title: Reversal of the postischaemic suppression of coronary function in perfused guinea pig heart by ischaemic preconditioning.
abstract: In the isolated guinea pig hearts suppression of endothelium-dependent (Acetylcholine, Substance P, postocclusive hyperaemia) and endothelium-independent (Sodium nitroprusside, PGE1) responses after 30 min subglobal ischaemia (reduction of coronary flow to 5%) were analysed in hearts which were not preconditioned or preconditioned by various protocols. Preconditioning consisted of single 5 min ischaemia (IP5) or single 10 min ischaemia (IP10) or double 5 min ischaemia (IP5 + 5). Thirty minutes of ischaemia followed by reperfusion reduced both endothelium-dependent and endothelium-independent responses approximately by 30-50% and slightly suppressed basal coronary flow by 10%. IP5 and IP5 + 5 protected against postischaemic suppression of responses to NaNP but not against postischaemic impairment of SP, ACh, and POH responses. The endothelium-dependent responses and postischaemic suppression of basal coronary flow were protected by IP10 only. In summary, in the isolated guinea pig heart the 30-min ischaemia impairs vasodilator responses to both endothelium-dependent and endothelium-independent agents. Ischaemic preconditioning protects both endothelial and smooth muscle cells function against this impairment, though endothelial cells require a more extensive preconditioning to put in motion protective mechanisms than smooth muscle cells do. Independent mechanisms of IP in endothelial cells and in smooth muscle cells are suggested.
authors.affiliation: Department of Pharmacology Medical College of Jagiellonian Uniwersity Cracow, Poland. mfschlop@cyf-kr.edu.pl
authors.forename: S
authors.initials: S
authors.lastname: Chlopicki
authors.forename: M
authors.initials: M
authors.lastname: Lomnicka
authors.forename: R J
authors.initials: RJ
authors.lastname: Gryglewski
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000527:Alprostadil / Q000494:pharmacology; D000818:Animals; D003331:Coronary Vessels / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006168:Guinea Pigs; D006940:Hyperemia / Q000473:pathology; D066298:In Vitro Techniques; D019157:Ischemic Preconditioning, Myocardial; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000503:physiopathology*; D009569:Nitric Oxide / Q000502:physiology*; D009599:Nitroprusside / Q000494:pharmacology; D010477:Perfusion; D013373:Substance P / Q000494:pharmacology; D013997:Time Factors; D014664:Vasodilation
chemical_list: D009599:Nitroprusside; D009569:Nitric Oxide; D013373:Substance P; D000527:Alprostadil; D000109:Acetylcholine