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Selected Publication:
Juránek, I; Bauer, V; Donnerer, J; Lembeck, F; Peskar, BA.
Severe hypoxia inhibits prostaglandin I(2) biosynthesis and vasodilatory responses induced by ionophore A23187 in the isolated rabbit ear.
Pharmacology. 2002; 66(4):199-205
Doi: 10.1159/000065534
Web of Science
PubMed
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- Co-authors Med Uni Graz
- Donnerer Josef
- Lembeck Fred
- Peskar Bernhard
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- Abstract:
- The present study was designed to test the hypothesis that lack of oxygen in severely hypoxic tissue may inhibit arachidonic acid oxygenation and thereby result in an inhibition of eicosanoid synthesis. Hypoxia was induced in the isolated rabbit ear, and arachidonate metabolism and peripheral resistance of the preparation were monitored simultaneously. Severe hypoxia completely inhibited the biosynthesis of prostaglandin I(2) induced by ionophore A23187 and converted the vasodilatory response observed under normoxia into vasoconstriction. The cyclooxygenase 1 inhibitor SC560 (1 micromol/l) effectively inhibited the normoxic prostaglandin I(2) biosynthesis, while the cyclooxygenase 2 inhibitor DFU (1 micromol/l) did not. Neither SC560 nor DFU affected normoxic vasodilatory responses, indicating no involvement of prostanoids. The nitric oxide (synthase inhibitor Nomega-nitro-L-arginine methyl ester (100 micromol/l) converted the vasodilation into vasoconstriction, similar to what was observed under hypoxia, suggesting that the hypoxia-mediated conversion might occur due to the inhibition of nitric oxide.
- Find related publications in this database (using NLM MeSH Indexing)
- Animals -
- Anoxia - metabolism
- Calcimycin - pharmacology
- Ear - pharmacology
- Epoprostenol - biosynthesis
- Female - biosynthesis
- Ionophores - pharmacology
- Male - pharmacology
- Muscle, Smooth, Vascular - drug effects
- Rabbits - drug effects
- Vasodilation - drug effects
- Find related publications in this database (Keywords)
- hypoxia
- isolated rabbit ear
- prostaglandin I-2
- vasodilation
- nitric oxide