title: Pulmonary vascular impedance and recipient chronic pulmonary hypertension following cardiac transplantation.
abstract: OBJECTIVE
  Recipient chronic pulmonary hypertension (CPH), secondary to long-standing congestive heart failure, represents a significant risk factor for right ventricular (RV) dysfunction following orthotopic cardiac transplantation (TX). This study was designed to characterize the changes occurring in pulmonary hemodynamics, pre-TX and post-TX, using Fourier analysis, a canine model of bicaval TX, and monocrotaline pyrrole (MCTP)-induced recipient CPH.
  
  
  METHODS
  Prospective, controlled study.
  
  
  METHODS
  Experimental laboratory.
  
  
  METHODS
  Twenty adult male mongrel dogs (23 to 26 kg).
  
  
  METHODS
  Recipients underwent pulmonary artery injection of 3 mg/kg MCTP 4 months pre-TX. On the day of TX, donor hearts were instrumented with an ultrasonic flow probe and micromanometers. Harmonic derivation of functional data was achieved with Fourier analysis.
  
  
  RESULTS
  At the time of TX, significant increases were observed in the mean pulmonary artery pressure and pulmonary vascular resistance of recipient animals in comparison to donors, which were further significantly increased following the termination of cardiopulmonary bypass. Significant increases were also observed in the input resistance, characteristic impedance, and RV hydraulic power post-TX compared to pre-TX, and occurred in association with a significant decrease in the transpulmonary efficiency.
  
  
  CONCLUSIONS
  In the setting of MCTP-induced recipient CPH donor hearts were exposed to significant alterations in cardiopulmonary hemodynamics following bicaval TX. Pulmonary blood flow is maintained by a significantly higher energy expenditure by the RV, but at a lower level of efficiency. This experimental model may provide a useful means by which to evaluate therapeutic options to better manage cardiopulmonary hemodynamics in order to prevent RV failure following TX in the setting of recipient CPH.
authors.affiliation: Department of Surgery, Duke University Medical Center, Durham, NC, USA. epchen@itsa.ucsf.edu
authors.forename: E P
authors.initials: EP
authors.lastname: Chen
authors.forename: H B
authors.initials: HB
authors.lastname: Bittner
authors.forename: R D
authors.initials: RD
authors.lastname: Davis
authors.forename: P
authors.initials: P
authors.lastname: Van Trigt
mesh_terms: D000818:Animals; D002908:Chronic Disease; D004195:Disease Models, Animal; D004285:Dogs; D017097:Electric Impedance; D005583:Fourier Analysis; D016027:Heart Transplantation / Q000379:methods / Q000502:physiology*; D006439:Hemodynamics; D006976:Hypertension, Pulmonary / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D016686:Monocrotaline / Q000031:analogs & derivatives; D011042:Poisons; D011446:Prospective Studies; D011651:Pulmonary Artery / Q000503:physiopathology*
chemical_list: D011042:Poisons; C014114:monocrotaline pyrrole; D016686:Monocrotaline