Abstract
The present study focuses on the sequential development of myocardial ultrastructural changes produced by oxygen radicals. Isolated rat hearts were perfused with oxygen radicals, generated by hypoxanthine and xanthine oxidase, for 5 and 10 min followed by a 35-min recovery period. The frequency of, and the association between, ultrastructural changes were examined by semiquantitative morphometry using the micrograph as unit. In each micrograph sarcolemmal, myocytic mitochondrial and myofilamental alterations were observed and graded as slight, moderate or severe. The myocytic nucleus and the endothelial cells were scored as normal or altered. Five min group: Among the cellular organelles examined, the myocytic mitochondria showed the highest frequency of alteration (in 15.3% of the micrographs). Among the grades of myocytic mitochondrial ultrastructural changes, slight alterations predominated (12.5%). Slight myocytic mitochondrial alterations were not significantly associated with the occurrence of ultrastructural changes of other cellular organelles. Endothelial ultrastructural alterations were sparse (1.5%). Ten min group: The frequency of altered organelles was greater when compared to the 5 min group. The myocytic mitochondria were still the most frequently altered component (61.7%), and myocytic mitochondrial ultrastructural alterations of all grades were strongly associated with the occurrence of other myocytic ultrastructural changes. In conclusion, the present study showed that myocytic mitochondrial changes predominated after both 5 and 10 min of oxygen radical exposure followed by recovery. In the 5 min group slight myocytic mitochondrial changes appeared independent of other myocardial changes, but in the 10 min group, however, myocytic mitochondrial changes were strongly associated with other myocardial ultrastructural changes. These results indicate that myocytic mitochondria are especially vulnerable to oxygen radicals, and further that myocytic mitochondrial ultrastructural changes may be a crucial step in the development of oxygen radical-induced myocardial damage.
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