title: Reduction of ST elevation in repeated coronary occlusion model depends on both altered metabolic response and conduction property.
abstract: The aim of this study was to elucidate the mechanisms of altered electrical response to ischemia in repeated coronary occlusion model. To test its dependence on metabolic response, extracellular K+ concentration (eKC), myocardial pH and PCO2 were simultaneously measured with epicardial ECG during three consecutive 4 min of left anterior descending coronary artery (LAD) occlusion separated by 15 min of reperfusion in canine hearts. ECG changes induced by infusion of high K+-buffer (10 mM) into the coronary arterial bed via carotid artery-LAD bypass (referred to as high K+-challenges: HKC) were also tested prior to (the first HKC), and during each reperfusion period (the second to the fourth HKC). ST elevation was significantly reduced in subsequent occlusions (3.14 +/- 0.48 and 2.98 +/- 0.47 mV in the second and third occlusion, both P<0.05, compared to 4.91 +/- 0.78 mV in the first). This was accompanied by significant attenuation of the changes in eKC, tissue pH and PCO2. ST elevation induced by HKC also significantly reduced after repeated occlusion (4.09 +/- 0.79 mV in the fourth HKC vs. 5.64 +/- 0.68 mV in the first, P<0.05) in spite of the identical changes in eKC during HKC. This progressive decrease in ST changes by HKC was rather consistent with augmented conduction delay (86.4 +/- 7.1% increase in activation time in the fourth vs. 54.3 +/- 3.4% in the first, P<0.01). These findings indicate that repeated ischemia induces altered electrical response to subsequent ischemia based on both attenuated metabolic response and altered conduction property.
authors.affiliation: The Second Department of Internal Medicine, Akita University, 1-1-1 Hondo, Akita 010-8543, Japan.tsaito@im2.med.akita-u.ac.jp
authors.forename: Takashi
authors.initials: T
authors.lastname: Saito
authors.forename: Hiroto
authors.initials: H
authors.lastname: Miura
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Kimura
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Watanabe
authors.forename: Akira
authors.initials: A
authors.lastname: Nakagomi
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Tamura
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Hasegawa
authors.forename: Satoshi
authors.initials: S
authors.lastname: Kibira
authors.forename: Mamoru
authors.initials: M
authors.lastname: Miura
mesh_terms: D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D003327:Coronary Disease; D004285:Dogs; D004562:Electrocardiography; D004734:Energy Metabolism; D005260:Female; D006329:Heart Conduction System / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology; D006863:Hydrogen-Ion Concentration; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism; D011188:Potassium / Q000378:metabolism
chemical_list: D002245:Carbon Dioxide; D011188:Potassium