title: Pulmonary blood flow regulates plasma tissue plasminogen activator concentrations in patients with congenital heart defects.
abstract: OBJECTIVE
  The wall shear stress generated by blood flow regulates the expression of fibrinolytic proteins by endothelial cells in vitro. In the present study, the effects of pulmonary blood flow on fibrinolytic activity were studied in patients with congenital heart defects and pulmonary hypertension.
  
  
  METHODS
  Twenty-seven patients who underwent cardiac operation because of congenital heart defects were divided into four groups according to the severity of pulmonary hypertension. Group I consisted of seven patients with normal pulmonary artery pressure, group II consisted of nine patients with pulmonary hypertension caused by increased pulmonary blood flow, group III consisted of six patients with pulmonary hypertension caused by increased pulmonary vascular resistance, and group IV consisted of five patients with tetralogy of Fallot. Plasma concentrations of tissue plasminogen activator, plasmin, and thrombin were assayed as the inhibitor-bound forms.
  
  
  RESULTS
  The preoperative concentration of tissue plasminogen activator was higher in group II than in all other groups (p = 0.0003). However, the postoperative concentration decreased only in patients in group II when compared with the preoperative value (p = 0.01). By Pearson's correlation analysis, pulmonary blood flow was found to correlate with the preoperative concentration of tissue plasminogen activator (95% confidence interval = 3.99 to 10.58, p = 0.0001). No definite conclusion was found for the relationship between tissue plasminogen activator and plasmin concentration. Further, the preoperative thrombin concentration was similar in all groups.
  
  
  CONCLUSIONS
  These findings suggest that pulmonary blood flow may regulate the plasma concentration of tissue plasminogen activator in patients with congenital heart defects.
authors.affiliation: First Department of Surgery, Nagoya City University Medical School, Nagoya, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Mishima
authors.forename: M
authors.initials: M
authors.lastname: Asano
authors.forename: T
authors.initials: T
authors.lastname: Saito
authors.forename: S
authors.initials: S
authors.lastname: Yamamoto
authors.forename: T
authors.initials: T
authors.lastname: Ukai
authors.forename: H
authors.initials: H
authors.lastname: Yoshitomi
authors.forename: K
authors.initials: K
authors.lastname: Matsumoto
authors.forename: T
authors.initials: T
authors.lastname: Manabe
mesh_terms: D002675:Child, Preschool; D005341:Fibrinolysin / Q000378:metabolism; D005342:Fibrinolysis; D005500:Follow-Up Studies; D006330:Heart Defects, Congenital / Q000150:complications / Q000201:enzymology* / Q000503:physiopathology* / Q000601:surgery; D006801:Humans; D006976:Hypertension, Pulmonary / Q000209:etiology*; D007223:Infant; D007231:Infant, Newborn; D010960:Plasminogen Activators / Q000097:blood*; D011652:Pulmonary Circulation; D013917:Thrombin / Q000378:metabolism; D010959:Tissue Plasminogen Activator / Q000097:blood*
chemical_list: D010960:Plasminogen Activators; D013917:Thrombin; D010959:Tissue Plasminogen Activator; D005341:Fibrinolysin