title: Ischemic preconditioning changes the pattern of coronary reactive hyperemia regardless of mitochondrial ATP-sensitive K(+) channel blockade.
abstract: Ischemic preconditioning increases the velocity of vasodilatation and reduces the total hyperemic flow (THF) of a subsequent coronary reactive hyperemia (CRH). The increase in the velocity of vasodilatation has been shown to depend on an up-regulation of the endothelial release of nitric oxide, while the reduction of THF is attributed to an adenosine A(1) receptor-mediated mechanism. We investigated whether the changes in CRH induced by preconditioning ischemia (PI) can still be obtained after blockade of mitochondrial ATP-sensitive K(+) channels by sodium 5-hydroxydecanoate (5-HD), and whether the blockade per se affects the pattern of CRH. In anesthetized goats, flow was recorded from the left circumflex coronary artery (LCCA). CRH was obtained with the occlusion of LCCA for 15 s. PI was obtained by 2 cycles of 2.5 min of LCCA occlusion with a 5 min interval of reperfusion between the two occlusions. CRH was studied before and after i.v. administration of 5-HD (20 mg/kg), as well as in the presence of 5-HD after PI. Following 5-HD, the pattern of CRH remained unchanged. After 5-HD and PI, velocity of vasodilatation and total hyperemic flow of CRH showed the same changes as in previous studies after PI alone. It was concluded that the blockade of mitochondrial ATP-sensitive K(+) channels, which is reported to prevent myocardial protection, does not affect CRH and does not prevent PI from increasing the velocity of vasodilatation and reducing THF. These results demonstrate that the changes induced in CRH by preconditioning are independent of the opening of the mitochondrial ATP-sensitive K(+) channels.
authors.affiliation: Dipartimento di Scienze Cliniche e Biologiche dell'Università di Torino, Orbassano, Italy.
authors.forename: Pasquale
authors.initials: P
authors.lastname: Pagliaro
authors.forename: Amedeo
authors.initials: A
authors.lastname: Chiribiri
authors.forename: Raffaella
authors.initials: R
authors.lastname: Rastaldo
authors.forename: Daniele
authors.initials: D
authors.lastname: Mancardi
authors.forename: Claudia
authors.initials: C
authors.lastname: Penna
authors.forename: Donatella
authors.initials: D
authors.lastname: Gattullo
authors.forename: Gianni
authors.initials: G
authors.lastname: Losano
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D000758:Anesthesia; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology*; D003652:Decanoic Acids / Q000494:pharmacology; D006041:Goats; D006439:Hemodynamics / Q000187:drug effects; D006880:Hydroxy Acids / Q000494:pharmacology; D006940:Hyperemia / Q000503:physiopathology*; D019157:Ischemic Preconditioning, Myocardial; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*
chemical_list: D000889:Anti-Arrhythmia Agents; D003652:Decanoic Acids; D006880:Hydroxy Acids; D015221:Potassium Channels; C052853:5-hydroxydecanoic acid; D000255:Adenosine Triphosphate