Document Detail


Coronary vascular injury after transient coronary artery occlusion.
MedLine Citation:
PMID:  8231114     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Microvascular function was examined in dog hearts subjected to transient coronary artery occlusion. EXPERIMENTAL DESIGN: Temporary coronary artery occlusion (15 or 30 minutes) followed by prolonged reperfusion (24 to 72 hours) was performed in dogs. Myocardial blood flow (radioactive microspheres), vascular permeability (human serum albumin uptake), and apparent vascular volume (radioactively labeled erythrocytes) were used as measures of vascular function. Myeloperoxidase was used as a measure of leukocyte uptake. Free radical formation was measured by electron spin resonance using a spin trapping agent (phenyl N-tert-butylnitrone). RESULTS: A 30-minute occlusion followed by reperfusion produced prolonged hyperemia, increased vascular permeability, increased apparent vascular volume, and increased leukocyte uptake. Extravasation of red blood cells and carbon black was present within the coronary artery distribution. The altered vascular function was temporally correlated with prolonged leukocyte uptake and free radical production, returning to control values only at 72 hours. A 15-minute occlusion increased vascular permeability at 24 hours, without altering myocardial blood flow or apparent vascular volume. Transmural myocardial leukocyte accumulation after a 15-minute occlusion was minimal in the absence of myocardial infarction or other histologic alterations. Active free radical formation was minimal at 24 hours, with a return of vascular permeability to control values at 48 hours. CONCLUSIONS: The data demonstrate prolonged dysfunction of the coronary microvasculature after a transient 30-minute occlusion of the left anterior descending coronary artery. The prolonged injury is associated temporally with leukocyte uptake and free radical formation in the presence of minimal infarction. A transient 15-minute occlusion produces a different pattern of vascular dysfunction with an abbreviated duration (24 hours), not associated with myocardial necrosis, extensive leukocyte uptake, nor prolonged free radical formation.
Authors:
E Patterson; R D Burow; C Y Hung; B J Scherlag
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Laboratory investigation; a journal of technical methods and pathology     Volume:  69     ISSN:  0023-6837     ISO Abbreviation:  Lab. Invest.     Publication Date:  1993 Oct 
Date Detail:
Created Date:  1993-11-29     Completed Date:  1993-11-29     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0376617     Medline TA:  Lab Invest     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  471-82     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, University of Oklahoma Health Sciences Center, Oklahoma City.
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MeSH Terms
Descriptor/Qualifier:
Animals
Capillary Permeability
Coronary Circulation*
Coronary Vessels / pathology*,  physiology*,  radionuclide imaging
Cyclic N-Oxides
Dogs
Electron Spin Resonance Spectroscopy
Free Radicals / metabolism
Humans
Leukocytes / physiology
Microcirculation / pathology*,  radionuclide imaging
Nitrogen Oxides
Papillary Muscles / cytology,  pathology
Peroxidase / metabolism
Reperfusion
Serum Albumin / metabolism
Spin Labels
Technetium Tc 99m Aggregated Albumin / diagnostic use
Time Factors
Grant Support
ID/Acronym/Agency:
GM-36512/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Cyclic N-Oxides; 0/Free Radicals; 0/Nitrogen Oxides; 0/Serum Albumin; 0/Spin Labels; 0/Technetium Tc 99m Aggregated Albumin; 3376-24-7/phenyl-N-tert-butylnitrone; EC 1.11.1.7/Peroxidase
Comments/Corrections
Comment In:
Lab Invest. 1994 Jun;70(6):953-4   [PMID:  7516987 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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