title: Endothelium-dependent pulmonary artery responses in chronic heart failure: influence of pulmonary hypertension.
abstract: OBJECTIVE
  The purpose of this study was to determine whether pulmonary artery responses to acetylcholine are abnormal in patients with chronic heart failure.
  
  
  BACKGROUND
  Defective pulmonary artery endothelium-dependent responses have been observed in chronic heart failure models in animals. However, pulmonary artery endothelial responses in humans with chronic heart failure are unknown.
  
  
  METHODS
  Twenty-two patients with chronic treated heart failure (12 with secondary pulmonary hypertension, Group I; 10 with normal pulmonary artery pressure, Group II) and 8 control patients constituted the study groups. Intravascular ultrasound measurements of pulmonary artery area just beyond the tip of an 8F infusion sheath were obtained in response to acetylcholine (10(-6), 10(-5) and 10(-4) mol/liter). The 10(-6) mol/liter infusion was repeated after methylene blue infusion. Indomethacin (5 micrograms/ml) was sequentially added to this combination in 17 patients.
  
  
  RESULTS
  There were no significant differences among the three groups in vascular area responses to the lowest concentration (10(-6) and 10(-5) mol/liter) of acetylcholine, but the 10(-4) mol/liter infusion resulted in significant constriction in Group II patients (p < 0.05, analysis of variance [ANOVA]). Pretreatment with methylene blue in Group II also resulted in significant pulmonary artery vasoconstriction to even the 10(-6) mol/liter acetylcholine infusion (10.4 +/- 7.8% in Group II vs. 1.7 +/- 3.9% in the control group and 0.1 +/- 4.3% in Group I, p < 0.05, ANOVA). The addition of indomethacin resulted in reversal of the constriction in Group II patients.
  
  
  CONCLUSIONS
  These responses indicate that the pulmonary artery endothelium may play a significant role in inhibiting vasoconstriction in patients with chronic heart failure who maintain normal pulmonary artery pressure.
authors.affiliation: McGuire Veterans Affairs Medical Center, Medical College of Virginia, Richmond.
authors.forename: T R
authors.initials: TR
authors.lastname: Porter
authors.forename: D O
authors.initials: DO
authors.lastname: Taylor
authors.forename: A
authors.initials: A
authors.lastname: Cycan
authors.forename: J
authors.initials: J
authors.lastname: Fields
authors.forename: C W
authors.initials: CW
authors.lastname: Bagley
authors.forename: N G
authors.initials: NG
authors.lastname: Pandian
authors.forename: P K
authors.initials: PK
authors.lastname: Mohanty
mesh_terms: D000109:Acetylcholine / Q000008:administration & dosage / Q000494:pharmacology*; D000368:Aged; D000704:Analysis of Variance; D016022:Case-Control Studies; D002407:Catheterization, Swan-Ganz; D002908:Chronic Disease; D003251:Constriction, Pathologic / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D006333:Heart Failure / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000000981:diagnostic imaging / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D007213:Indomethacin / Q000008:administration & dosage / Q000494:pharmacology*; D007262:Infusions, Intravenous; D016555:Matched-Pair Analysis; D008751:Methylene Blue / Q000008:administration & dosage / Q000494:pharmacology*; D008875:Middle Aged; D009569:Nitric Oxide / Q000502:physiology; D011651:Pulmonary Artery / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D011669:Pulmonary Wedge Pressure; D012720:Severity of Illness Index; D014463:Ultrasonography
chemical_list: D009569:Nitric Oxide; D000109:Acetylcholine; D008751:Methylene Blue; D007213:Indomethacin