title: Regional metabolism during coronary occlusion, reperfusion, and reocclusion using phosphorus31 nuclear magnetic resonance spectroscopy in the intact rabbit.
abstract: Few studies have examined metabolic consequences of coronary occlusion and reperfusion using phosphorus31 nuclear magnetic resonance (31P-NMR) in an intact animal model. Accordingly, we developed a model to study serial changes in myocardial metabolism in the intact open-chest rabbit. Ten animals underwent 20 +/- 2 minutes of regional coronary occlusion and 60 +/- 10 minutes of reperfusion followed by reocclusion. Cardiac-gated 31P-NMR spectra were obtained with a regional surface coil over the ischemic area during baseline, occlusion, reperfusion, and reocclusion conditions. Phosphocreatine fell with both the initial and second ischemic insults to 65% +/- 5% of baseline for the first occlusion (p less than 0.01) and tended to decrease to 89% +/- 8% of baseline for the second occlusion (p = 0.07), with normal levels reattained in the intervening period of reperfusion (99% +/- 5% of baseline, p = NS). Concordant inverse changes were seen with inorganic phosphates. At occlusion levels of inorganic phosphates were 135% +/- 10% of baseline (p less than 0.05) and 139% +/- 10% of baseline at reocclusion (p less than 0.05). Levels of adenosine triphosphate decreased during occlusion to 78% +/- 9% of baseline and were significantly lower than baseline during the second occlusion (75% +/- 5% of baseline, p less than 0.01). The ratio of phosphocreatine to inorganic phosphates, when compared with values at baseline, decreased at occlusion (49.6% +/- 4.7% of baseline, p less than 0.01) and at reocclusion (64.7% +/- 4.9% of baseline, p less than 0.01), with a normal ratio reattained in the intervening period of reperfusion (93.3% +/- 3.1% of baseline, p = NS). We conclude that reperfusion restores levels of phosphocreatine and adenosine triphosphate while returning levels of inorganic phosphates to baseline. Deleterious changes in high-energy phosphate metabolism are not potentiated by reocclusion in this model. 31P-NMR spectroscopy holds promise as a technique to noninvasively monitor intracellular biochemical processes serially during various interventions in the intact animal model.
authors.affiliation: Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109.
authors.forename: K M
authors.initials: KM
authors.lastname: Kavanaugh
authors.forename: A M
authors.initials: AM
authors.lastname: Aisen
authors.forename: K P
authors.initials: KP
authors.lastname: Fechner
authors.forename: T L
authors.initials: TL
authors.lastname: Chenevert
authors.forename: W R
authors.initials: WR
authors.lastname: Dunham
authors.forename: A J
authors.initials: AJ
authors.lastname: Buda
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003327:Coronary Disease / Q000378:metabolism* / Q000503:physiopathology; D009682:Magnetic Resonance Spectroscopy; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism*; D010710:Phosphates / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D011817:Rabbits
chemical_list: D010710:Phosphates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate