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J Thorac Cardiovasc Surg 1996;111:1248-1256
© 1996 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

EFFECTS OF CARDIOPULMONARY BYPASS AND CIRCULATORY ARREST ON ENDOTHELIUM-DEPENDENT VASODILATATION IN THE LUNG

Received for publication May 30, 1995 Accepted for publication August 28, 1995 Address for reprints: J. William Gaynor, MD, Pediatric Cardiothoracic Surgery, Children's Hospital of Philadelphia, 34th St. and Civic Center Blvd., Philadelphia, PA 19104.

Abstract

Endothelial injury with failure of pulmonary endothelium–dependent vasodilatation has been proposed as a possible cause for the increased pulmonary vascular resistance observed after cardiopulmonary bypass, but the mechanisms underlying this response are not understood. An in vivo piglet model was used to investigate the role of endothelium-dependent vasodilatation in postbypass pulmonary hypertension. The pulmonary vascular responses to acetylcholine, a receptor-mediated endothelium-dependent vasodilator, and nitric oxide, an endothelium-independent vasodilator, were studied in one group of animals after preconstriction with the thromboxane A₂analog U46619 (n= 6); a second group was studied after bypass with 30 minutes of deep hypothermic circulatory arrest (n= 6). After preconstriction with U46619, both acetylcholine and nitric oxide caused significant decreases in pulmonary vascular resistance (34% ± 6% decrease, p= 0.007, and 39% ± 4% decrease, p= 0.001). After cardiopulmonary bypass with circulatory arrest, acetylcholine did not significantly change pulmonary vascular resistance (0% ± 8% decrease, p= 1.0), whereas nitric oxide produced a 32% ± 4% decrease in pulmonary vascular resistance (p= 0.007). These results demonstrate a loss of receptor- mediated endothelium-dependent vasodilatation with normal vascular smooth muscle function after circulatory arrest. Administration of the nitric oxide synthase blocker N-nitro-L-arginine-methyl-ester after circulatory arrest significantly increased pulmonary vascular resistance; thus, although endothelial cell production of nitric oxide may be diminished, it continues to be a major contributor to pulmonary vasomotor tone after cardiopulmonary bypass with deep hypothermic circulatory arrest. In summary, cardiopulmonary bypass with deep hypothermic circulatory arrest results in selective pulmonary endothelial cell dysfunction with loss of receptor-mediated endothelium-dependent vasodilatation despite preserved ability of the endothelium to produce nitric oxide and intact vascular smooth muscle function. (J THORACCARDIOVASCSURG1996;111:1248-56)

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