title: A semi-immobilization of a partial auricle induces hypertrophy and ultrastructural alteration of cardiomyocytes.
abstract: Semi-immobilization of a partial area of the ventral edge, lateral epicardium of the left auricle (ventrolateral of left auricle), by using quick adhesion glue induces moderate hypertrophy of myocytes with an average increase of 34% in cross-sectional area. Intercellular connective tissues increased, and cellular sizes varied markedly. The ultrastructure of immobilized (semi-immobilized) myocytes commonly exhibited degenerating features in myofibrils, various cytoplasmic organelles including mitochondrial cristae and sarcoplasmic reticulum (SR) were disrupted, and T-tubules disappeared. Z-line streaming and widening (hypertrophic Z-line, rod bodies) and increase of metabolic particle deposition are typical phenomena in addition to intercalated disc (Id) disorganization. The results suggest that semi-immobilization of the auricle induces hypertrophy of myocytes in association with degeneration and disruption of myofibrils and other cytoplasmic organelles, and an increase of intercellular connective tissues, rather than increase of myofibril mass. This is the first study to immobilize only a part of the heart rather than the whole animal. Our results using artificial immobilization of cardiac myocytes were extremely significant since the structural alterations obtained were similar to that observed in cardiomyopathies. This suggests that myocytes progressing to heart failure are also subjected to inhibition of movement. Therefore, this experiment may prove very useful as a model for studying the functional effect of heart failure observed in cardiomyopathy.
authors.affiliation: Department of Veterinary Surgery, Azabu University, Kanagawa, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Muto
authors.forename: Y
authors.initials: Y
authors.lastname: Wakao
authors.forename: M
authors.initials: M
authors.lastname: Morimoto
authors.forename: W
authors.initials: W
authors.lastname: Klomkleaw
authors.forename: G A
authors.initials: GA
authors.lastname: Fuller
authors.forename: T
authors.initials: T
authors.lastname: Nakayama
authors.forename: T
authors.initials: T
authors.lastname: Oba
authors.forename: Y
authors.initials: Y
authors.lastname: Kasashima
authors.forename: R L
authors.initials: RL
authors.lastname: Hamlin
authors.forename: M
authors.initials: M
authors.lastname: Yamaguchi
mesh_terms: D019412:Anatomy, Cross-Sectional; D000818:Animals; D016275:Atrial Function; D006332:Cardiomegaly / Q000209:etiology* / Q000473:pathology*; D004195:Disease Models, Animal; D004285:Dogs; D006325:Heart Atria / Q000473:pathology; D007103:Immobilization; D008854:Microscopy, Electron; D008955:Models, Cardiovascular; D009206:Myocardium / Q000166:cytology* / Q000648:ultrastructure*; D010210:Papillary Muscles / Q000166:cytology* / Q000473:pathology* / Q000648:ultrastructure; D012519:Sarcoplasmic Reticulum / Q000648:ultrastructure