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Ann Thorac Surg 2008;85:585-586. doi:10.1016/j.athoracsur.2007.09.025
© 2008 The Society of Thoracic Surgeons
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Craig H. Selzman
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Original Articles: Cardiovascular

Invited Commentary

Craig H. Selzman, MD

Division of Cardiothoracic Surgery, University of North Carolina, CB #7065, 3040 Burnett-Womack Building, Chapel Hill, NC 27599-7065

(Email: selzman@med.unc.edu).

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

Pulmonary hypertension, regardless of the cause, represents a significant challenge to cardiothoracic surgeons with regard to preoperative risk assessment, perioperative management, and postoperative outcomes. Despite multiple pharmacologic strategies, including prostanoids, endothelin-receptor antagonists, and phosphodiesterase inhibitors, pulmonary hypertension remains a source of significant morbidity and mortality. One of the most recognized regulators of pulmonary vascular vasomotor tone is nitric oxide (NO). Otherwise known as endothelial-derived relaxation factor, NO is biosynthesized from L-arginine in the vasculature by two forms of nitric oxide synthase: constitutive nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS). Upregulation of endogenous NO or exogenous delivery of NO has been well studied in a variety of cardiovascular models as well as humans. . . . [Full Text of this Article]


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Ann. Thorac. Surg. 2008 85: 581-585. [Abstract] [Full Text] [PDF]





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