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Impaired myocardial function following chronic cobalt exposure in an isolated rat heart model

Haga, Y.; Clyne, N. LU ; Hatori, N.; Hoffman-Bang, C.; Pehrsson, S. K. and Rydén, L. (1996) In Trace Elements and Electrocytes 13(2). p.69-74
Abstract

Objectives: The effects of chronic cobalt exposure were studied in an isolated working model in a modified Langendorff preparation. Methods: Thirty-six rats were given either a conventional (control group) or a cobalt supplemented diet (cobalt group; 40 mg CoSO4 x 7 H2O/kg body weight/day). Sixteen of the animals were sacrificed and their hearts were excised after 16 weeks and the remaining 20 after 24 weeks. Ventricular function was determined on a working-mode Langendorff's circuit (16 weeks: control n = 8, cobalt n = 7, 24 weeks: control n = 9, cobalt n = 8) at different afterloads (70 and 90 cm H2O) and preloads (10, 15 and 20 cm H2O). Myocardial cobalt concentration was determined in 20... (More)

Objectives: The effects of chronic cobalt exposure were studied in an isolated working model in a modified Langendorff preparation. Methods: Thirty-six rats were given either a conventional (control group) or a cobalt supplemented diet (cobalt group; 40 mg CoSO4 x 7 H2O/kg body weight/day). Sixteen of the animals were sacrificed and their hearts were excised after 16 weeks and the remaining 20 after 24 weeks. Ventricular function was determined on a working-mode Langendorff's circuit (16 weeks: control n = 8, cobalt n = 7, 24 weeks: control n = 9, cobalt n = 8) at different afterloads (70 and 90 cm H2O) and preloads (10, 15 and 20 cm H2O). Myocardial cobalt concentration was determined in 20 rats given a conventional or a cobalt supplemented diet on the same protocol (16 weeks: control n = 4, cobalt n = 5, 24 weeks: control n = 5, cobalt n = 6). Results: Myocardial cobalt concentration significantly increased after 16 and 24 weeks of cobalt exposure as compared with those respective controls. Body weight was significantly lower in the cobalt groups than the corresponding control groups. Sixteen weeks of cobalt exposure did not significantly affect left ventricular function. After 24 weeks of cobalt exposure we found myocardial dysfunction characterized by a significantly reduced left ventricular pressure rise and decay (small absolute values of positive and negative dp/dt) in the cobalt group. At an afterload of 70 cm H2O maximal positive dp/dt was significantly higher in the control group only for a preload of 10 cm H2O. At an afterload of 90 cm H2O it was significantly higher in the control group for preloads of 10 and 15 cm H2O. The differences did not reach statistical significance in other settings. Maximal negative dp/dt in the control group at an afterload of 70 cm H2O was significantly lower than that in the cobalt group for preloads of 10 and 15 cm H2O while it was significantly lower for all preload levels at an afterload of 90 cm H2O. In general, dysfunction was more pronounced at low preloads. The ratio of left ventricular weight to body weight at 24 weeks was significantly higher in the cobalt group. Both cobalt groups had a significantly higher coronary flow in proportion to body weight as compared to the respective control groups. Conclusions: Chronic cobalt exposure caused poor weight gain, left ventricular hypertrophy and impaired left ventricular systolic and diastolic functions in an isolated working rat heart model. The mechanism remains uncertain, although left ventricular hypertrophy seemed to be an important contributory factor.

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author
publishing date
type
Contribution to journal
publication status
published
keywords
Cobalt, Myocardial function, Rat model
in
Trace Elements and Electrocytes
volume
13
issue
2
pages
6 pages
publisher
Dustri-Verlag Dr. Karl Feistle
external identifiers
  • Scopus:0029991130
ISSN
0946-2104
language
English
LU publication?
no
id
927d95d7-e25a-4370-8b1f-2bc3f3e6c798
date added to LUP
2016-08-30 22:01:43
date last changed
2016-09-16 15:09:50
@misc{927d95d7-e25a-4370-8b1f-2bc3f3e6c798,
  abstract     = {<p>Objectives: The effects of chronic cobalt exposure were studied in an isolated working model in a modified Langendorff preparation. Methods: Thirty-six rats were given either a conventional (control group) or a cobalt supplemented diet (cobalt group; 40 mg CoSO<sub>4</sub> x 7 H<sub>2</sub>O/kg body weight/day). Sixteen of the animals were sacrificed and their hearts were excised after 16 weeks and the remaining 20 after 24 weeks. Ventricular function was determined on a working-mode Langendorff's circuit (16 weeks: control n = 8, cobalt n = 7, 24 weeks: control n = 9, cobalt n = 8) at different afterloads (70 and 90 cm H<sub>2</sub>O) and preloads (10, 15 and 20 cm H<sub>2</sub>O). Myocardial cobalt concentration was determined in 20 rats given a conventional or a cobalt supplemented diet on the same protocol (16 weeks: control n = 4, cobalt n = 5, 24 weeks: control n = 5, cobalt n = 6). Results: Myocardial cobalt concentration significantly increased after 16 and 24 weeks of cobalt exposure as compared with those respective controls. Body weight was significantly lower in the cobalt groups than the corresponding control groups. Sixteen weeks of cobalt exposure did not significantly affect left ventricular function. After 24 weeks of cobalt exposure we found myocardial dysfunction characterized by a significantly reduced left ventricular pressure rise and decay (small absolute values of positive and negative dp/dt) in the cobalt group. At an afterload of 70 cm H<sub>2</sub>O maximal positive dp/dt was significantly higher in the control group only for a preload of 10 cm H<sub>2</sub>O. At an afterload of 90 cm H<sub>2</sub>O it was significantly higher in the control group for preloads of 10 and 15 cm H<sub>2</sub>O. The differences did not reach statistical significance in other settings. Maximal negative dp/dt in the control group at an afterload of 70 cm H<sub>2</sub>O was significantly lower than that in the cobalt group for preloads of 10 and 15 cm H<sub>2</sub>O while it was significantly lower for all preload levels at an afterload of 90 cm H<sub>2</sub>O. In general, dysfunction was more pronounced at low preloads. The ratio of left ventricular weight to body weight at 24 weeks was significantly higher in the cobalt group. Both cobalt groups had a significantly higher coronary flow in proportion to body weight as compared to the respective control groups. Conclusions: Chronic cobalt exposure caused poor weight gain, left ventricular hypertrophy and impaired left ventricular systolic and diastolic functions in an isolated working rat heart model. The mechanism remains uncertain, although left ventricular hypertrophy seemed to be an important contributory factor.</p>},
  author       = {Haga, Y. and Clyne, N. and Hatori, N. and Hoffman-Bang, C. and Pehrsson, S. K. and Rydén, L.},
  issn         = {0946-2104},
  keyword      = {Cobalt,Myocardial function,Rat model},
  language     = {eng},
  number       = {2},
  pages        = {69--74},
  publisher    = {ARRAY(0x9919340)},
  series       = {Trace Elements and Electrocytes},
  title        = {Impaired myocardial function following chronic cobalt exposure in an isolated rat heart model},
  volume       = {13},
  year         = {1996},
}