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Extracellular superoxide dismutase transgene overexpression preserves postischemic myocardial function in isolated murine hearts.

Publication ,  Journal Article
Chen, EP; Bittner, HB; Davis, RD; Folz, RJ; Van Trigt, P
Published in: Circulation
November 1, 1996

BACKGROUND: Myocardial injury after ischemia and reperfusion may be mediated, at least in part, by oxygen-derived free radicals; this supposition is supported by the observation that significant quantities of these radicals are generated during reperfusion. To directly assess the protective effect of extracellular superoxide dismutase (EC-SOD), this study was designed to investigate the ability of EC-SOD overexpression in the hearts of transgenic mice to protect myocardial tissue against ischemiareperfusion injury by use of an isolated work performing murine heart preparation and functional analysis. METHODS AND RESULTS: Ten transgenic mice (EC.SOD, 28 to 31 g) were studied and compared with 10 control mice (Ctl, 28 to 31 g) in terms of preischemic and postischemic myocardial function. All hearts underwent cardiac harvest and arrest, followed by instrumentation and subsequent reperfusion with warm Krebs-Henseleit solution. Preload-dependent functional analysis was then performed to evaluate cardiac output, contractility (dP/dt), heart rate, stroke work, and stroke volume before and after a 7-minute period of warm ischemia. Results are expressed as mean +/- SEM (ANOVA, paired unpaired t tests). There was no significant difference in preischemic myocardial performance for Ctl and EC-SOD mice. After warm ischemia, cardiac output in EC-SOD was significantly improved compared with Ctl (EC-SOD, 4.55 +/- 0.37 mL/min; Ctl, 2.55 +/- 0.28 mL/min; P < .05). Postischemic dP/dt, stroke work, and stroke volume were also significantly improved in EC-SOD compared with Ctl mice (EC-SOD, 1808 +/- 39 mm Hg/s, 745 +/- 67 dyne.cm, and 13.1 +/- 1.2 microL, respectively; Ctl, 1497 +/- 87 mm Hg/s, 472 +/- 83 dyne.cm, and 8.2 +/- 1.5 microL; P < .05). CONCLUSIONS: EC-SOD overexpressed mice showed significant improvement in postischemic cardiac function compared with Ctl mice. Thus, EC-SOD overexpressed hearts are less susceptible to mild degrees of ischemia-reperfusion injury than normal hearts.

Duke Scholars

Published In

Circulation

ISSN

0009-7322

Publication Date

November 1, 1996

Volume

94

Issue

9 Suppl

Start / End Page

II412 / II417

Location

United States

Related Subject Headings

  • Transgenes
  • Superoxide Dismutase
  • Myocardial Ischemia
  • Mice, Transgenic
  • Mice
  • Humans
  • Heart
  • Cardiovascular System & Hematology
  • Cardiac Output
  • Animals
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Chen, E. P., Bittner, H. B., Davis, R. D., Folz, R. J., & Van Trigt, P. (1996). Extracellular superoxide dismutase transgene overexpression preserves postischemic myocardial function in isolated murine hearts. Circulation, 94(9 Suppl), II412–II417.
Chen, E. P., H. B. Bittner, R. D. Davis, R. J. Folz, and P. Van Trigt. “Extracellular superoxide dismutase transgene overexpression preserves postischemic myocardial function in isolated murine hearts.Circulation 94, no. 9 Suppl (November 1, 1996): II412–17.
Chen EP, Bittner HB, Davis RD, Folz RJ, Van Trigt P. Extracellular superoxide dismutase transgene overexpression preserves postischemic myocardial function in isolated murine hearts. Circulation. 1996 Nov 1;94(9 Suppl):II412–7.
Chen, E. P., et al. “Extracellular superoxide dismutase transgene overexpression preserves postischemic myocardial function in isolated murine hearts.Circulation, vol. 94, no. 9 Suppl, Nov. 1996, pp. II412–17.
Chen EP, Bittner HB, Davis RD, Folz RJ, Van Trigt P. Extracellular superoxide dismutase transgene overexpression preserves postischemic myocardial function in isolated murine hearts. Circulation. 1996 Nov 1;94(9 Suppl):II412–II417.

Published In

Circulation

ISSN

0009-7322

Publication Date

November 1, 1996

Volume

94

Issue

9 Suppl

Start / End Page

II412 / II417

Location

United States

Related Subject Headings

  • Transgenes
  • Superoxide Dismutase
  • Myocardial Ischemia
  • Mice, Transgenic
  • Mice
  • Humans
  • Heart
  • Cardiovascular System & Hematology
  • Cardiac Output
  • Animals