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Myocardial Oxygenation in Infarcted Hearts Predicted by a Microvascular Transport Model
Author(s) -
Wang Bin,
Scott Robert C,
Pattillo Christopher B,
Pandian B. Prabhakar,
Sundaram Shankar,
Kiani Mohammad F
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a713
Subject(s) - cardiology , hypoxia (environmental) , oxygenation , myocardial infarction , heart failure , medicine , ligation , oxygen transport , myocyte , biomedical engineering , oxygen , chemistry , organic chemistry
Chronic heart failure is most commonly due to ischemic cardiomyopathy with previous myocardial infarction (MI). Rebuilding lost myocardium to prevent heart failure mandates a neovasculature able to nourish new cardiomyocytes. Previously we have used a series of novel techniques adapted from field of tumor biology to directly measure the scar neovasculature at 1–4 weeks post‐MI in rats following left coronary artery ligation and with a view towards its ability to deliver and exchange oxygen (AJP, 2005, 289(1):H108–H113). In this study, we have developed an anatomically and functionally realistic mathematical model of oxygen transport in cardiac tissue to help us in deciding what angiogenic strategies should be used to rebuild the neovasculature. The model is constructed to match the microvascular anatomy of cardiac tissue based on available morphometric image and is used to predict tissue hypoxia in the MI rat hearts. Our results indicated that our model predictions match experimentally measured tissue hypoxia values, and can be used to predict distributions of oxygen concentration in the hearts, which is mainly dependant on the density of perfused vessels in the heart tissue. From the minimal oxygen concentration needed by myocytes to maintain their normal function, we can calculate the number of perfused vessels needed in the heart to avoid hypoxia; this can guide our work in rebuilding vascular networks using targeted delivery of pro‐angiogenic compounds to infarcted myocardium. Supported by AHA.