title: Vascular rhexis in mice subjected to non-sustained myocardial ischemia and its therapeutic implications.
abstract: We previously described the death of vascular cells (vascular rhexis) following persistent coronary occlusion. The present study was designed to determine whether non-sustained ischemia can initiate vascular rhexis and if so, whether relatively brief ischemic insults are sufficient. C57BL6 mice were subjected to coronary ligation for 15 min or 3 h followed by reperfusion. Soluble fractions of left ventricular (LV) homogenates were obtained 48 h after the onset of transitory coronary occlusion. They were assayed by Western blotting for quantification of alpha smooth muscle actin (α-SMA) and smooth muscle myosin heavy chain (SM-MHC) that we have shown reflect vascular rhexis delineated immunohistochemically. Non-sustained coronary occlusion for 3 h initiated vascular rhexis evident 45 h after reperfusion, but not earlier, as judged from Western blotting of α-SMA and SM-MHC. The number of small- and medium-sized vessels in the previously ischemic zones was reduced at 45 h after reperfusion as well. Thus, vascular rhexis occurs after ischemia as brief as 3 h but evolves slowly and is not evident for 45 h. The delayed disintegration of the vasculature makes it likely that it can be ameliorated by interventions initiated after non-sustained ischemia, rendering it an attractive target for diminution of phenomena such as late negative LV remodeling, and 'no reflow.'
authors.affiliation: Department of Medicine, Cardiovascular Research Institute, University of Vermont, Colchester, 05446, USA.
authors.forename: A K M Tarikuz
authors.initials: AK
authors.lastname: Zaman
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: French
authors.forename: Jeffrey L
authors.initials: JL
authors.lastname: Spees
authors.forename: Azan S
authors.initials: AS
authors.lastname: Binbrek
authors.forename: Burton E
authors.initials: BE
authors.lastname: Sobel
mesh_terms: D000199:Actins / Q000378:metabolism; D042702:Angiopoietin-2 / Q000097:blood; D000818:Animals; D016923:Cell Death; D042783:Endothelial Cells / Q000473:pathology; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology; D006470:Hemorrhage / Q000150:complications / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D051379:Mice; D008810:Mice, Inbred C57BL; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology*; D009203:Myocardial Infarction / Q000097:blood / Q000150:complications / Q000473:pathology; D017202:Myocardial Ischemia / Q000097:blood / Q000150:complications / Q000473:pathology* / Q000628:therapy*; D032389:Myocytes, Smooth Muscle / Q000473:pathology; D018995:Myosin Heavy Chains / Q000378:metabolism; D009336:Necrosis
chemical_list: D000199:Actins; D042702:Angiopoietin-2; D018995:Myosin Heavy Chains