title: Hyperglycaemia alters the endothelium-dependent relaxation of canine coronary arteries.
abstract: The aim of the present study was to investigate the effects of experimental diabetes and hyperglycaemia per se on the endothelium-dependent relaxation of isolated canine coronary arteries and to analyse the possible involvement of the cyclooxygenase pathway in the alterations induced by hyperglycaemia. Rings from the left anterior descending coronary arteries of 18 metabolically healthy, six alloxan-diabetic and six insulin-treated alloxan diabetic dogs were set up for isometric tension recording. Diabetic coronaries as well as healthy vessels subjected to in vitro hyperglycaemia (25.5 mmol L-1 glucose) showed impaired (P < 0.05) relaxation to acetylcholine (3 nmol L-1-10 micromol L-1) compared with normoglycaemic, i.e. metabolically healthy and insulin-treated diabetic controls, either before or after indomethacin (3 micromol L-1) administration. The maximal dilation elicited by acetylcholine was further decreased (P < 0.05) by the cyclooxygenase inhibitor in the diabetic coronaries only. Relaxation to sodium nitroprusside did not differ among groups. These results suggest that hyperglycaemia may result in impaired endothelium-dependent dilation of coronary arteries. Diminished relaxation of diabetic coronaries is worsened by the inhibition of the synthesis of vasodilator cyclooxygenase products.
authors.affiliation: Research Department, György Gottsegen National Institute of Cardiology, Budapest, Hungary.
authors.forename: E
authors.initials: E
authors.lastname: Kocsis
authors.forename: P
authors.initials: P
authors.lastname: Pacher
authors.forename: I
authors.initials: I
authors.lastname: Pósa
authors.forename: E
authors.initials: E
authors.lastname: Nieszner
authors.forename: G
authors.initials: G
authors.lastname: Pogátsa
authors.forename: M Z
authors.initials: MZ
authors.lastname: Koltai
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001786:Blood Glucose; D003331:Coronary Vessels / Q000378:metabolism / Q000503:physiopathology*; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000503:physiopathology*; D015237:Dinoprost / Q000494:pharmacology; D004285:Dogs; D004730:Endothelium, Vascular / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D006943:Hyperglycemia / Q000378:metabolism*; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D019335:Nitroarginine / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D009994:Osmolar Concentration; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D001786:Blood Glucose; D016861:Cyclooxygenase Inhibitors; D004791:Enzyme Inhibitors; D014665:Vasodilator Agents; D009599:Nitroprusside; D019335:Nitroarginine; D015237:Dinoprost; D000109:Acetylcholine; D007213:Indomethacin