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Cisternal and lumbar CSF concentration of arachidonate metabolites in vasospasm following subarachnoid hemorrhage from ruptured aneurysm: biochemical and clinical considerations.

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Two representative cases of subarachnoid hemorrhage in which prostaglandin D2 (PGD2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), stable metabolite of prostacyclin (PGI2), were monitored with serial lumbar punctures and detected in cisternal CSF during operations for aneurysm, are

Gastric bleeding and increased gastric vascular permeability induced by platelet activating factor (PAF): effect of drugs that affect arachidonate metabolism.

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The injurious effect of platelet activating factor (PAF) on gastric mucosa was studied by measuring bleeding in the acid perfused stomach of anesthetized rats. The effect of PAF on gastric mucosal vascular permeability (GMVP) was assessed by dye-leakage in the saline perfused stomach of anesthetized

Arachidonate metabolites and vasospasm after subarachnoid haemorrhage.

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A wide literature exists about the pathogenesis of cerebral arterial spasm following subarachnoid haemorrhage: several compounds have been identified in human cerebrospinal fluid as possible vasoactive agents involved in the biochemical mechanism of vasospasm onset. Many experimental evidences exist

Cisternal and lumbar CSF levels of arachidonate metabolites after subarachnoid haemorrhage: an assessment of the biochemical hypothesis of vasospasm.

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Several naturally occurring compounds have been identified in human cerebrospinal fluid (CSF) after subarachnoid haemorrhage (SAH) as possible vasoactive agents involved in the biochemical mechanism of vasospasm. The authors have measured, in 30 patients admitted for SAH, CSF concentrations of two

[Effects of the subarachnoid hemorrhage on the release of arachidonate metabolites from canine cerebral arteries].

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Release of arachidonate metabolites from isolated canine cerebral arteries into perfusing medium were estimated using radioimmunoassay (RIA) in vitro. The cerebral arteries were isolated from dogs sustained experimental subarachnoid hemorrhages (SAH) and the results were compared with that of normal

Activation of the arachidonate 5-lipoxygenase pathway in the canine basilar artery after experimental subarachnoidal hemorrhage.

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Severe cerebral vasospasm as confirmed by angiography was induced in dogs by injection of autologous blood into the cisterna magna, and the resultant leukotriene formation in the isolated basilar artery was examined. When stimulated with calcium ionophore (A 23187), the arteries of the treated

Bleeding disorder associated with albumin-dependent partial deficiency in platelet thromboxane production. Effect of albumin on arachidonate metabolism in platelets.

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The authors describe a patient with a longstanding bleeding disorder associated with impaired platelet aggregation and secretion despite normal granule contents. Thrombin-induced platelet thromboxane A2 production, measured using a radioimmunoassay for thromboxane B2, was markedly decreased or

Role of the arachidonate cascade in the pathogenetic mechanism of cerebral vasospasm following subarachnoid hemorrhage.

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Familial and constitutional bleeding disorder due to platelet cyclo-oxygenase deficiency.

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Three family members from two successive generations had a bleeding tendency. Their template bleeding time was prolonged and platelet aggregation induced by ADP and adrenaline showed no second wave; collagen at low to moderate concentrations failed to aggregate and release ATP, whereas higher

[Antiplatelet therapy can unmask an inherited bleeding disorder. Aspirin-like defect of platelets does not protect against atherosclerosis].

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Some inherited platelet disorders may be revealed late, as in the presented case of a 68-year-old-man. Recurrent epistaxis following peri-interventional antiplatelet therapy (after three elective percutaneous coronary interventions) and an episode of upper gastrointestinal haemorrhage required

Abnormal platelet function and arachidonate metabolism in chronic idiopathic thrombocytopenic purpura.

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We observed several patients with chronic idiopathic thrombocytopenic purpura (ITP) whose bleeding times were more prolonged than would have been expected from their platelet counts. To investigate this further, we performed in vivo and in vitro platelet function studies, assessed arachidonate

Valproate treatment and platelet function: the role of arachidonate metabolites.

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OBJECTIVE Valproate (VPA) is an extensively used drug in the therapy of epilepsies. One of the most frequently reported side effects of VPA is hemorrhagic diathesis. Some authors emphasized the decreased platelet count as the basis of VPA-induced hemorrhagic diathesis, but some reports suggested

Familial bleeding disorder associated with deficiencies in platelet signal processing and glycoproteins.

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Aggregation responses to low concentrations of ADP, epinephrine, collagen and cationophore A23187 in platelets from two family members with marked bleeding tendencies were virtually absent, whereas shape change with ADP was normal. The contribution to factor X activation by collagen-treated

The release of radioactive arachidonate from lipids of red blood cells during prolonged incubations in vitro.

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Red blood cells were isolated from rat blood and incubated in the presence of [3H]arachidonate. A sizeable quantity (18%) of the radioactivity was incorporated into red cell lipids, of which phosphatidylcholine was the most highly labelled. Radioactive arachidonate was found at position 2 of this

Bimoclomol protects against vascular consequences of experimental subarachnoid hemorrhage in rats.

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Bimoclomol (BRLP-42) is a novel antiischemic compound acting against peripheral vascular complications of diabetes mellitus (neuropathy, retinopathy, and nephropathy). In the present study the activity of bimoclomol was tested in experimental subarachnoid hemorrhage (SAH) and arachidonic acid

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