title: Attenuation of cardiac vascular rhexis: a promising therapeutic target.
abstract: BACKGROUND
  We have previously identified a phenomenon that we called vascular rhexis (VR) after coronary occlusion in mice. To explore its potential pathogenetic impact on the destruction of vessels described, its potential universality, and its characterization as a scaffolding for evaluating amelioration, we studied Sprague-Dawley rats from which multiple blood samples and robust tissue samples can be obtained.
  
  
  METHODS
  Rats were subjected to nonsustained coronary occlusion for 15 min, 1 h, 90 min, 3 h, or 4 h, followed by reperfusion. Soluble fractions of left ventricular (LV) homogenates were obtained 48 h later and assayed by western blotting for quantification of α-smooth muscle actin, diminution of which has been immunohistochemically shown to reflect delineation of VR. The functional integrity of vessel walls was assessed 24 h after induction of ischemia for selected intervals, followed by reperfusion using fluorescein isothiocyanate-tagged albumin injected through the tail vein 2 h before harvesting tissue.
  
  
  RESULTS
  Nonsustained coronary occlusion for 1 h initiated VR, evident 47 h after reperfusion; however, more brief ischemic insults did not. Loss of functional integrity was evident as judged from increases in extravasated fluorescein isothiocyanate-conjugated albumin in LV walls.
  
  
  CONCLUSIONS
  Because VR occurs early and may be ameliorated by interventions that can be initiated soon after the onset of nonsustained ischemia before myocardial cell death is substantial, its amelioration is an attractive target for diminution of late negative LV remodeling associated with the 'no reflow' phenomenon to which it can contribute.
authors.affiliation: Department of Medicine, Cardiovascular Research Institute, University of Vermont College of Medicine, Colchester Research Facility, Colchester, Vermont 05446, USA.
authors.forename: A K M
authors.initials: AK
authors.lastname: Tarikuz Zaman
authors.forename: Jeffrey L
authors.initials: JL
authors.lastname: Spees
authors.forename: Burton E
authors.initials: BE
authors.lastname: Sobel
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D015153:Blotting, Western; D002199:Capillary Permeability; D016923:Cell Death; D054059:Coronary Occlusion / Q000378:metabolism / Q000473:pathology*; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology*; D003402:Creatine Kinase / Q000378:metabolism; D004195:Disease Models, Animal; D016650:Fluorescein-5-isothiocyanate / Q000031:analogs & derivatives / Q000378:metabolism; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology; D007120:Immunochemistry; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology* / Q000517:prevention & control; D054318:No-Reflow Phenomenon / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012709:Serum Albumin / Q000378:metabolism; D024745:Smooth Muscle Myosins / Q000378:metabolism; D013997:Time Factors; D020257:Ventricular Remodeling
chemical_list: D000199:Actins; D015415:Biomarkers; D003402:Creatine Kinase; D016650:Fluorescein-5-isothiocyanate; D012709:Serum Albumin; D024745:Smooth Muscle Myosins; C518288:FITC-albumin; C498862:Acta2 protein, rat