Myocardial ultrastructural alterations in ducklings with isoproterenol-induced cardiotoxicosis.
Fifty-two, 8-week-old, male White Pekin ducklings (Anas platyrhynchos domesticus) were allotted into control (n = 7) and isoproterenol-injected groups (n = 45). One control duck and 5 to 7 isoproterenol-injected (200 mg/kg of body weight) ducklings were euthanatized at postinjection hours (PIH) 1, 12, and 24 and at postinjection days (PID) 2, 4, 7, and 14. The left ventricular myocardium was examined, using electron microscopy. The earliest ultrastructural alteration in damaged myocytes was myofibrillar lysis at PIH 12. At PIH 24, affected myocytes had necrosis with mineralization of mitochondria. By PID 2, macrophages had invaded into areas of myocardial necrosis, mineralization was prominent in myocyte mitochondria, and dedifferentiated myocytes with reduced numbers of myofibrils, increased numbers of polysomes, large nuclei, and prominent nucleoli were first observed. The primary myocardial finding at PID 4, 7, and 14 was 2 populations of sublethally damaged myocytes. One population of injured myocytes had numerous polysomes in the sarcoplasm and large nuclei with prominent nucleoli, indicating attempts at repair of myofibrillar damage. The 2nd population of myocytes with myofibrillar lysis did not have morphologic evidence of myofibrillar repair. Therefore, the sequential ultrastructural alterations of damage and repair induced by isoproterenol in the duckling myocardium provided model for comparative studies of cardiotoxicity.
D000818:Animals; D009202:Cardiomyopathies / Q000139:chemically induced / Q000473:pathology*; D004372:Ducks; D007545:Isoproterenol; D008297:Male; D008854:Microscopy, Electron; D009206:Myocardium / Q000473:pathology / Q000648:ultrastructure*; D009336:Necrosis
D007545:Isoproterenol