title: Prolonged repolarization during hypoxemia in epicardial electrogram: difference from ischemia and a competitive action of cyclic AMP.
abstract: The effects of regional hypoxemia and ischemia on epicardial electrogram were studied in anesthetized, open-chest dogs. The left circumflex artery (LCx) was cannulated and perfused with either arterial blood or hypoxic solution. A contact electrode for recording monophasic action potential (MAP) was applied to the epicardial site of the LCx area. Epicardial electrograms and MAP in the LCx perfusion territory were recorded 1) just before and at the end of a 2-min coronary occlusion (ischemia) and 2) just before and at the end of a 2-min perfusion of hypoxic solution (hypoxemia). The activation-recovery interval (ARI), defined as an interval from the minimum derivative of the QRS complex to the maximum derivative of the T-wave in the unipolar electrogram, changed linearly with MAP duration during above interventions. The ARI decreased by 29% from 189 +/- 14 to 134 +/- 30 ms during ischemia (p < .001), and it increased by 39% from 183 +/- 11 to 254 +/- 31 ms during hypoxemia (p < .001). Hypoxemia produced a giant negative T-wave whose pattern was not modified by pretreatments with autonomic nerve blockers (propranolol and atropine), a Ca2+ channel blocker (verapamil), an ATP-sensitive K+ channel (KATP blocker (5-hydroxydecanoate or transient outward K+ current (I(to) blocker (4-aminopyridine). Isoproterenol, forskolin or aminophylline inhibited both the appearances of giant negative T and the ARI prolongation. Accordingly, unlike ischemia, hypoxemia prolongs repolarization process and this prolongation is inhibited by the augmentation of intracellular cyclic AMP.
authors.affiliation: First Department of Internal Medicine Yamagata University School of Medicine, Japan.
authors.forename: E
authors.initials: E
authors.lastname: Ikeno
authors.forename: I
authors.initials: I
authors.lastname: Kubota
authors.forename: T
authors.initials: T
authors.lastname: Kondo
authors.forename: M
authors.initials: M
authors.lastname: Yamaki
authors.forename: T
authors.initials: T
authors.lastname: Shibata
authors.forename: H
authors.initials: H
authors.lastname: Tomoike
mesh_terms: D000200:Action Potentials; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D000242:Cyclic AMP / Q000378:metabolism*; D004285:Dogs; D004562:Electrocardiography; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D007545:Isoproterenol / Q000494:pharmacology; D017202:Myocardial Ischemia / Q000378:metabolism / Q000503:physiopathology*; D010477:Perfusion; D011433:Propranolol / Q000494:pharmacology; D013565:Sympatholytics / Q000494:pharmacology
chemical_list: D000318:Adrenergic beta-Agonists; D007473:Ion Channels; D013565:Sympatholytics; D011433:Propranolol; D000242:Cyclic AMP; D007545:Isoproterenol