Why the study?
Does systolic stretching affect ischemic contracture and postischemic recovery in isolated rabbit hearts during severe or moderate global ischemia?
Does systolic stretching affect ischemic contracture and postischemic recovery in isolated rabbit hearts during severe or moderate global ischemia?
Systolic stretching prevents ischemic contracture and improves recovery during severe ischemia but has deleterious effects during moderate ischemia when opposed by weakly contracting fibers.
SS effects on recovery vary by ischemia severity in rabbit hearts; leaves open clinical translation and human trials.
During regional myocardial ischemia, the ischemic segment is subjected to "paradoxical" systolic stretch; with severe global ischemia and asystole, the myocardial fibers are motionless.Both of these abnormal states of fiber motion may contribute directly to ischemic injury and, therefore, were assessed in isolated rabbit hearts paced at 180 beats/min and subjected to 90 minutes of severe or moderate global ischemia, followed by 60 minutes of reperfusion.A nonpulsatile isovolumic fluid-filled balloon occupied the left ventricular (LV) cavity in the controls; in experimental groups, the LV balloon was repetitively expanded in systole throughout the ischemic period to recreate the preischemic LV systolic pressure and simulate the paradoxical or systolic stretching (SS) which occurs in an ischemic ventricular segment.During severe ischemia, when inherent contractile activity was absent, 32 ± 5 mm Hg of contracture occurred; SS completely prevented ischemic contracture.Postischemic recovery of developed pressure without SS was 32 ± 6% vs. 72 ± 5% in the SS group (P < 0.001).Postischemia ATP and CP levels were higher in the SS group (ATP: 9.7 ± 0.5 vs. 6.1 ± 0.5 /imol/g, P< 0.001; CP: 55.0 ± 7.2 vs. 30.1 ± 4.8 /imol/g, P < 0.025).During moderate ischemia, 25% of preischemic contractile function persisted, and SS was opposed by weakly, but actively, contracting fibers.During moderate ischemia, SS decreased inherent developed pressure from 22 ± 1 to 10 ± 2 mm Hg (P< 0.001); recovery also was decreased in the SS group (86 ± 2 vs. 73 ± 4% of preischemic developed pressure (P< 0.01), as was tissue ATP (16.6 ± 1.8 vs. 11.8 ± 0.8 jumol/g (P< 0.05).Thus, abnormal fiber motion during ischemia directly contributes to myocardial injury.In the absence of active contraction, SS was beneficial.When SS was opposed by weakly contracting fibers during moderate ischemia, it appeared to impose an afterload and had deleterious effects on the ischemic myocardium.
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Apstein et al. (1980) studied this question.
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