Functional consequences of acute collagen degradation studied in crystalloid perfused rat hearts

K. Todaka, T. Jiang, J. T. Chapman, A. Gu, S. M. Zhu, E. Herzog, J. S. Hochman, S. F. Steinberg, D. Burkhoff

研究成果: ジャーナルへの寄稿記事

13 引用 (Scopus)

抄録

Objectives: The impact of acute collagen disruption by the disulfide donor, 5,5'-dithio-2-nitrobenzoic acid (DTNB) on ventricular properties was tested in rat hearts. Methods: Collagen was degraded acutely in 13 isolated, isovolumically contracting rat hearts by perfusion with 1 mM DTNB added to Krebs Henseleit solution for 1 hour followed by 2-hour perfusion with normal solution. Another 13 hearts were perfused with normal solution for 3 hours (Control). Results: Collagen content was 3.5 ± 0.5% of ventricular dry weight in control group compared with 2.1 ± 0.4% in DTNB group (decrease by 40%, p < 0.01). Scanning electron micrographs revealed loss of the delicate collagen network surrounding muscle fibers in DTNB treated hearts. Developed pressure at a fixed volume decreased to 86 ± 17% of the baseline value after 3-hour perfusion in the control group, whereas in DTNB treated hearts developed pressure fell to 68 ± 13% (p < 0.01). End-diastolic pressure was set at 5 mmHg at the beginning of the experiment and rose to 15 ± 8 mmHg in control and 30 ± 13 mmHg (p < 0.01) in the treated hearts. Concomitantly, wet-to-dry weight ratio increased from 5.63 ± 0.26 in control to 6.07 ± 0.11 (p < 0.05) in the DTNB treated hearts. A separate set of experiments on isolated myocytes excluded the possibility of a direct effect of DTNB on myocyte contractile function. Conclusions: These data suggested that with 40% collagen disruption by DTNB there is a significant increase in tissue edema that results in a decrease in chamber capacitance; in addition, there is a significant decrease in systolic performance which reflects the combined effect of edema and loss of collagen.

元の言語英語
ページ(範囲)147-158
ページ数12
ジャーナルBasic Research in Cardiology
92
発行部数3
DOI
出版物ステータス出版済み - 1 1 1997
外部発表Yes

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Nitrobenzoates
Collagen
Perfusion
Muscle Cells
Edema
Pressure
Weights and Measures
Control Groups
crystalloid solutions
Disulfides
Electrons
Blood Pressure
Muscles

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

これを引用

Functional consequences of acute collagen degradation studied in crystalloid perfused rat hearts. / Todaka, K.; Jiang, T.; Chapman, J. T.; Gu, A.; Zhu, S. M.; Herzog, E.; Hochman, J. S.; Steinberg, S. F.; Burkhoff, D.

:: Basic Research in Cardiology, 巻 92, 番号 3, 01.01.1997, p. 147-158.

研究成果: ジャーナルへの寄稿記事

Todaka, K, Jiang, T, Chapman, JT, Gu, A, Zhu, SM, Herzog, E, Hochman, JS, Steinberg, SF & Burkhoff, D 1997, 'Functional consequences of acute collagen degradation studied in crystalloid perfused rat hearts', Basic Research in Cardiology, 巻. 92, 番号 3, pp. 147-158. https://doi.org/10.1007/BF00788632
Todaka, K. ; Jiang, T. ; Chapman, J. T. ; Gu, A. ; Zhu, S. M. ; Herzog, E. ; Hochman, J. S. ; Steinberg, S. F. ; Burkhoff, D. / Functional consequences of acute collagen degradation studied in crystalloid perfused rat hearts. :: Basic Research in Cardiology. 1997 ; 巻 92, 番号 3. pp. 147-158.
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abstract = "Objectives: The impact of acute collagen disruption by the disulfide donor, 5,5'-dithio-2-nitrobenzoic acid (DTNB) on ventricular properties was tested in rat hearts. Methods: Collagen was degraded acutely in 13 isolated, isovolumically contracting rat hearts by perfusion with 1 mM DTNB added to Krebs Henseleit solution for 1 hour followed by 2-hour perfusion with normal solution. Another 13 hearts were perfused with normal solution for 3 hours (Control). Results: Collagen content was 3.5 ± 0.5{\%} of ventricular dry weight in control group compared with 2.1 ± 0.4{\%} in DTNB group (decrease by 40{\%}, p < 0.01). Scanning electron micrographs revealed loss of the delicate collagen network surrounding muscle fibers in DTNB treated hearts. Developed pressure at a fixed volume decreased to 86 ± 17{\%} of the baseline value after 3-hour perfusion in the control group, whereas in DTNB treated hearts developed pressure fell to 68 ± 13{\%} (p < 0.01). End-diastolic pressure was set at 5 mmHg at the beginning of the experiment and rose to 15 ± 8 mmHg in control and 30 ± 13 mmHg (p < 0.01) in the treated hearts. Concomitantly, wet-to-dry weight ratio increased from 5.63 ± 0.26 in control to 6.07 ± 0.11 (p < 0.05) in the DTNB treated hearts. A separate set of experiments on isolated myocytes excluded the possibility of a direct effect of DTNB on myocyte contractile function. Conclusions: These data suggested that with 40{\%} collagen disruption by DTNB there is a significant increase in tissue edema that results in a decrease in chamber capacitance; in addition, there is a significant decrease in systolic performance which reflects the combined effect of edema and loss of collagen.",
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T1 - Functional consequences of acute collagen degradation studied in crystalloid perfused rat hearts

AU - Todaka, K.

AU - Jiang, T.

AU - Chapman, J. T.

AU - Gu, A.

AU - Zhu, S. M.

AU - Herzog, E.

AU - Hochman, J. S.

AU - Steinberg, S. F.

AU - Burkhoff, D.

PY - 1997/1/1

Y1 - 1997/1/1

N2 - Objectives: The impact of acute collagen disruption by the disulfide donor, 5,5'-dithio-2-nitrobenzoic acid (DTNB) on ventricular properties was tested in rat hearts. Methods: Collagen was degraded acutely in 13 isolated, isovolumically contracting rat hearts by perfusion with 1 mM DTNB added to Krebs Henseleit solution for 1 hour followed by 2-hour perfusion with normal solution. Another 13 hearts were perfused with normal solution for 3 hours (Control). Results: Collagen content was 3.5 ± 0.5% of ventricular dry weight in control group compared with 2.1 ± 0.4% in DTNB group (decrease by 40%, p < 0.01). Scanning electron micrographs revealed loss of the delicate collagen network surrounding muscle fibers in DTNB treated hearts. Developed pressure at a fixed volume decreased to 86 ± 17% of the baseline value after 3-hour perfusion in the control group, whereas in DTNB treated hearts developed pressure fell to 68 ± 13% (p < 0.01). End-diastolic pressure was set at 5 mmHg at the beginning of the experiment and rose to 15 ± 8 mmHg in control and 30 ± 13 mmHg (p < 0.01) in the treated hearts. Concomitantly, wet-to-dry weight ratio increased from 5.63 ± 0.26 in control to 6.07 ± 0.11 (p < 0.05) in the DTNB treated hearts. A separate set of experiments on isolated myocytes excluded the possibility of a direct effect of DTNB on myocyte contractile function. Conclusions: These data suggested that with 40% collagen disruption by DTNB there is a significant increase in tissue edema that results in a decrease in chamber capacitance; in addition, there is a significant decrease in systolic performance which reflects the combined effect of edema and loss of collagen.

AB - Objectives: The impact of acute collagen disruption by the disulfide donor, 5,5'-dithio-2-nitrobenzoic acid (DTNB) on ventricular properties was tested in rat hearts. Methods: Collagen was degraded acutely in 13 isolated, isovolumically contracting rat hearts by perfusion with 1 mM DTNB added to Krebs Henseleit solution for 1 hour followed by 2-hour perfusion with normal solution. Another 13 hearts were perfused with normal solution for 3 hours (Control). Results: Collagen content was 3.5 ± 0.5% of ventricular dry weight in control group compared with 2.1 ± 0.4% in DTNB group (decrease by 40%, p < 0.01). Scanning electron micrographs revealed loss of the delicate collagen network surrounding muscle fibers in DTNB treated hearts. Developed pressure at a fixed volume decreased to 86 ± 17% of the baseline value after 3-hour perfusion in the control group, whereas in DTNB treated hearts developed pressure fell to 68 ± 13% (p < 0.01). End-diastolic pressure was set at 5 mmHg at the beginning of the experiment and rose to 15 ± 8 mmHg in control and 30 ± 13 mmHg (p < 0.01) in the treated hearts. Concomitantly, wet-to-dry weight ratio increased from 5.63 ± 0.26 in control to 6.07 ± 0.11 (p < 0.05) in the DTNB treated hearts. A separate set of experiments on isolated myocytes excluded the possibility of a direct effect of DTNB on myocyte contractile function. Conclusions: These data suggested that with 40% collagen disruption by DTNB there is a significant increase in tissue edema that results in a decrease in chamber capacitance; in addition, there is a significant decrease in systolic performance which reflects the combined effect of edema and loss of collagen.

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