Stuttering Reperfusion of Ischemic Myocardium Does Not Exacerbate Myocardial Infarction: Evidence Against Lethal Cell Reperfusion Injury in the Rabbit.
Journal: 2017/August - Journal of Thrombosis and Thrombolysis
ISSN: 1573-742X
PUBMED: 10613981
Abstract:
In the clinical setting of acute myocardial infarction, coronary reperfusion may occur intermittently. Whether this intermittent or stuttering reperfusion exacerbates reperfusion cell injury is not known. To investigate whether stuttering reperfusion affects the development of necrosis, anesthetized male rabbits were randomized to either control or stuttering-reperfusion groups. The control rabbits underwent 40 minutes of continuous left anterior descending (LAD) occlusion followed by 3 hours of continuous reperfusion. The stuttering-reperfusion rabbits were occluded for the same 40 minutes but were reperfused for 1 minute at 37, 39, and 41 minutes into the occlusion period. Each of these brief reperfusion periods was followed by 1 minute of occlusion. After 40 minutes of occlusion (43 minutes after initial occlusion), the stuttering-reperfusion group was continuously reperfused for 3 hours. Regional myocardial blood flow was measured during occlusion and 30 minutes after final repe rfusion in both groups. Area at risk (AR, %LV) was delineated by in vivo blue dye injection and the area of necrosis (AN) by in vitro tetrazolium staining. Results: There was no difference in AR blood flow between groups, Ischemic blood flow (ml/min/g) was 0.05 +/- 0.02 in the control group and 0.09 +/- 0.04 in stuttering-reperfusion group. After reperfusion, blood flow in the ischemic area was 1.36 +/- 0.13 in control and 1.87 +/- 0.40 in stuttering-reperfusion rabbits. The AN expressed as a percentage of the AR was 43 +/- 8 in the control rabbits and 36 +/- 6 in the stuttering-reperfusion rabbits. Stuttering-reperfusion did not augment the development of necrosis compared with the control group. Conclusion: Reperfusing the myocardium in a stuttering fashion had no effect on the amount of necrosis and did not contribute to lethal cell reperfusion injury in this model.
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