Ligation of the coronary artery of rabbit hearts produced ultrastructural evidence of ischemic damage that progressed over a 2-hour period. Changes indicative of irreversible necrosis in myocytes (margination of nuclear chromatin, near total glycogen depletion, and development of osmiophilic mitochondria densities) appeared at 45 to 60 minutes, and by 2 hours all myocytes in the center of the ischemic area appeared dead. Lysosomal dense and residual bodies were observed most frequently in the paranuclear regions of myocytes, and no evidence of rupture of lysosomal membranes was observed over the 1st hour; after 2 hours, however, lysosomal profiles were rarely present. In myocytes, acid phosphatase, arylsulfatase, and thioacetic acid reaction products were normally present primarily in the Golgi complex and GERL, with little activity in dense or residual bodies. Little change was noted until after 1 hour of ischemia, when reaction products were observed in the cytosol as well as in organelles. In contrast to myocytes, interstitial cells (which normally contained many positively staining vacuoles of multiple types) developed hypertrophied Golgi and numerous secondary lysosomes after 30 minutes of ischemia, with increased reaction products in the Golgi complex and GERL. Longer periods of ischemia failed to alter further the appearance of interstitial cells. It is concluded that: lysosomal changes during ischemia are different in interstitial cells than in cardiac myocytes; myocytic lysosomes appear structurally intact for 1 hour but disappear by 2 hours of ischemia; and definitive ultrastructural evidence of myocytic necrosis precedes obvious changes in myocytic lysosomal structure but follows changes in lysosomal properties as measured biochemically and immunohistochemically.
|Original language||English (US)|
|Number of pages||12|
|State||Published - Dec 1 1978|
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Molecular Biology
- Cell Biology