5-hydroxy-6-8-11-14-eicosatetraenoic-acid and Ischemic-Attack--Transient
5-hydroxy-6-8-11-14-eicosatetraenoic-acid has been researched along with Ischemic-Attack--Transient* in 3 studies
Other Studies
3 other study(ies) available for 5-hydroxy-6-8-11-14-eicosatetraenoic-acid and Ischemic-Attack--Transient
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Ebselen (DR3305) ameliorates delayed cerebral vasospasm in a canine two-hemorrhage model.
Ebselen, a seleno-organic compound which inhibits arachidonic acid lipoxygenase activity and exerts glutathione peroxidase-like activity, ameliorated delayed cerebral vasospasm in a canine two-hemorrhage model. Twenty-five dogs were exposed to subarachnoid hemorrhage and divided into two groups. In the Ebselen-treated group (6 dogs), 50 mg kg-1 of Ebselen was administered twice a day, for 7 days. The other 19 dogs without administration of Ebselen were used as a control group. In the Ebselen-treated group, the basilar artery on Day 7 after subarachnoid hemorrhage was constricted to 68.1 +/- 6.4% (mean +/- SD, n = 6) of the angiographic diameter on Day 0, before subarachnoid hemorrhage. This percentage was significantly larger than the 41.3 +/- 4.6% (n = 19) in the control group. The basilar artery segment obtained on Day 7 in the Ebselen-treated group produced 3.32 +/- 1.82 nmol of 5-hydroxyeicosatetraenoic acid/mg protein/5 minutes (n = 5), significantly less than the 6.73 +/- 0.95 (n = 3) produced by the artery in the control group. Thus, administration of Ebselen suppressed arachidonate 5-lipoxygenase activation and had a beneficial effect on angiographically detected delayed vasospasm. Topics: Animals; Arachidonate 5-Lipoxygenase; Azoles; Basilar Artery; Dogs; Hydroxyeicosatetraenoic Acids; Ischemic Attack, Transient; Isoindoles; Organoselenium Compounds; Subarachnoid Hemorrhage; Time Factors; Vasoconstriction | 1997 |
Participation of lipoxygenase products from arachidonic acid in the pathogenesis of cerebral vasospasm.
To examine the possible involvement of lipoxygenase products from arachidonic acid in the pathogenesis of delayed vasospasm after subarachnoid hemorrhage (SAH), we measured the contents of hydroxyeicosatetraenoic acids (HETEs) in the subarachnoid clot, the cerebrospinal fluid, and the basilar artery, using the canine "two-hemorrhage" model. Lipoxygenase activity in the subarachnoid clot and the basilar artery was measured, ex vivo, using samples obtained 7 days after SAH. For a quantitative analysis of HETEs, each sample was homogenized with either ice-cold saline or methanol. The lipid extract was then submitted to reverse-phase HPLC. The identity of each HETE was further confirmed using straight-phase HPLC and gas chromatography-mass spectrometry. When the basilar artery was homogenized with ice-cold saline, a significant increase in the 5-HETE content was observed on SAH day 8. However, when the artery was homogenized with methanol, HETEs were not detected. In the case of incubation in the presence of arachidonic acid and calcium ionophore A23187, the 5-lipoxygenase activity was remarkably increased in the basilar artery exposed to SAH, compared to that of normal dogs. The subarachnoid clot contained a significant amount of 12-HETE (average 1.8 nmol/g wet weight) from day 2 to day 8. The administration of 1,2-bis(nicotinamido)propane significantly ameliorated vasospasm in the two-hemorrhage model, simultaneously inhibiting the 5-lipoxygenase activity of the basilar artery. Our observations show that the activities of 12- and 5-lipoxygenases are significantly increased after SAH in the subarachnoid clot and the basilar artery, respectively.(ABSTRACT TRUNCATED AT 250 WORDS) Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Animals; Arachidonic Acid; Arachidonic Acids; Basilar Artery; Chromatography, High Pressure Liquid; Dogs; Gas Chromatography-Mass Spectrometry; Hydroxyeicosatetraenoic Acids; Ischemic Attack, Transient; Lipoxygenase; Subarachnoid Hemorrhage | 1988 |
[Cerebral vasospasm and lipid peroxidation--lipid peroxides in the cerebrospinal fluid after subarachnoid hemorrhage].
The relationship between lipid peroxides in cerebrospinal fluid (CSF) and the occurrence of cerebral vasospasm following subarachnoid hemorrhage (SAH) was evaluated by analyzing CSF with high-performance liquid chromatography (HPLC) and gas chromatography mass spectrometry (GC-MS). Hydroperoxy eicosatetraenoic acids (HPETEs) and hydroxy eicosatetraenoic acids (HETEs) were synthesized by the treatment of arachidonic acid with hydrogen peroxide and cupric chloride. The retention time of these HPETEs and HETEs were determined on HPLC. The position of oxydation occurred was determined after methylation, reduction and trimethyl silylation using GC-MS. Thus the elucidation of positional isomers of HPETEs and HETEs was made possible by the retention time on HPLC. The supernant of CSF after SAH was adjusted to pH 3.0 and then absorbed to octadecyl silyl silica column. The eluted fraction with 15% ethanol-water from octadecyl silyl silica column was analyzed by HPLC detecting at 238 nm. No peak was observed on HPLC at the region of HPETEs and HETEs in the CSF obtained from healthy person. In SAH patients, several peaks were recognized in accordance with the occurrence of cerebral vasospasm. One of the peaks was identified as 5-HETE by HPLC and GC-MS. In 10 SAH patients, semi-quantitative analysis of 5-HETE in the CSF was performed by measuring the height of the peak identified as 5-HETE on HPLC. The close correlation was recognized between the occurrence of cerebral vasospasm and the appearance of 5-HETE in the CSF. The results of the present study suggest that lipid peroxidation is involved in the pathogenesis of chronic vasospasm after SAH. Topics: Arachidonic Acids; Humans; Hydroxyeicosatetraenoic Acids; Ischemic Attack, Transient; Lipid Peroxides; Oxidation-Reduction; Subarachnoid Hemorrhage | 1982 |