title: Bidirectional cavopulmonary shunt with right ventricular outflow patency: the impact of pulsatility on pulmonary endothelial function.
abstract: OBJECTIVE
  Although in vitro studies have suggested the importance of flow pulsatility in endothelial function, few reports have focused on pulmonary endothelial function under decreased pulsatile flow after a bidirectional cavopulmonary shunt with or without an additional pulmonary flow source. The purpose of the present study was to assess the pulmonary endothelial function after bidirectional cavopulmonary shunt.
  
  
  RESULTS
  Pulmonary vasodilating response was evaluated in 10 patients 0.4 to 7.0 years (median 1.6 years) after bidirectional cavopulmonary shunt who were provided an additional flow source by retaining the pulmonary outflow tract and in 8 control subjects. Average pulmonary flow velocity was measured with a Doppler flow wire placed in the segmental lower lobe pulmonary artery during incremental infusion of acetylcholine (10(-8), 10(-7), 10(-6), and 10(-5) mol/L) and then of nitroglycerin (0.5 and 1.0 microg. kg(-1). min(-1)) after recovery. In the control subjects, a dose-dependent increase in flow velocity was observed in response to acetylcholine (maximum increase was 155% +/- 17% of baseline) and to nitroglycerin (maximum increase was 151% +/- 20% of baseline). In contrast, patients showed a significantly impaired response to acetylcholine (maximum increase was 124% +/- 17% of baseline; P <.01 vs control), whereas the response to nitroglycerin was preserved (138% +/- 12% of baseline; P =.09 vs control). In addition, the maximum response to acetylcholine correlated significantly with the pulmonary pulse pressure (r = 0.89, P <.01) and with the pulmonary flow pulsatility (r = 0.88, P <.01).
  
  
  CONCLUSIONS
  These results clearly suggest that patients after bidirectional cavopulmonary shunt show pulmonary endothelial functional attenuation and, of more importance, that decreased pulsatility of cavopulmonary flow is mainly responsible for this endothelial abnormality.
authors.affiliation: Department of Pediatrics and First Department of Surgery, Osaka University, Osaka, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Kurotobi
authors.forename: T
authors.initials: T
authors.lastname: Sano
authors.forename: S
authors.initials: S
authors.lastname: Kogaki
authors.forename: T
authors.initials: T
authors.lastname: Matsushita
authors.forename: T
authors.initials: T
authors.lastname: Miwatani
authors.forename: M
authors.initials: M
authors.lastname: Takeuchi
authors.forename: H
authors.initials: H
authors.lastname: Matsuda
authors.forename: S
authors.initials: S
authors.lastname: Okada
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000293:Adolescent; D001166:Arteriovenous Shunt, Surgical / Q000379:methods*; D001783:Blood Flow Velocity / Q000502:physiology; D002648:Child; D002675:Child, Preschool; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology* / Q000503:physiopathology*; D005260:Female; D005500:Follow-Up Studies; D006330:Heart Defects, Congenital / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000601:surgery*; D006801:Humans; D007223:Infant; D016014:Linear Models; D008297:Male; D005996:Nitroglycerin / Q000494:pharmacology; D011651:Pulmonary Artery / Q000503:physiopathology / Q000601:surgery*; D011673:Pulsatile Flow / Q000187:drug effects; D012016:Reference Values; D016896:Treatment Outcome; D018608:Ultrasonography, Doppler; D014682:Vena Cava, Inferior / Q000601:surgery*
chemical_list: D005996:Nitroglycerin; D000109:Acetylcholine