Recovery of left ventricular segmental function after long-term reperfusion following temporary coronary occlusion in conscious dogs. Comparison of 2- and 4-hour occlusions.

Abstract

We compared the recovery of left ventricular segmental function with long-term reperfusion after two periods of coronary artery occlusion in conscious dogs to determine the relationship between the severity and duration of a temporary ischemic insult and the potential for recovery of contractile function. Twenty-seven awake dogs, previously instrumented with ultrasonic crystals for measuring regional left ventricular net systolic wall thickening, underwent 2 (group I) or 4 (group II) hours of left anterior descending coronary artery occlusion, followed by 1 month of reperfusion. Dogs were studied 24 hours after reperfusion and at weekly intervals for 1 month, after which the contractile reserve of left ventricular segments was assessed by their response to dopamine and postextrasystolic potentiation. The myocardial infarctions produced in the experimental model were relatively small. Left ventricular segments were classified by their severity of contractile dysfunction 1 hour after left anterior descending occlusion: class 1, >67% pre-occlusion net systolic wall thickening; class 2, 0-66.9%; class 3, <0% (paradoxical thinning). Class 1 segments in both groups showed trivial changes in net systolic wall thickening and regional myocardial blood flow (measured with 9-15 jtm microspheres) with left anterior descending occlusion and reperfusion. Class 2 segmental net systolic wall thickening was 32 5 (SEM) and 30 4% of control (P < 0.005 vs. control values) 1 hour after left anterior descending occlusion in groups I and II, respectively; endocardial blood flow to these segments decreased 56 13% and 49 12% (P < 0.05 vs. control values). Class 3 segments displayed severe dyskinesis (net systolic wall thickening = -43 6% and -33 5%, groups I and II) and reductions in endocardial blood flow during left anterior descending occlusion [-81 10% and -78 8% (P < 0.05)]. Segmental function of class 2 and 3 segments in group I dogs improved significantly with long-term reperfusion, attaining values of net systolic wall thickening of 66 9 and 26 9% control, respectively, at 1 month. Mean values of net systolic wall thickening attained by class 2 and 3 segments in this group during postextrasystolic potentiation were 93 7 and 50 13, respectively. In contrast, the net systolic wall thickening of class 2 segments in group II dogs did not change significantly with long-term reperfusion (net systolic wall thickening = 37 12 at 1 month) and the average net systolic wall thickening attained by these segments with postextrasystolic potentiation was 51 10%. Class 3 segments in group II dogs underwent a reversal of paradoxical thinning, but were essentially akinetic (net systolic wall thickening = 12 12%) after 1 month of reperfusion and did not demonstrate significant inotropic reserve. The extent of segmental necrosis paralleled the degree of contractile dysfunction in the three segment classes, but was not significantly different between groups I and II. Similarly, macrohistochemically determined area-at-risk and gross infarct size were not different between the two groups of dogs. Thus, reperfusion after 2 hours of left anterior descending occlusion eventually improves the contractile function at sites of moderate and severe dysfunction, whereas long-term reperfusion after 4 hours of left anterior descending occlusion does not restore contractile function to class 2 segments significantly, nor does it restore important degrees of contractile function to severely dyskinetic segments. These differences in recovery of contractile function apparently are not attributable to greater segmental necrosis, larger areas of infarction, or ultimate alterations in segmental coronary blood flow. (Circ Res 53: 248-263, 1983) THE influence of reperfusion on the extent of even-perfusion exerts important beneficial effects (Meertual myocardial ischemic injury has received much baum and Corday, 1975). This controversy probably attention in recent years, but disagreement exists is the result of differences in experimental methodregarding the duration of ischemia after which re-ology (e.g., species differences, anesthetized vs. un-Downloaded from http://ahajournals.org