2-methyl-3-(4-(3-pyridinylmethyl)phenyl)-2-propenoic-acid and Subarachnoid-Hemorrhage

2-methyl-3-(4-(3-pyridinylmethyl)phenyl)-2-propenoic-acid has been researched along with Subarachnoid-Hemorrhage* in 5 studies

Other Studies

5 other study(ies) available for 2-methyl-3-(4-(3-pyridinylmethyl)phenyl)-2-propenoic-acid and Subarachnoid-Hemorrhage

ArticleYear
Pathological changes in cerebral arteries following experimental subarachnoid hemorrhage: role of blood platelets.
    The Anatomical record, 1988, Volume: 220, Issue:2

    The role of blood platelets in producing early intimal changes in cerebral arteries following subarachnoid hemorrhage (SAH) was examined by using 18 cats. Experimental SAH was produced by a rupture of the proximal portion of the right middle cerebral artery. Following SAH, the scanning electron microscope revealed that structural alterations in the intimal layer of major cerebral arteries occurred as early as 2 hours and became more severe by 48 hours. Vascular alterations, which were predominantly detected in the ruptured vessel, consisted of endothelial cell corrugation, detachment, crater formation, intimal adhesion of platelets and red blood cells, intimal thrombi, and reendothelialization. When cats were pretreated prior to SAH with an anti-platelet-aggregating agent, OKY-1581, the intimal blood elements and thrombi were clearly reduced, and reendothelialization was not observed. However, endothelial cell changes in the OKY-1581-treated group were very similar to those occurring in the nontreated group. While these results suggest that bioactive substances contained within blood platelets, such as growth factors, serotonin, and norepinephrine, have little effect on producing endothelial cell injury, platelets may be important in the initiation of reendothelialization following vessel injury.

    Topics: Animals; Blood Platelets; Cell Adhesion; Cerebral Arteries; Erythrocytes; Methacrylates; Microscopy, Electron, Scanning; Subarachnoid Hemorrhage

1988
Prevention of cerebral vasospasm with OKY-046 an imidazole derivative and a thromboxane synthetase inhibitor. A preliminary co-operative clinical study.
    Acta neurochirurgica, 1985, Volume: 77, Issue:3-4

    The prevention of cerebral vasospasm with OKY-046, an imidazole derivative and a thromboxane synthetase inhibitor, was studied co-operatively at ten neurosurgical services. Intravenous administrations of 2, 5 or 10 mu/kg/minute of OKY-046 were given continuously from the earliest possible day to the 14th SAH-day to 82 patients with ruptured cerebral aneurysm. Sixty-eight patients (83%) showed moderate to high high-density (SAH) in their initial CTs. Angiographic vasospasms were seen in 58 patients, representing 71% of all cases or 81% of the 72 cases for which angiograms were available: the vasospasms of 45 patients (55 or 63%) were moderate to severe. Symptomatic vasospasm occurred, however, only in 27 patients (33%): in 18 of those cases, moreover, the symptoms were mild or transient. The conditions of the patients at one month after the SAH were classified into 9 grades from 0 (normal) to 8 (deceased). Fifty-two patients (63%) were classified as 0 or 1, and 64 (78%) as better than 3 (possible daily life unaided). The administration of OKY-046 was proven to decrease TXB2 in the blood. This paper emphasizes the effectiveness of the drug for symptomatic vasospasm, and supports our previous contention that cerebral microthrombosis may play an important role in the pathogenesis of cerebral vasospasm.

    Topics: Acrylates; Adult; Aged; Drug Eruptions; Female; Hemorrhage; Humans; Intracranial Aneurysm; Ischemic Attack, Transient; Male; Meclofenamic Acid; Methacrylates; Middle Aged; Recurrence; Subarachnoid Hemorrhage; Thromboxane-A Synthase

1985
The role of the prostacyclin-thromboxane system in cerebral vasospasm following induced subarachnoid hemorrhage in the rabbit.
    Journal of neurosurgery, 1984, Volume: 61, Issue:6

    Subarachnoid hemorrhage (SAH) was induced in 50 rabbits by injecting 1.25 cc/kg of autologous, well heparinized, fresh arterial blood into the cisterna magna, followed by suspending the animals in a head-down position at 30 degrees for 15 minutes. The animals were evenly divided into five groups: a control group, or groups receiving post-SAH prostacyclin (PGI2), carbacyclin, thromboxane A2 (TXA2) synthetase inhibitor (OKY-1581), or nutralipid. Radiographic vertebrobasilar arterial spasm was demonstrated on the 3rd day post-SAH in the control animals. This was decreased in the prostacyclin and the carbacyclin groups and was absent in the OKY-1581 and the nutralipid groups. Cerebral blood flow (CBF) measurements on the 4th day post-SAH using the xenon-133 technique failed to reveal any significant difference between the prostacyclin, the carbacyclin, and the control groups, but flows in the nutralipid and the OKY-1581 groups were significantly higher. There was a good correlation between the clinical status and the CBF. Intracytoplasmic vacuolation and detachment of the vascular endothelium, seen ultrastructurally, may account for the impaired synthesis of prostacyclin. Exogenous prostacyclin and carbacyclin decreased vasospasm but failed to improve cerebral perfusion. OKY-1581 blocked the synthesis of the potent vasoconstrictor, TXA2, which is not only formed during platelet aggregation but also induces platelet aggregation. Nutralipid contains linolenic acid, a precursor of eicosapentaenoic acid (EPA), which is more potent in inhibiting platelet aggregation and in blocking TXA2 production. The various fatty acid constituents of nutralipid bind to albumin and thereby shorten the half-life of TXA2.

    Topics: Acrylates; Animals; Cerebrovascular Circulation; Epoprostenol; Fatty Acids; Female; Ischemic Attack, Transient; Male; Methacrylates; Rabbits; Subarachnoid Hemorrhage; Thromboxane A2; Thromboxane-A Synthase

1984
Effect of selective inhibitor of thromboxane A2 synthetase on cerebral vasospasm after early surgery.
    Journal of neurosurgery, 1984, Volume: 61, Issue:1

    The authors report the results of inhibition of thromboxane A2 synthetase in 49 consecutive patients with subarachnoid hemorrhage (SAH). These unselected Grade I to IV patients all had a ruptured aneurysm of the anterior circle of Willis, and were operated on within 72 hours after SAH. Twenty-seven patients were treated postoperatively by an intravenous infusion of sodium (E)-3- [4-(3-pyridylmethyl)-phenyl] -2- propenoate (OKY-1581), a selective inhibitor of thromboxane A2 synthetase, at 5 micrograms/kg/min for 10 to 14 days, and the remaining 22 patients did not receive this drug. Both groups of patients had similar age distribution and preoperative neurological conditions. A suggestive but statistically insignificant improvement was found in postoperative angiographic vasospasm, ischemic symptoms, and overall outcome in the group receiving OKY-1581. The incidence of low-density areas on the postoperative computerized tomography scans was significantly decreased in patients treated with OKY-1581 infusion.

    Topics: Acrylates; Adult; Aged; Cerebral Angiography; Humans; Intracranial Aneurysm; Ischemic Attack, Transient; Methacrylates; Middle Aged; Rupture, Spontaneous; Subarachnoid Hemorrhage; Thromboxane-A Synthase; Tomography, X-Ray Computed

1984
Prevention of cerebral vasospasm after SAH with a thromboxane synthetase inhibitor, OKY-1581.
    Journal of neurosurgery, 1982, Volume: 57, Issue:1

    The efficacy of thromboxane synthetase inhibitor in the prevention of cerebral vasospasm after subarachnoid hemorrhage (SAH) was evaluated in a prolonged experiment using dogs. Changes in the diameter of the basilar artery were followed by angiography, and morphological changes were studied by photomicroscopy and electron microscopy. As a thromboxane synthetase inhibitor, OKY-1581 (sodium-(E)-3-(4(-3-pyridylmethyl)phenyl)-2-methylacrylate) was used. Dogs received intravenous injections of 160 mg of OKY-1581 dissolved in 2 ml of physiological saline immediately after subarachnoid blood injection. Subsequently, the animals received continuous intravenous infusion of the drug at the rate of 4 gm/50 ml/24 hours until sacrifice 4 days after induction of SAH. Control dogs received subarachnoid blood injection without treatment with OKY-1581. Angiographic examination revealed that the late spasm was almost completely abolished by the treatment with OKY-1581. Early spasm was also prevented, but the drug's effect was less prominent than it was on the late spasm. Morphological study revealed degenerative changes in the endothelium and myonecrotic changes in the tunica media following SAH in the basilar arteries of the treated as well as the untreated dogs. However, corrugation of the internal elastic lamina was almost completely absent in the treated dogs. The above results indicate that a disproportionate synthesis of thromboxane A2 plays an important role in the evolution of chronic cerebral vasospasm following SAH, and that drugs such as OKY-1581 that selectively inhibit thromboxane synthetase might be useful in the prevention of vasospasm.

    Topics: Acrylates; Angiography; Animals; Basilar Artery; Dogs; Ischemic Attack, Transient; Methacrylates; Subarachnoid Hemorrhage; Thromboxane-A Synthase

1982