title: Disturbed lipid metabolism in diabetic coronary vessels.
abstract: The aim of this study was to clarify whether or not arachidonic acid metabolic disorders are caused by a substrate inavailability and whether such disorders might contribute to circulatory disturbances in the diabetic myocardium. Norepinephrine induced a decrease in the conductivity of both coronary arterial bed and myocardial microcirculation in alloxan-diabetic dogs. It was markedly (p less than 0.05) attenuated both by indomethacin and acetylsalicylic acid pretreatments indicating an imbalance among the vasoactive prostanoids in diabetes. TXA2 release from the diabetic coronary rings was found to be elevated and could be normalized after the blockade of vascular adrenoceptors by phentolamine (p less than 0.05). PGI2 synthesis was also enhanced by adrenergic blockade in the diabetic arterial rings. After pretreatment with 14C arachidonic acid, in order to measure substrate availability, the arachidonic acid metabolic rate was less in the diabetic coronary arteries than in healty vessels (p less than 0.05). Ten mumol/l norepinephrine decreased arachidonic acid metabolism in the presence of prelabelled substrate in the diabetic animals, compared to an increase observed in metabolically healthy dogs. Therefore diabetes appears to diminish arachidonic acid metabolism and uptake independent of adrenoceptors and to induce an imbalance between vasoconstrictor and vasodilator cyclooxygenase products, resulting in elevated TXA2 release controlled by adrenergic mechanisms which may contribute to an impairment in myocardial microcirculation.
authors.affiliation: National Institute of Cardiology, Budapest, Hungary.
authors.forename: M Z
authors.initials: MZ
authors.lastname: Koltai
authors.forename: P
authors.initials: P
authors.lastname: Rösen
authors.forename: P
authors.initials: P
authors.lastname: Hadházy
authors.forename: Z
authors.initials: Z
authors.lastname: Aranyi
authors.forename: G
authors.initials: G
authors.lastname: Ballagi-Pordány
authors.forename: G
authors.initials: G
authors.lastname: Pogátsa
mesh_terms: D000496:Alloxan; D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism*; D001241:Aspirin / Q000494:pharmacology; D003326:Coronary Circulation / Q000187:drug effects; D003331:Coronary Vessels / Q000378:metabolism*; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D004285:Dogs; D011464:Epoprostenol / Q000378:metabolism; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D008833:Microcirculation / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects; D013928:Thromboxane A2 / Q000378:metabolism; D014661:Vasoconstriction / Q000187:drug effects
chemical_list: D001095:Arachidonic Acids; D011942:Receptors, Adrenergic, alpha; D013928:Thromboxane A2; D000496:Alloxan; D011464:Epoprostenol; D011451:Prostaglandin-Endoperoxide Synthases; D001241:Aspirin; D009638:Norepinephrine; D011224:Prazosin; D007213:Indomethacin; D010646:Phentolamine