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J Thorac Cardiovasc Surg 2002;123:1031-1034
© 2002 The American Association for Thoracic Surgery

Editorials

The bioactive peptide endothelin causes multiple biologic responses relevant to myocardial and vascular performance after cardiac surgery

Francis G. Spinale, MD, PhD

From the Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, SC.

Received for publication Dec 28, 2001. Accepted for publication March 5, 2002. Address for reprints: Francis G. Spinale, MD, PhD, Cardiothoracic Surgery, Strom Thurmond Research Building, 770 MUSC Complex, Suite 625, Medical University of South Carolina, Charleston, SC 29425.


   Introduction
 
See related articles on pages 1114 and 1120.


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  		Dr Spinale and associates

 
Over one-half million cardiac surgical procedures are performed in the United States and a large number of these procedures require cardiopulmonary bypass (CPB) and cardioplegic arrest. However, transient left ventricular (LV) dysfunction can occur with reperfusion and separation from CPB and result in a complex postoperative course. The causes for this LV pump dysfunction are multifactorial and include intrinsic defects in myocardial contractile performance and alterations in hemodynamic loading conditions. Neurohormonal system activation and subsequent release of bioactive peptides occur during and after CPB and cardioplegic arrest. One of the more potent bioactive peptides released into the systemic vasculature under these conditions is endothelin-1 (ET).Go Go 1-9 Increased synthesis and release of ET has been implicated to exacerbate LV pump dysfunction in a number of cardiovascular diseases.Go Go 8-12 Thus, elevated ET in patients during and after cardiac surgery may compromise LV function and contribute to a complex postoperative course.Go Go 13-17 In the two companion studies by Verma and colleaguesGo Go 18,19 in this issue of the Journal, of Thoracic and Cardiovascular Surgery, the authors demonstrated that ET can contribute to myocardial cell injury and microvascular constriction after an episode of controlled ischemia-reperfusion, which was particularly pronounced in the context of hyperglycemia or diabetes. These findings add to the body of knowledge to suggest that ET contributes to abnormalities in cardiovascular regulation after cardioplegic arrest and CPB and can further exacerbate these processes in pre-existing disease states such as diabetes. Comprehensive reviews and texts on the molecular biology, biosynthesis, and signaling of ET have been published.Go Go 7-10 However, a brief review with respect to the biology of ET and the different cellular functions within the cardiovascular system would be appropriate to place these recent studies into context with our emerging understanding of the importance of . . . [Full Text of this Article]


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Increased endothelin-1 production in diabetic patients after cardioplegic arrest and reperfusion impairs coronary vascular reactivity: Reversal by means of endothelin antagonism
Subodh Verma, Andrew Maitland, Richard D. Weisel, Paul W. M. Fedak, Shu-Hong Li, Donald A. G. Mickle, Ren-Ke Li, Lawrence Ko, and Vivek Rao
J. Thorac. Cardiovasc. Surg. 2002 123: 1114-1119. [Abstract] [Full Text] [PDF]

Hyperglycemia exaggerates ischemia-reperfusion–induced cardiomyocyte injury: Reversal with endothelin antagonism
Subodh Verma, Andrew Maitland, Richard D. Weisel, Shu-Hong Li, Paul W. M. Fedak, Neil C. Pomroy, Donald A. G. Mickle, Ren-Ke Li, Lawrence Ko, and Vivek Rao
J. Thorac. Cardiovasc. Surg. 2002 123: 1120-1124. [Abstract] [Full Text] [PDF]



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