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QUANTIFICATION OF CARDIAC FIBROSIS BY COLOUR‐SUBTRACTIVE COMPUTER‐ASSISTED IMAGE ANALYSIS
Author(s) -
Gaspard Gerard J,
Pasumarthi Kishore BS
Publication year - 2008
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2008.04930.x
Subject(s) - cardiac fibrosis , fibrosis , myocardial fibrosis , medicine , cardiology , pathology
SUMMARY1 Quantification of fibrosis is a key parameter in the assessment of the severity of cardiovascular disease and efficacy of future candidate therapies. Computer‐assisted methods are frequently used to assess cardiac fibrosis in several experimental models. A brief survey indicated that there is a clear dearth of literature outlining detailed methodologies for computer‐based assessment of cardiac fibrosis. The purpose of the present study was to provide a reliable method for a systematic assessment of cardiac fibrosis. 2 We induced cardiac fibrosis by isoproterenol (ISO) infusion in adult CD1 male mice and quantified fibrosis using a recently developed colour‐subtractive computer‐assisted image analysis (CS‐CAIA) technique. Here, we provided a detailed description of our methodology to facilitate its wider use by other researchers. 3 We showed that the severity of ISO‐induced cardiac fibrosis was similar in the apex, mid‐ventricular ring and base of the adult CD1 mouse heart. In contrast with other species, such as rats and dogs, we found that uniform expression of b 1 ‐adrenoceptors between different regions in CD1 mouse hearts correlated well with uniform induction of cardiac fibrosis. 4 A previous study found a negative correlation between levels of myocardial fibrosis and the degree of cardiac hypertrophy in ISO‐treated Wistar rats. In contrast, we found a similar degree of cardiac fibrosis in our ISO‐treated CD1 mice. 5 Our results suggest that CD1 mice are an ideal model system to study catecholamine‐induced cardiac remodelling, as well as to screen candidate antifibrotic agents for future therapies.