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15 Hydroperoxyarachidonic Acid

The Experts below are selected from a list of 12 Experts worldwide ranked by ideXlab platform

John R. Vane – 1st expert on this subject based on the ideXlab platform

  • HUMAN ARTERIAL AND VENOUS TISSUES GENERATE PROSTACYCLIN (PROSTAGLANDIN X), A POTENT INHIBITOR OF PLATELET AGGREGATION
    The Lancet, 2003
    Co-Authors: S. Moncada, E.a. Higgs, John R. Vane

    Abstract:

    Abstract Fresh rings of arteries and veins obtained from surgical specimens generated an unstable substance, prostacyclin (prostaglandin X, [P.G.X]) which is a potent inhibitor of platelet aggregation. The spontaneous generation of prostacyclin as well as its generation from exogenous arachidonic Acid was inhibited by incubation of the tissues with a prostaglandin-synthetase inhibitor such as indomethacin, whilst the generation induced by prostaglandin endoper-oxides was not. 15Hydroperoxyarachidonic Acid (a lipid hydroperoxide) inhibited the generation of prostacyclin in all three situations. It is postulated that prostacyclin is important for prevention of deposition of plastelets on the vessel wall and that the inhibition or prevention of the generation of prostacyclin is important in the genesis of diseases, especially those in which increased lipid peroxidation occurs, such as atherosclerosis.

  • Transformation of arachidonic Acid and prostaglandin endoperoxides by the guinea pig heart. Formation of RCS and prostacyclin.
    European Journal of Pharmacology, 2002
    Co-Authors: Karsten Schrör, Salvador Moncada, Fernando B. Ubatuba, John R. Vane

    Abstract:

    Abstract The metabolism of arachidonic Acid (AA) was studied in perfused isolated hearts from guinea pigs. The coronary effluent was continuously bioassayed for prostaglandin-like substances (PLS) using the cascade technique of Vane. Injections of AA in doses between 1–50 μg into the perfusion fluid prior to the heart produced vasodilatation of the coronary vascular bed followed by a contraction of the rat stomach strip (RSS), chick rectum (CR) and rat colon (RC) as well as relaxation of the bovine coronary artery (BCA). At the higher doses of AA there was also contraction of the rabbit aorta (RbA). The same pattern of effects on the bioassay tissues was seen when prostaglandin endoperoxide (PGH2) was perfused through the heart. The response of the bank of superfused tissues provided evidence for the formation of prostacyclin (PGX or PGI2), PGE2 and PGF2α. Chromatographic studies showed that 6-oxo-PGF1α together with other prostaglandins was present in the perfusate after Acidification, which suggested that the bovine coronary relaxing substance consists mainly of PGI2. Moreover, the rabbit aorta contracting substance (RCS) released in the perfusate was due to prostaglandin endoperoxides and not to thromboxane (TXA2. The formation of PLS from AA was completely blocked after treatment of the heart with the cyclo-oxygenase inhibitors, indomethacin or meclofenamic Acid. Pretreatment of the heart with 15Hydroperoxyarachidonic Acid (15-HPAA), a selective inhibitor of prostacyclin synthetase, inhibited the effect of AA on the coronary vasculature and diverted the metabolic transformation of AA towards PGE2 and PGF2α.

Kintomo Takakura – 2nd expert on this subject based on the ideXlab platform

  • Enhancement of ATPase activity by a lipid peroxide of arachidonic Acid in rat brain microvessels.
    Journal of Neurochemistry, 2006
    Co-Authors: Tohru Koide, Takao Asano, Hiroshi Matsushita, Kintomo Takakura

    Abstract:

    Abstract: The effects of 15Hydroperoxyarachidonic Acid (15-hpaa) on Na+, K+- and Mg + -ATPase activities in the blood-brain barrier (BBB) were examined using rat brain microvessels (MV). 15-HPAA markedly stimulated these ATPase activities in MV at low concentrations whereas the synaptosomal Na+, K+ -ATPase activity was inhibited in a dose-dependent manner. Further neurochemical analysis revealed that this stimulatory effect of 15-HPAA in MV was not due to a simple detergent-like action of the compound on the membranes but rather to stimulation of the phospholipase A2 and lipoxygenase activity within MV. In addition, it was shown that free radical reactions were involved in the mechanism. Since such anti-edema drugs as 1,2-bis(nicotinamido)propane were proved to be potent suppressors of the enhanced ATPase activity, further speculations on the role of this effect for ischemic brain edema are offered.

Karsten Schrör – 3rd expert on this subject based on the ideXlab platform

  • Transformation of arachidonic Acid and prostaglandin endoperoxides by the guinea pig heart. Formation of RCS and prostacyclin.
    European Journal of Pharmacology, 2002
    Co-Authors: Karsten Schrör, Salvador Moncada, Fernando B. Ubatuba, John R. Vane

    Abstract:

    Abstract The metabolism of arachidonic Acid (AA) was studied in perfused isolated hearts from guinea pigs. The coronary effluent was continuously bioassayed for prostaglandin-like substances (PLS) using the cascade technique of Vane. Injections of AA in doses between 1–50 μg into the perfusion fluid prior to the heart produced vasodilatation of the coronary vascular bed followed by a contraction of the rat stomach strip (RSS), chick rectum (CR) and rat colon (RC) as well as relaxation of the bovine coronary artery (BCA). At the higher doses of AA there was also contraction of the rabbit aorta (RbA). The same pattern of effects on the bioassay tissues was seen when prostaglandin endoperoxide (PGH2) was perfused through the heart. The response of the bank of superfused tissues provided evidence for the formation of prostacyclin (PGX or PGI2), PGE2 and PGF2α. Chromatographic studies showed that 6-oxo-PGF1α together with other prostaglandins was present in the perfusate after Acidification, which suggested that the bovine coronary relaxing substance consists mainly of PGI2. Moreover, the rabbit aorta contracting substance (RCS) released in the perfusate was due to prostaglandin endoperoxides and not to thromboxane (TXA2. The formation of PLS from AA was completely blocked after treatment of the heart with the cyclo-oxygenase inhibitors, indomethacin or meclofenamic Acid. Pretreatment of the heart with 15Hydroperoxyarachidonic Acid (15-HPAA), a selective inhibitor of prostacyclin synthetase, inhibited the effect of AA on the coronary vasculature and diverted the metabolic transformation of AA towards PGE2 and PGF2α.