The effects of chronic renal failure on cardiac performance and myocardial
morphology were studied in rats: 17 with 5/6 nephrectomy (CRF rats) and 12
with sham operation (controls). Cardiac function was assessed 8 weeks posto
peratively, using the Langendorff technique for an isolated working heart m
odel. After the hemodynamic study the hearts were fixed for electron and li
ght microscopy. In the CRF rats left ventricular systolic pressure was sign
ificantly higher at all preloads (10-20 cmH(2)O) and afterloads (70-90 cmH(
2)O), and left ventricular stroke work was significantly increased at prelo
ad 20 cmH(2)O with afterloads 70 or 90 cmH(2)O. Light microscopy revealed f
ibronecrotic lesions consisting of fibroblastic proliferation with newly fo
rmed collagen interposed between or entrapping degenerative myocytes. The c
hanges were focally distributed, with perivascular accentuation and were mo
st frequent in the basal half of the ventricular wall. Electron microscopy
of non-necrotic myocytes showed intact myocytes, with mitochondria morphome
trically similar in the 2 groups, but a significantly lower incidence of mi
tochondrial granules in the CRF rats. Thus 8 weeks of CRF showed no cardiac
dysfunction associated with the focally distributed fibronecrotic myocardi
al lesions and decrease in mitochondrial granules. The precise mechanism of
the discrepancy between the morphological change and the cardiac function
is unclear. One possible explanation may be that because the pathological c
hanges in the myocardium were focal or mild to moderate, some compensation
mechanism may be involved or it may be the turning point of functional chan
ge from acute renal failure to the chronic state.