title: Remodeling of myocyte dimensions in hypertrophic and atrophic rat hearts.
abstract: Changes in hemodynamic load cause alterations in cardiac myocyte size, with regional variations in myocyte size distribution possible within the ventricular wall. We studied regional changes in cellular dimensions and their distribution in two models of cardiac hypertrophy and in cardiac atrophy in the rat. Combined volume-pressure overload was produced by 3,3',5-triiodo-L-thyronine (T3) treatment; atrophy was produced by heterotopic isotransplantation. Our previous data from long-term pressure overload after aortic constriction were used for comparison. Isolated ventricular myocytes were obtained after in vitro coronary perfusion with collagenase. Cell volume and its distribution were determined; cell length was directly measured by image analysis, and cross-sectional area was estimated from the cell volume/cell length ratio, assuming a cylindrical model. Myocyte hypertrophy resulting from hyperthyroidism and aortic constriction was primarily due to increased cross-sectional area. In both cases, the relative response was greater in the right ventricle than in the left ventricle. Within the left ventricle, epimyocardial myocytes enlarged the most. Aortic constriction and T3 treatment predominantly increased the size of smaller myocytes. Heterogeneity in myocyte size increased after constriction but remained relatively unaffected after T3 treatment. Atrophy of left ventricular myocytes was due to a proportional decrease in cell length and cross-sectional area, with the greatest decrease in the left ventricular endomyocardium. Atrophy predominantly affected larger myocytes, resulting in a more homogeneous overall population of smaller myocytes. We conclude that various alterations in load lead to diverse remodeling in the myocyte population throughout the ventricular wall. In general, smaller myocytes show the highest growth potential, whereas larger myocytes exhibit the highest potential to atrophy.
authors.affiliation: Department of Physiology, University of Ottawa Health Sciences Center, Ontario, Canada.
authors.forename: S E
authors.initials: SE
authors.lastname: Campbell
authors.forename: B
authors.initials: B
authors.lastname: Korecky
authors.forename: K
authors.initials: K
authors.lastname: Rakusan
mesh_terms: D000818:Animals; D001011:Aorta / Q000502:physiology; D001284:Atrophy; D001835:Body Weight / Q000187:drug effects; D006332:Cardiomegaly / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D006321:Heart / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology*; D016027:Heart Transplantation / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D008955:Models, Cardiovascular; D009206:Myocardium / Q000473:pathology*; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D011917:Rats, Inbred Lew; D011919:Rats, Inbred Strains; D012016:Reference Values; D014284:Triiodothyronine / Q000494:pharmacology
chemical_list: D014284:Triiodothyronine