title: Periarteritis in lung from a continuous-flow right ventricular assist device: role of the local Renin-Angiotensin system.
abstract: BACKGROUND
  We previously reported renal arterial periarteritis after implantation of a continuous-flow left ventricular assist device in calves. The purpose of the present study was to investigate whether the same periarteritis changes occur in the intrapulmonary arteries after implantation of a continuous-flow right ventricular assist device (CFRVAD) in calves and to determine the mechanism of those histologic changes.
  
  
  METHODS
  Ten calves were implanted with a CFRVAD for 29 ± 7 days, and we compared pulmonary artery samples and hemodynamic data before and after CFRVAD implantation prospectively.
  
  
  RESULTS
  After implantation, the pulsatility index (pulmonary arterial pulse pressure/pulmonary arterial mean pressure) significantly decreased (0.88 ± 0.40 before vs 0.51 ± 0.22 after; p < 0.05), with severe periarteritis of the intrapulmonary arteries in all animals. Periarterial pathology included hyperplasia and inflammatory cell infiltration. The number of inflammatory cells positive for the angiotensin II type 1 receptor was significantly higher after implantation (7.8 ± 6.5 pre-CFRVAD vs 313.2 ± 145.2 at autopsy; p < 0.01). Serum angiotensin-converting enzyme activity significantly decreased after implantation from 100% to 49.7 ± 17.7% at week 1 (p = 0.01). Tissue levels of angiotensin-converting enzyme also demonstrated a significant reduction (0.381 ± 0.232 before implantation vs 0.123 ± 0.096 at autopsy; p = 0.043).
  
  
  CONCLUSIONS
  Periarteritis occurred in the intrapulmonary arteries of calves after CFRVAD implantation. The local renin-angiotensin system (not the angiotensin-converting enzyme pathway) plays an important role in such changes.
authors.affiliation: Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA.
authors.forename: Chiyo
authors.initials: C
authors.lastname: Ootaki
authors.forename: Michifumi
authors.initials: M
authors.lastname: Yamashita
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Ootaki
authors.forename: Diyar
authors.initials: D
authors.lastname: Saeed
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Horai
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Fumoto
authors.forename: Alex L
authors.initials: AL
authors.lastname: Massiello
authors.forename: Steven N
authors.initials: SN
authors.lastname: Emancipator
authors.forename: Leonard A R
authors.initials: LA
authors.lastname: Golding
authors.forename: Kiyotaka
authors.initials: K
authors.lastname: Fukamachi
mesh_terms: D000818:Animals; D001167:Arteritis / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D015153:Blotting, Western; D002417:Cattle; D004195:Disease Models, Animal; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology / Q000601:surgery*; D006353:Heart-Assist Devices / Q000009:adverse effects*; D006439:Hemodynamics; D007150:Immunohistochemistry; D008168:Lung / Q000098:blood supply*; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D011651:Pulmonary Artery; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology*
chemical_list: D044140:Receptor, Angiotensin, Type 1; D007703:Peptidyl-Dipeptidase A