| The impact of pressure overload on coronary vascular changes following myocardial infarction in rats. | |
MedLine Citation:
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PMID: 23275620 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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This study investigates the impact of pressure overload on vascular changes after myocardial infarction (MI) in rats. To evaluate the effect of pressure overload, MI was induced in three groups: 1) left coronary artery ligation for 1 mo (MI-1m), 2) ischemia 30 min/reperfusion for 1 mo (I/R-1m), and 3) ischemia-reperfusion (I/R) was performed after pressure overload induced by aortic banding for 2 mo; 1 mo post-I/R, aortic constriction was released (Ab+I/R+DeAb). Heart function was assessed by echocardiography and in vivo hemodynamics. Resin casting and three-dimensional imaging with microcomputed tomography were used to characterize changes in coronary vasculature. TTC (triphenyltetrazohum chloride) staining and Masson's Trichrome were conducted in parallel experiments. In normal rats, MI induced by I/R and permanent occlusion was transmural or subendocardial. Occluded arterial branches vanished in MI-1m rats. A short residual tail was retained, distal to the occluded site in the ischemic area in I/R-1m hearts. Vascular pathological changes in transmural MI mostly occurred in ischemic areas and remote vasculature remained normal. In pressure overloaded rats, I/R injury induced a sub-MI in which ischemia was transmural, but myocardium in the involved area had survived. The ischemic arterial branches were preserved even though the capillaries were significantly diminished and the pathological changes were extended to remote areas, characterized by fibrosis, atrial thrombus, and pulmonary edema in the Ab+I/R+DeAb group. Pressure overload could increase vascular tolerance to I/R injury, but also trigger severe global ventricular fibrosis and results in atrial thrombus and pulmonary edema. |
Authors:
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Jiqiu Chen; Artiom Petrov; Elisa Yaniz-Galende; Lifan Liang; Hans J de Haas; Jagat Narula; Roger J Hajjar |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S. Date: 2012-12-28 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 304 ISSN: 1522-1539 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2013 Mar |
Date Detail:
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Created Date: 2013-03-04 Completed Date: 2013-04-18 Revised Date: 2013-05-06 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H719-28 Citation Subset: IM |
Affiliation:
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Cardiovascular Research Center, Mount Sinai School of Medicine, New York, NY 10029, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Capillaries / physiology, radiography, ultrasonography Cardiac Imaging Techniques Coronary Circulation / physiology* Coronary Vessels / physiology*, radiography, ultrasonography Disease Models, Animal Echocardiography Fibrosis / diagnosis, physiopathology Heart Failure / diagnosis, physiopathology* Male Myocardial Infarction / diagnosis, physiopathology* Myocardial Reperfusion Injury / diagnosis, physiopathology Myocardium / pathology Rats Rats, Sprague-Dawley Tomography, X-Ray Computed Ventricular Pressure / physiology* |
| Grant Support | |
ID/Acronym/Agency:
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HHSN268201000045C/HL/NHLBI NIH HHS; HHSN268201000045C//PHS HHS; HL-088434/HL/NHLBI NIH HHS; P20 HL100396/HL/NHLBI NIH HHS; P20-HL-100396/HL/NHLBI NIH HHS; P50-HL-112324/HL/NHLBI NIH HHS; R01 HL080498/HL/NHLBI NIH HHS; R01 HL083156/HL/NHLBI NIH HHS; R01 HL088434/HL/NHLBI NIH HHS; R01-HL-093183/HL/NHLBI NIH HHS |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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