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Esmolol Improves Left Ventricular Function via  Enhanced β-Adrenergic Receptor Signaling in a Canine Model of Coronary Revascularization
Journal article

Esmolol Improves Left Ventricular Function via  Enhanced β-Adrenergic Receptor Signaling in a Canine Model of Coronary Revascularization

  • Booth, John V. Assistant Professor of Anesthesiology.
  • Spahn, Donat R. Professor and Chairman of Anesthesiology, Department of Anesthesiology, University Hospital Lausanne, Switzerland.
  • McRae, Robert L. Laboratory Research Analyst II.
  • Chesnut, Lynn C. Laboratory Research Analyst I, Department of Anesthesiology.
  • El-Moalem, Habib Assistant Professor of Biostatistics, Department of Community and Family Medicine.
  • Atwell, Darryl M. Assistant Professor of Anesthesiology.
  • Leone, Bruce J. Associate Professor of Anesthesiology, Department of Anesthesiology, Mayo Clinic, Jacksonville, Florida.
  • Schwinn, Debra A. Professor of Anesthesiology, Department of Anesthesiology, Professor of Surgery, Department of Surgery, and Professor of Pharmacology/Cancer Biology, Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina.
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Published in:
  • Anesthesiology. - Ovid Technologies (Wolters Kluwer Health). - 2002, vol. 97, no. 1, p. 162-169
Anesthesiology and Pain Medicine
English
Background
Recent American Heart Association guidelines highlight the paucity of data on effectiveness and/or mechanisms underlying use of beta-adrenergic receptor (beta AR) antagonists after acute coronary syndromes in patients subsequently undergoing revascularization. It is important to assess whether beta AR antagonists might protect the heart and improve ventricular function in this scenario. The authors therefore used esmolol (an ultra-short-acting beta AR antagonist) to determine whether beta AR antagonist treatment improves left ventricular function in a canine model of acute reversible coronary ischemia followed by coronary reperfusion during cardiopulmonary bypass (CPB). The authors also tested whether the mechanism includes preserved beta AR signaling.


Methods
Dogs were randomized to either esmolol or saline infusions administered during CPB (n = 29). Pre-CPB and end-CPB transmyocardial left ventricular biopsies were obtained; plasma catecholamine concentrations, myocardial beta AR density, and adenylyl cyclase activity were measured. In addition, left ventricular systolic shortening and postsystolic shortening were determined immediately prior to each biopsy.


Results
While beta AR density remained unchanged in each group, isoproterenol-stimulated adenylyl cyclase activity decreased 26 +/- 6% in the control group but increased 38 +/- 10% in the esmolol group (pre-CPB to end-CPB, mean +/- SD, P = 0.0001). Left ventricular systolic shortening improved in both groups after release of coronary (LAD) ligature; however, the esmolol group increased to 72 +/- 23% of pre-CPB values compared to 48 +/- 12% for the control group (P = 0.0008).


Conclusions
These data provide prospective evidence that esmolol administration results in improved myocardial function. Furthermore, the mechanism appears to involve enhanced myocardial beta AR signaling.
Language
  • English
Open access status
closed
Identifiers
Persistent URL
https://sonar.ch/global/documents/46417
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