Heart & Lung: The Journal of Acute and Critical Care
Volume 36, Issue 2 , Pages 140-147, March 2007

Direct inotropic effect of the beta-2 receptor agonist terbutaline on impaired diaphragmatic contractility in septic rats

  • Mitsuru Uzuki, MD, PhD

      Affiliations

    • Department of Anesthesiology, Sapporo Medical University School of Medicine, Sapporo, Japan
  • ,
  • Michiaki Yamakage, MD, PhD

      Affiliations

    • Department of Anesthesiology, Sapporo Medical University School of Medicine, Sapporo, Japan
    • Corresponding Author InformationReprint requests: Michiaki Yamakage, MD, PhD, Assistant Professor, Department of Anesthesiology, Sapporo Medical University School of Medicine, South 1, West 16, Chuo-ku, Sapporo, Hokkaido 060-8543, Japan.
  • ,
  • Naoyuki Fujimura, MD, PhD

      Affiliations

    • Division of Emergency and Critical Care Medicine, Okayama University School of Medicine, Okayama, Japan.
  • ,
  • Akiyoshi Namiki, MD, PhD

      Affiliations

    • Department of Anesthesiology, Sapporo Medical University School of Medicine, Sapporo, Japan

The purpose of this study was to determine which beta-adrenoceptor agonist (1 or 2) is responsible for the direct inotropic effects on diaphragmatic contractility during sepsis. Rats were divided into two groups: a cecal ligation and perforation (CLP) group and a sham group. The hemidiaphragm was removed at 16 hours after the operation. Dobutamine (a beta-1 agonist) or terbutaline (a beta-2 agonist) was administered to an organ bath containing diaphragmatic tissues, and muscle contractility was assessed. Muscle contractility was diminished in the CLP group. Terbutaline increased peak twitch tension, caused an upward shift in the force-frequency curves, and improved contractility of the fatigued diaphragm in the CLP group. Dobutamine did not have any effect on these parameters in the CLP group. We conclude that activation of beta-2 adrenoceptors might be responsible for the direct inotropic effects on the diaphragm in an intra-abdominal septic model.

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 This study was supported by grants-in-aid for scientific research (No. 13770848, 15591648 and 15591915) from the Japanese Ministry of Education, Science, Sports and Culture.

PII: S0147-9563(06)00178-6

doi:10.1016/j.hrtlng.2006.06.006

Heart & Lung: The Journal of Acute and Critical Care
Volume 36, Issue 2 , Pages 140-147, March 2007