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Dynamic changes of endothelin-1, nitric oxide, and cyclic GMP in patients with congenital heart disease

K Bando1, P Vijayaraghavan, M W Turrentine

  • 1Section of Cardiothoracic Surgery, James W. Riley Hospital for Children and Indiana University Medical Center, Indianapolis 46202-5123, USA. kbando@wpo.iupui.edu

Circulation
|December 31, 1997
PubMed

Insights

High endothelin-1 (ET-1) levels and inadequate nitric oxide (NO) may cause pulmonary hypertension after heart surgery. This study in children shows ET-1 increases with pulmonary pressure, while NO response is impaired in high-pressure cases.

Area of Science:

  • Cardiovascular Physiology
  • Pediatric Cardiology
  • Surgical Outcomes Research

Background:

  • Pulmonary hypertension is a significant complication following congenital heart surgery.
  • The precise mechanisms driving post-cardiac surgery pulmonary hypertension remain incompletely understood.

Purpose of the Study:

  • To investigate the roles of endothelin-1 (ET-1) and nitric oxide (NO) in the development of pulmonary hypertension after cardiopulmonary bypass (CPB).
  • To analyze the relationship between ET-1, NO, and pulmonary pressure in pediatric patients undergoing CPB.

Main Methods:

  • Assayed plasma ET-1, NO metabolites, and cyclic GMP (cGMP) in 50 children at multiple time points around CPB.
  • Categorized patients into low flow (LF), high flow/low pressure (HF-LP), and high flow/high pressure (HF-HP) groups based on pulmonary hemodynamics.
  • Administered alpha-blockers and NO donors to specific patient groups as clinically indicated.

Main Results:

  • Endothelin-1 (ET-1) levels peaked 6 hours post-CPB, with significantly higher concentrations observed in the high flow/high pressure (HF-HP) group.
  • ET-1 levels at 6 hours strongly correlated with the systolic pulmonary pressure/systemic pressure ratio (Pp/Ps).
  • Despite NO donor administration, nitric oxide (NO) metabolites and cyclic GMP (cGMP) levels were similarly elevated in both HF-HP and high flow/low pressure (HF-LP) groups, suggesting potential impaired NO response in HF-HP.

Conclusions:

  • Elevated ET-1, coupled with potentially inadequate NO production or response, likely contributes to increased pulmonary pressure in HF-HP patients.
  • Endogenous NO may play a role in maintaining lower pulmonary pressure in HF-LP patients.
  • Understanding these vasoactive pathways is crucial for managing post-operative pulmonary hypertension in pediatric cardiac surgery.
Abstract

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