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Myocardial morphology and cardiac function in rats with renal failure

Hatori, N. ; Havu, N. ; Hofman-Bang, C. ; Clyne, N. LU orcid and Pehrsson, S. K. (2000) In Japanese Circulation Journal 64(8). p.606-610
Abstract

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 postoperatively, using the Langendorff technique for an isolated working heart model. After the hemodynamic study the hearts were fixed for electron and light microscopy. In the CRF rats left ventricular systolic pressure was significantly higher at all preloads (10-20 cmH2O) and afterloads (70-90 cmH2O), and left ventricular stroke work was significantly increased at preload 20 cmH2O with afterloads 70 or 90 cmH2O. Light microscopy revealed fibronecrotic lesions consisting of... (More)

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 postoperatively, using the Langendorff technique for an isolated working heart model. After the hemodynamic study the hearts were fixed for electron and light microscopy. In the CRF rats left ventricular systolic pressure was significantly higher at all preloads (10-20 cmH2O) and afterloads (70-90 cmH2O), and left ventricular stroke work was significantly increased at preload 20 cmH2O with afterloads 70 or 90 cmH2O. Light microscopy revealed fibronecrotic lesions consisting of fibroblastic proliferation with newly formed collagen interposed between or entrapping degenerative myocytes. The changes were focally distributed, with perivascular accentuation and were most frequent in the basal half of the ventricular wall. Electron microscopy of non-necrotic myocytes showed intact myocytes, with mitochondria morphometrically similar in the 2 groups, but a significantly lower incidence of mitochondrial granules in the CRF rats. Thus 8 weeks of CRF showed no cardiac dysfunction associated with the focally distributed fibronecrotic myocardial 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 changes in the myocardium were focal or mild to moderate, some compensation mechanism may be involved or it may be the turning point of functional change from acute renal failure to the chronic state.

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author
; ; ; and
publishing date
type
Contribution to journal
publication status
published
keywords
Hemodynamics, Mitochondrial granules, Rat morphology, Renal failure
in
Japanese Circulation Journal
volume
64
issue
8
pages
5 pages
publisher
Japanese Circulation Society
external identifiers
  • pmid:10952158
  • scopus:0033857135
ISSN
0047-1828
DOI
10.1253/jcj.64.606
language
English
LU publication?
no
id
1f79dbca-e226-4ad2-8434-5dc349404e73
date added to LUP
2016-08-30 21:53:57
date last changed
2024-01-04 11:41:19
@article{1f79dbca-e226-4ad2-8434-5dc349404e73,
  abstract     = {{<p>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 postoperatively, using the Langendorff technique for an isolated working heart model. After the hemodynamic study the hearts were fixed for electron and light microscopy. In the CRF rats left ventricular systolic pressure was significantly higher at all preloads (10-20 cmH<sub>2</sub>O) and afterloads (70-90 cmH<sub>2</sub>O), and left ventricular stroke work was significantly increased at preload 20 cmH<sub>2</sub>O with afterloads 70 or 90 cmH<sub>2</sub>O. Light microscopy revealed fibronecrotic lesions consisting of fibroblastic proliferation with newly formed collagen interposed between or entrapping degenerative myocytes. The changes were focally distributed, with perivascular accentuation and were most frequent in the basal half of the ventricular wall. Electron microscopy of non-necrotic myocytes showed intact myocytes, with mitochondria morphometrically similar in the 2 groups, but a significantly lower incidence of mitochondrial granules in the CRF rats. Thus 8 weeks of CRF showed no cardiac dysfunction associated with the focally distributed fibronecrotic myocardial 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 changes in the myocardium were focal or mild to moderate, some compensation mechanism may be involved or it may be the turning point of functional change from acute renal failure to the chronic state.</p>}},
  author       = {{Hatori, N. and Havu, N. and Hofman-Bang, C. and Clyne, N. and Pehrsson, S. K.}},
  issn         = {{0047-1828}},
  keywords     = {{Hemodynamics; Mitochondrial granules; Rat morphology; Renal failure}},
  language     = {{eng}},
  number       = {{8}},
  pages        = {{606--610}},
  publisher    = {{Japanese Circulation Society}},
  series       = {{Japanese Circulation Journal}},
  title        = {{Myocardial morphology and cardiac function in rats with renal failure}},
  url          = {{http://dx.doi.org/10.1253/jcj.64.606}},
  doi          = {{10.1253/jcj.64.606}},
  volume       = {{64}},
  year         = {{2000}},
}