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[Beneficial effect of a selective TXA2 synthetase inhibitor, OKY-046, both on thromboxane B2 production and vascular damage after spinal cord injury in rat spinal cord].
Nihon Seikeigeka Gakkai Zasshi. 1990 Jan; 64(1):82-8.NS

Abstract

Thromboxane A2 (TXA2) is an eicosanoid with potent platelet aggregation and vasoconstricting activity, while prostaglandin I2 (PGI2) antagonizes its activity. But these eicosanoids are so labile that the stable degradation products, thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), are determined in biological materials. In a rat spinal cord compression injury model, a production of TXB2 reached a peak (133.6 +/- 13.8 pmol/g cord) 5 minutes after compression injury, while that of 6-keto-PGF1 alpha slightly increased (26.2 +/- 11.7 pmol/g cord). And the magnitude of the increase in TXB2 and the extent of post-traumatic vascular damage as determined by fluorescein uptake were both dependent on the degree of spinal cord compression injury. We also studied the effect of a selective TXA2 synthetase inhibitor, OKY-046 [E)-3-[4-(1-imidazolylmethyl)phenyl]-2-propenoic acid), both on TXB2 production in the injured spinal cord and post-traumatic vascular damage. When OKY-046 was administered intravenously 10 minutes prior to compression injury at a dose of 500 micrograms/kg body weight, the increased production of TXB2 was inhibited by about 80% and uptake of sodium fluorescein was reduced by a maximum of 40%. When the compression injury was induced before OKY-046 was administered, the inhibitory effect of OKY-046 on TXB2 production decreased depending on the duration before administration. In contrast, the 6-keto-PGF1 alpha level was not affected in the presence of OKY-046.

Authors+Show Affiliations

Department of Orthopaedic Surgery, Tokushima University, School of Medicine, Japan.No affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Research Support, Non-U.S. Gov't

Language

jpn

PubMed ID

2319197

Citation

Morimoto, K, et al. "[Beneficial Effect of a Selective TXA2 Synthetase Inhibitor, OKY-046, Both On Thromboxane B2 Production and Vascular Damage After Spinal Cord Injury in Rat Spinal Cord]." Nihon Seikeigeka Gakkai Zasshi, vol. 64, no. 1, 1990, pp. 82-8.
Morimoto K, Ikata T, Tounai T. [Beneficial effect of a selective TXA2 synthetase inhibitor, OKY-046, both on thromboxane B2 production and vascular damage after spinal cord injury in rat spinal cord]. Nihon Seikeigeka Gakkai Zasshi. 1990;64(1):82-8.
Morimoto, K., Ikata, T., & Tounai, T. (1990). [Beneficial effect of a selective TXA2 synthetase inhibitor, OKY-046, both on thromboxane B2 production and vascular damage after spinal cord injury in rat spinal cord]. Nihon Seikeigeka Gakkai Zasshi, 64(1), 82-8.
Morimoto K, Ikata T, Tounai T. [Beneficial Effect of a Selective TXA2 Synthetase Inhibitor, OKY-046, Both On Thromboxane B2 Production and Vascular Damage After Spinal Cord Injury in Rat Spinal Cord]. Nihon Seikeigeka Gakkai Zasshi. 1990;64(1):82-8. PubMed PMID: 2319197.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Beneficial effect of a selective TXA2 synthetase inhibitor, OKY-046, both on thromboxane B2 production and vascular damage after spinal cord injury in rat spinal cord]. AU - Morimoto,K, AU - Ikata,T, AU - Tounai,T, PY - 1990/1/1/pubmed PY - 1990/1/1/medline PY - 1990/1/1/entrez SP - 82 EP - 8 JF - Nihon Seikeigeka Gakkai zasshi JO - Nihon Seikeigeka Gakkai Zasshi VL - 64 IS - 1 N2 - Thromboxane A2 (TXA2) is an eicosanoid with potent platelet aggregation and vasoconstricting activity, while prostaglandin I2 (PGI2) antagonizes its activity. But these eicosanoids are so labile that the stable degradation products, thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), are determined in biological materials. In a rat spinal cord compression injury model, a production of TXB2 reached a peak (133.6 +/- 13.8 pmol/g cord) 5 minutes after compression injury, while that of 6-keto-PGF1 alpha slightly increased (26.2 +/- 11.7 pmol/g cord). And the magnitude of the increase in TXB2 and the extent of post-traumatic vascular damage as determined by fluorescein uptake were both dependent on the degree of spinal cord compression injury. We also studied the effect of a selective TXA2 synthetase inhibitor, OKY-046 [E)-3-[4-(1-imidazolylmethyl)phenyl]-2-propenoic acid), both on TXB2 production in the injured spinal cord and post-traumatic vascular damage. When OKY-046 was administered intravenously 10 minutes prior to compression injury at a dose of 500 micrograms/kg body weight, the increased production of TXB2 was inhibited by about 80% and uptake of sodium fluorescein was reduced by a maximum of 40%. When the compression injury was induced before OKY-046 was administered, the inhibitory effect of OKY-046 on TXB2 production decreased depending on the duration before administration. In contrast, the 6-keto-PGF1 alpha level was not affected in the presence of OKY-046. SN - 0021-5325 UR - https://www.unboundmedicine.com/medline/citation/2319197/[Beneficial_effect_of_a_selective_TXA2_synthetase_inhibitor_OKY_046_both_on_thromboxane_B2_production_and_vascular_damage_after_spinal_cord_injury_in_rat_spinal_cord]_ L2 - https://www.medicalonline.jp/meteo_linkout.php?issn=0021-5325&volume=64&issue=1&spage=82 DB - PRIME DP - Unbound Medicine ER -