title: Mechanical tissue resuscitation protects against myocardial ischemia-reperfusion injury.
abstract: OBJECTIVE
  Reperfusion injury is a complex inflammatory response involving numerous mechanisms and pathways. Mechanical tissue resuscitation is a newly described therapeutic strategy that reduces reperfusion injury. This study further investigates potential mechanisms for the protective effects of mechanical tissue resuscitation while utilizing a bio-absorbable matrix.
  
  
  METHODS
  Anesthetized swine were subjected to 80 minutes of coronary ischemia and three hours of reperfusion. An absorbable matrix was used to cover the ischemic-reperfused myocardium and apply the mechanical tissue resuscitation (-50 mmHg) throughout reperfusion. Infarct size, myocardial blood flow (microspheres), apoptosis, edema, and hemodynamics were analyzed.
  
  
  RESULTS
  Both control and treated groups displayed similar hemodynamics and physiologic parameters. Mechanical tissue resuscitation significantly reduced early infarct size (16.6 ± 3.8% vs. 27.3 ± 2.5% of area at risk, p < 0.05). This reduction of infarct size was accompanied by reduced edema formation in both epicardial (27% reduction) and endocardial (58% reduction) samples. Histological examination of both epicardial and endocardial tissues also revealed a reduction in apoptosis (80% and 44% reductions) in MTR-treated hearts.
  
  
  CONCLUSIONS
  Treatment with mechanical tissue resuscitation during reperfusion reduces both early cell death and the delayed, programmed cell death after ischemia-reperfusion. This cardioprotection is also associated with a significant reduction in interstitial water. Additional cardioprotection may be derived from mechanical tissue resuscitation-induced increased blood flow. Mechanical tissue resuscitation, particularly with a resorbable device, is a straightforward and efficacious mechanical strategy for decreasing cardiomyocyte death following myocardial infarction as an adjunctive therapy to surgical revascularization.
authors.affiliation: Department of Cardiothoracic Surgery, Wake Forest School of Medicine, Winston-Salem, North Carolina.
authors.forename: James E
authors.initials: JE
authors.lastname: Jordan
authors.forename: Jennifer J
authors.initials: JJ
authors.lastname: Mays
authors.forename: Julie E
authors.initials: JE
authors.lastname: Shelton
authors.forename: Allyson K
authors.initials: AK
authors.lastname: Bryant
authors.forename: Magan R
authors.initials: MR
authors.lastname: Lane
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Morykwas
authors.forename: Louis C
authors.initials: LC
authors.lastname: Argenta
mesh_terms: D000818:Animals; D017209:Apoptosis; D001274:Atmospheric Pressure; D004699:Endocardium / Q000166:cytology / Q000473:pathology; D009203:Myocardial Infarction / Q000473:pathology / Q000628:therapy; D015425:Myocardial Reperfusion / Q000009:adverse effects; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000473:pathology; D010496:Pericardium / Q000166:cytology / Q000473:pathology; D012151:Resuscitation / Q000379:methods*; D013552:Swine