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Mechanical Tissue Resuscitation (MTR) reduces myocardial tissue injury following myocardial ischemia‐reperfusion (MI/R)
Author(s) -
Jordan James E.,
Mays Jennifer J.,
Shelton Julie E.,
Thompson Edreca A.,
Bryant Allyson K.,
Lane Magan R.,
Morykwas Michael J.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1130.1
Subject(s) - medicine , endocardium , myocardial infarction , edema , reperfusion injury , cardiology , ischemia , resuscitation , apoptosis , infarction , tunel assay , anesthesia , biology , biochemistry , immunohistochemistry
Background Reperfusion following an ischemic myocardial event increases cell death by activation of inflammatory processes. Reducing reperfusion injury may improve morbidity and mortality following AMI. We have previously shown MTR to reduce infarct size following MI/R. Here, we determine the effects of MTR on apoptosis and edema using a novel, bio‐absorbable patch. Methods A left, anterior free‐wall ischemic lesion (80 minutes) was created using reversible tourniquets in swine. Animals were randomized to receive either no treatment (Control) or MTR (− 50mmHg) using a bio‐absorbable patch at reperfusion. Following 3 hours of reperfusion, infarct size, apoptosis and edema were determined. Results While both groups had similar areas at risk (AAR/LV, 13.2 ± 0.7% and 14.8 ± 0.5%; p=.09), infarct size (AN/AAR) was significantly reduced in MTR‐treated animals (16.8±2.8%, p <.05) compared to controls (26.4±2.8%). This myocardial protection was accompanied by a reduction in epicardial apoptosis (7.7 ± 1.9% vs. 29.3 ± 7.7% TUNEL positive cells). MTR also reduced interstitial space in the endocardium by 53% and in the epicardium by 34%. Conclusions MTR applied directly over the infarcted area of the heart by means of a bio‐absorbable patch results in tissue preservation which may be the result of changes in apoptosis and edema formation. These data suggest that MTR could be an appropriate therapeutic approach to decrease myocyte death following a myocardial infarction.