title: Smaller infarct after preconditioning does not predict extent of early functional improvement of reperfused heart.
abstract: We evaluated the ability of ischemic preconditioning to restore function to salvaged myocardium in rabbits. Although ischemic preconditioning reduces infarct size, few investigators studying recovery of function after coronary occlusions lasting >/=30 min have reported any mechanical benefit in preconditioned hearts. However, because myocardial function was seldom evaluated beyond 5 h after reperfusion stunning may have masked the benefit. Accordingly, rabbits were chronically instrumented with a pneumatic occluder around a branch of the left coronary artery, a pair of 1-mm ultrasonic crystals in the myocardial territory destined to become ischemic, and electrocardiogram (ECG) leads. One week after surgery the ECG and segment length tracing were recorded at rest, during 30-min occlusion and 1 h of reflow, and again at 24, 48, and 72 h. In ischemically preconditioned rabbits, 5-min coronary occlusion and 10-min reperfusion preceded the long occlusion. The beginning and end of systole were determined by recording the first and second heart sounds with a hand-held precordial microphone. Postmortem infarct size was measured with triphenyltetrazolium chloride. During the 30-min coronary occlusion all segments became nearly akinetic or bulged during systole. After 60 min of reflow there was little return of function in either group. Between 24 and 72 h there was minimal recovery in the control group (segment shortening equals 13.3 +/- 4.1% of baseline), whereas function was much better in preconditioned hearts (44.2 +/- 7.4% of baseline, P < 0.02). Infarct size as a percentage of risk zone was much smaller in preconditioned hearts (10.2 +/- 1.4 vs. 29.7 +/- 1.8%, P < 0.001). Thus there is a gradual recovery of systolic function of reperfused myocardium after a coronary occlusion. Although early mechanical recovery is significantly better after preconditioning, it is much less than would be predicted by the reduction of infarct size.
authors.affiliation: Department of Medicine, University of South Alabama, College of Medicine, Mobile, Alabama 36688, USA.
authors.forename: M V
authors.initials: MV
authors.lastname: Cohen
authors.forename: X M
authors.initials: XM
authors.lastname: Yang
authors.forename: J M
authors.initials: JM
authors.lastname: Downey
mesh_terms: D000818:Animals; D004562:Electrocardiography; D005260:Female; D005544:Forecasting; D006321:Heart / Q000503:physiopathology*; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000473:pathology; D010701:Phonocardiography; D011817:Rabbits; D020127:Recovery of Function