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Effects of cardiopulmonary bypass and circulatory arrest on endothelium-dependent vasodilation in the lung.

Publication ,  Journal Article
Kirshbom, PM; Jacobs, MT; Tsui, SS; DiBernardo, LR; Schwinn, DA; Ungerleider, RM; Gaynor, JW
Published in: J Thorac Cardiovasc Surg
June 1996

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 A2 analog 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 Ngamma-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.

Duke Scholars

Published In

J Thorac Cardiovasc Surg

DOI

ISSN

0022-5223

Publication Date

June 1996

Volume

111

Issue

6

Start / End Page

1248 / 1256

Location

United States

Related Subject Headings

  • Vasodilation
  • Vascular Resistance
  • Swine
  • Respiratory System
  • Nitric Oxide Synthase
  • Nitric Oxide
  • Muscle, Smooth, Vascular
  • Lung
  • Hypertension, Pulmonary
  • Heart Arrest, Induced
 

Citation

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Kirshbom, P. M., Jacobs, M. T., Tsui, S. S., DiBernardo, L. R., Schwinn, D. A., Ungerleider, R. M., & Gaynor, J. W. (1996). Effects of cardiopulmonary bypass and circulatory arrest on endothelium-dependent vasodilation in the lung. J Thorac Cardiovasc Surg, 111(6), 1248–1256. https://doi.org/10.1016/s0022-5223(96)70228-3
Kirshbom, P. M., M. T. Jacobs, S. S. Tsui, L. R. DiBernardo, D. A. Schwinn, R. M. Ungerleider, and J. W. Gaynor. “Effects of cardiopulmonary bypass and circulatory arrest on endothelium-dependent vasodilation in the lung.J Thorac Cardiovasc Surg 111, no. 6 (June 1996): 1248–56. https://doi.org/10.1016/s0022-5223(96)70228-3.
Kirshbom PM, Jacobs MT, Tsui SS, DiBernardo LR, Schwinn DA, Ungerleider RM, et al. Effects of cardiopulmonary bypass and circulatory arrest on endothelium-dependent vasodilation in the lung. J Thorac Cardiovasc Surg. 1996 Jun;111(6):1248–56.
Kirshbom, P. M., et al. “Effects of cardiopulmonary bypass and circulatory arrest on endothelium-dependent vasodilation in the lung.J Thorac Cardiovasc Surg, vol. 111, no. 6, June 1996, pp. 1248–56. Pubmed, doi:10.1016/s0022-5223(96)70228-3.
Kirshbom PM, Jacobs MT, Tsui SS, DiBernardo LR, Schwinn DA, Ungerleider RM, Gaynor JW. Effects of cardiopulmonary bypass and circulatory arrest on endothelium-dependent vasodilation in the lung. J Thorac Cardiovasc Surg. 1996 Jun;111(6):1248–1256.
Journal cover image

Published In

J Thorac Cardiovasc Surg

DOI

ISSN

0022-5223

Publication Date

June 1996

Volume

111

Issue

6

Start / End Page

1248 / 1256

Location

United States

Related Subject Headings

  • Vasodilation
  • Vascular Resistance
  • Swine
  • Respiratory System
  • Nitric Oxide Synthase
  • Nitric Oxide
  • Muscle, Smooth, Vascular
  • Lung
  • Hypertension, Pulmonary
  • Heart Arrest, Induced