ABNORMAL IMMUNOSTAINING FOR DYSTROPHIN IN ISOPROTERENOL-INDUCED ACUTEMYOCARDIAL INJURY IN RATS - EVIDENCE FOR CHANGE IN DYSTROPHIN IN THE ABSENCE OF GENETIC-DEFECT

Abnormalities in the gene for Duchenne muscular dystrophy produce skel etal and myocardial changes, by impairing dystrophin production in pat ients with Duchenne and Pecker muscular dystrophy. However, it is not known whether myocardial dystrophin may be altered in patients with ot her heart diseases. To investigate whether changes in myocardial dystr ophin may be induced by acute myocardial injury, the immunostaining pa tterns of myocardial dystrophin were examined, together with those of myocardial actin, in rats with isoproterenol-induced myocardial damage . Hearts were excised at 6, 12, 24 and 48 h, and 1 and 4 weeks after t he subcutaneous administration of 100 mg/kg of isoproterenol, Frozen s erial sections were prepared for haematoxylin and eosin staining, and for immunostaining for dystrophin and actin. The immunostaining patter ns of actin were used as an indicator of cell injury, The myocardial c ells observed were classified into four types, according to staining p attern: normal for both actin and dystrophin (Type 1); normal for acti n, but abnormal for dystrophin (Type 2); abnormal for actin, but norma l for dystrophin (Type 3); and abnormal for both actin and dsytrophin (Type 4). The percentage of myocardial cells with abnormal staining (T ypes 2, 3 and 4) at 6, 12, 24 and 48 h after isoproterenol injection w as 22.4, 12.6, 16.0 and 2.4%, respectively; most cells were Types 3 an d 4. One week after injection or later, no Type 3 or 4 cells were dete cted, while the percentages of Type 2 cells were 2.7% for 1 week and 2 .2% for 4 weeks, significantly higher than the corresponding value in the control group. In conclusion, changes in myocardial dystrophin may occur in isoproterenol-induced myocardial injury in rats. (C) 1997 Ac ademic Press Limited.