Document Detail


A novel strategy for increasing wall thickness of coronary venules prior to retroperfusion.
MedLine Citation:
PMID:  16603695     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The sudden exposure of veins to arterial pressures during coronary venous retroperfusion may cause rupture of small venules. Our rationale is to first occlude the coronary vein, which will cause an increase in pressure intermediate to arterial and venous values, and hence lead to remodeling and increased wall thickness of the veins prior to retroperfusion. To accomplish this objective, five pigs were subjected to left anterior descending (LAD) vein ligation while six pigs served as sham. Myocardial tissue samples were obtained from the area adjacent to the LAD vein at four transmural locations of the left ventricular free wall: epicardial surface, subepicardium, midmyocardium, and endocardium. Arterioles and venules from the experimental and sham control groups were photographed, and the following measurements were made: inner and outer circumferences, inner and outer areas, major and minor diameters, and intima-media thickness. Each vessel was categorized in four different orders according to lumen diameter. Our results show that intima-media thickness was larger in the experimental group in all four regions of the heart and in all four orders of the vessels, although venules from the epicardial region showed the largest increase in thickness. The intima-media thickness-to-radius ratio was also larger in the experimental group and decreased from epicardial to endocardial region of the heart and from order 1 to order 4 of the vessels. The present study provides a rationale for the development of coronary retroperfusion strategy that avoids vessel rupture and hemorrhage in the postcapillary venules.
Authors:
Jenny Susana Choy; Ghassan S Kassab
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2006-04-07
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  291     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2006 Aug 
Date Detail:
Created Date:  2006-07-14     Completed Date:  2006-08-18     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H972-8     Citation Subset:  IM    
Affiliation:
Dept. of Biomedical Engineering, Univ. of California, Irvine, 204 Rockwell Engineering Center, Irvine, CA 92697-2715, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arterioles / cytology,  physiology
Coronary Vessels / anatomy & histology,  physiology*
Edema / pathology
Endocardium / cytology,  physiology
Hemorrhage / pathology
Ligation
Myocardium / cytology
Perfusion
Pericardium / cytology,  physiology
Swine
Ventricular Remodeling
Venules / anatomy & histology,  physiology
Grant Support
ID/Acronym/Agency:
2-R01-HL-055554-06/HL/NHLBI NIH HHS

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


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