acta neurologica, 1986, Volume: 8, Issue:6

    Topics: Adult; Aged; Cerebral Infarction; Humans; Ischemic Attack, Transient; Male; Middle Aged; Thromboxane B2

1986
[Thromboxane in rat brain following incomplete ischemia].
    Harefuah, 1982, Nov-15, Volume: 103, Issue:10

    Topics: Animals; Cerebral Cortex; Electroencephalography; Indomethacin; Ischemic Attack, Transient; Prostaglandins; Rats; Thromboxane B2; Thromboxanes

1982
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