Physiologic role of coronary PGl2 and PGE2 in modulating coronary vascular response to sympathetic stimulation

Gian Gastone Neri Serneri; Gian Franco Gensini; Rosanna Abbate; Sergio Castellani; Francesco Bonechi; Armando Dagianti; Luciano Arata; Francesco Fedele; Carlo Iacoboni; Domenico Prisco

doi:10.1016/S0002-8703(05)80322-9

Physiologic role of coronary PGl2 and PGE2 in modulating coronary vascular response to sympathetic stimulation

Gian Gastone Neri Serneri, Gian Franco Gensini, Rosanna Abbate, Sergio Castellani, Francesco Bonechi, Armando Dagianti, Luciano Arata, Francesco Fedele, Carlo Iacoboni, Domenico Prisco

Fondazione Don Carlo Gnocchi Onlus

Research output: Contribution to journal › Article › peer-review

Abstract

To investigate a physiologic role of coronary prostacyclin (PG12) and prostaglandin E₂ (PGE₂) 30 patients who were not affected by coronary heart dlsease were evaluated for coronary hemodynamics and coronary PGl₂ and PGE₂ production. Inhibition of coronary prostaglandin biosynthesis by ketoprofen (1 mg/kg) or aspirin (15 mg/kg) administered intravenously did not significantly change coronary hemodynamics in resting conditions. In all patients cold pressor tests induced significant increases in coronary blood flow (p2 (as 6-keto-PGF_1α) and PGE₂ formation was observed (p2 and PGE₂ formation that was induced by cold pressor test and caused a paradoxical increase in coronary vascular resistance (ketoprofen: p

Original language	English
Pages (from-to)	848-854
Number of pages	7
Journal	American Heart Journal
Volume	119
Issue number	4
DOIs	https://doi.org/10.1016/S0002-8703(05)80322-9
Publication status	Published - 1990

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

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10.1016/S0002-8703(05)80322-9

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title = "Physiologic role of coronary PGl2 and PGE2 in modulating coronary vascular response to sympathetic stimulation",

abstract = "To investigate a physiologic role of coronary prostacyclin (PG12) and prostaglandin E2 (PGE2) 30 patients who were not affected by coronary heart dlsease were evaluated for coronary hemodynamics and coronary PGl2 and PGE2 production. Inhibition of coronary prostaglandin biosynthesis by ketoprofen (1 mg/kg) or aspirin (15 mg/kg) administered intravenously did not significantly change coronary hemodynamics in resting conditions. In all patients cold pressor tests induced significant increases in coronary blood flow (p2 (as 6-keto-PGF1α) and PGE2 formation was observed (p2 and PGE2 formation that was induced by cold pressor test and caused a paradoxical increase in coronary vascular resistance (ketoprofen: p",

author = "{Neri Serneri}, {Gian Gastone} and Gensini, {Gian Franco} and Rosanna Abbate and Sergio Castellani and Francesco Bonechi and Armando Dagianti and Luciano Arata and Francesco Fedele and Carlo Iacoboni and Domenico Prisco",

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T1 - Physiologic role of coronary PGl2 and PGE2 in modulating coronary vascular response to sympathetic stimulation

AU - Neri Serneri, Gian Gastone

AU - Gensini, Gian Franco

AU - Abbate, Rosanna

AU - Castellani, Sergio

AU - Bonechi, Francesco

AU - Dagianti, Armando

AU - Arata, Luciano

AU - Fedele, Francesco

AU - Iacoboni, Carlo

AU - Prisco, Domenico

PY - 1990

Y1 - 1990

N2 - To investigate a physiologic role of coronary prostacyclin (PG12) and prostaglandin E2 (PGE2) 30 patients who were not affected by coronary heart dlsease were evaluated for coronary hemodynamics and coronary PGl2 and PGE2 production. Inhibition of coronary prostaglandin biosynthesis by ketoprofen (1 mg/kg) or aspirin (15 mg/kg) administered intravenously did not significantly change coronary hemodynamics in resting conditions. In all patients cold pressor tests induced significant increases in coronary blood flow (p2 (as 6-keto-PGF1α) and PGE2 formation was observed (p2 and PGE2 formation that was induced by cold pressor test and caused a paradoxical increase in coronary vascular resistance (ketoprofen: p

AB - To investigate a physiologic role of coronary prostacyclin (PG12) and prostaglandin E2 (PGE2) 30 patients who were not affected by coronary heart dlsease were evaluated for coronary hemodynamics and coronary PGl2 and PGE2 production. Inhibition of coronary prostaglandin biosynthesis by ketoprofen (1 mg/kg) or aspirin (15 mg/kg) administered intravenously did not significantly change coronary hemodynamics in resting conditions. In all patients cold pressor tests induced significant increases in coronary blood flow (p2 (as 6-keto-PGF1α) and PGE2 formation was observed (p2 and PGE2 formation that was induced by cold pressor test and caused a paradoxical increase in coronary vascular resistance (ketoprofen: p

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Physiologic role of coronary PGl2 and PGE2 in modulating coronary vascular response to sympathetic stimulation

Abstract

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