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J Thorac Cardiovasc Surg 2003;125:S92-S93
© 2003 The American Association for Thoracic Surgery

Editorials

Endothelial and myocardial stunning

Gerald D. Buckberg, MD

From the Department of Cardiothoracic Surgery, University of California at Los Angeles Medical Center, Los Angeles, Calif.

Received for publication July 13, 2000. Accepted for publication July 13, 2000. Address for reprints: Gerald D. Buckberg, MD, Department of Cardiothoracic Surgery, UCLA Medical Center, Rm 62-258 CHS, Box 951741, Los Angeles, CA 90095-1741.

The first 20% of the full text of this article appears below.

Until recently, myocyte stunning from inadequate cardiac protection has been the main focus of interest and is most relevant in damaged hearts (ie, hypertrophy, unstable angina, and reduced ejection fraction) in which vulnerability is accentuated. This injury is transient, since stunning recovers after brief inotropic or mechanical support. This editorial focuses on an expanding recognition that both the myocyte and the endothelium can be injured or stunned, as the two limbs are interrelated.

Damaged hearts exhibit loss of endothelium-dependent factors and reduced nitric oxide formation. The result is perioperative vasospasm, adherence of platelets, and leukocyte attachment that also causes capillary obstruction with inhomogeneous flow. The essential theme is that the endothelium is injured, because neutrophils do not attach, then roll, and finally have parenchymal influence for oxygen radical injury without such damage. This clinical report is the application of an experimentally proven . . . [Full Text of this Article]






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