Male Sprague-Dawley rats aged 3 weeks that were maintained on an iron-
deficient diet for 4-5 weeks developed severe anemia with markedly red
uced hemoglobin levels (3.94 +/- 0.14 Hb g% versus controls 12.9 +/- 0
.11 Hb g%). Iron-deficiency resulted in marked cardiac hypertrophy (ca
rdiomegaly). On sacrifice, the hearts were processed for light and tra
nsmission electron microscopy. The major ultrastructural changes were
found in the hypertrophied left ventricle and left papillary muscles.
Iron-deficiency caused marked edema in myocytes, sarcomeres were out o
f register, and degeneration and discontinuities in myofilaments were
common. Iron-deficiency resulted in the enlargement of the interfibril
lar mitochondria, changes in the matrix and the formation of electrond
ense amorphous bodies. The ultrastructural changes in myocytes in resp
onse to experimental iron-deficiency were similar to those described b
y others in cases of experimental ischemia or hypoxia. Mitochondrial c
hanges were also found in the atria of iron-deficient rats. Quantitati
ve cytochemical measurement of succinate dehydrogenase activity was de
termined and was shown to be substantially reduced in the iron-deficie
nt heart. In severely iron-deficient rats restored to a normal iron-su
fficient diet for two weeks, hemoglobin levels recovered, however the
myocytes of the hypertrophied left ventricles and papillary muscles co
ntinued to show severe degenerative changes.