Document Detail


Oxygen-dependent quenching of phosphorescence used to characterize improved myocardial oxygenation resulting from vasculogenic cytokine therapy.
MedLine Citation:
PMID:  21292844     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study evaluates a therapy for infarct modulation and acute myocardial rescue and utilizes a novel technique to measure local myocardial oxygenation in vivo. Bone marrow-derived endothelial progenitor cells (EPCs) were targeted to the heart with peri-infarct intramyocardial injection of the potent EPC chemokine stromal cell-derived factor 1α (SDF). Myocardial oxygen pressure was assessed using a noninvasive, real-time optical technique for measuring oxygen pressures within microvasculature based on the oxygen-dependent quenching of the phosphorescence of Oxyphor G3. Myocardial infarction was induced in male Wistar rats (n = 15) through left anterior descending coronary artery ligation. At the time of infarction, animals were randomized into two groups: saline control (n = 8) and treatment with SDF (n = 7). After 48 h, the animals underwent repeat thoracotomy and 20 μl of the phosphor Oxyphor G3 was injected into three areas (peri-infarct myocardium, myocardial scar, and remote left hindlimb muscle). Measurements of the oxygen distribution within the tissue were then made in vivo by applying the end of a light guide to the beating heart. Compared with controls, animals in the SDF group exhibited a significantly decreased percentage of hypoxic (defined as oxygen pressure ≤ 15.0 Torr) peri-infarct myocardium (9.7 ± 6.7% vs. 21.8 ± 11.9%, P = 0.017). The peak oxygen pressures in the peri-infarct region of the animals in the SDF group were significantly higher than the saline controls (39.5 ± 36.7 vs. 9.2 ± 8.6 Torr, P = 0.02). This strategy for targeting EPCs to vulnerable peri-infarct myocardium via the potent chemokine SDF-1α significantly decreased the degree of hypoxia in peri-infarct myocardium as measured in vivo by phosphorescence quenching. This effect could potentially mitigate the vicious cycle of myocyte death, myocardial fibrosis, progressive ventricular dilatation, and eventual heart failure seen after acute myocardial infarction.
Authors:
William Hiesinger; Sergei A Vinogradov; Pavan Atluri; J Raymond Fitzpatrick; John R Frederick; Rebecca D Levit; Ryan C McCormick; Jeffrey R Muenzer; Elaine C Yang; Nicole A Marotta; John W MacArthur; David F Wilson; Y Joseph Woo
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-02-03
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  110     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-05-12     Completed Date:  2011-09-30     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1460-5     Citation Subset:  IM    
Affiliation:
Division of Cardiovascular Surgery, Department of Surgery, University of Pennsylvania, Philadelphia, PA 19104, USA.
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MeSH Terms
Descriptor/Qualifier:
Angiogenesis Inducing Agents / therapeutic use
Animals
Chemokine CXCL12 / therapeutic use*
Luminescent Measurements / methods*
Male
Metalloporphyrins / pharmacokinetics*
Myocardial Infarction / drug therapy*,  metabolism*,  pathology
Myocardium / metabolism*
Oxygen / metabolism*
Rats
Rats, Wistar
Tissue Distribution
Treatment Outcome
Grant Support
ID/Acronym/Agency:
1K08-HL-072812/HL/NHLBI NIH HHS; 1R01-HL-089315-01/HL/NHLBI NIH HHS; T32-HL-007843-13/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Angiogenesis Inducing Agents; 0/Chemokine CXCL12; 0/Metalloporphyrins; 0/oxyphor G2; 7782-44-7/Oxygen
Comments/Corrections

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


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