title: Reduced pulsatility induces periarteritis in kidney: role of the local renin-angiotensin system.
abstract: OBJECTIVE
  The need for pulsatility in the circulation during long-term mechanical support has been a subject of debate. We compared histologic changes in calf renal arteries subjected to various degrees of pulsatile circulation in vivo. We addressed the hypothesis that the local renin-angiotensin system may be implicated in these histologic changes.
  
  
  RESULTS
  Sixteen calves were implanted with devices giving differing degrees of pulsatile circulation: 6 had a continuous flow left ventricular assist device (LVAD); 6 had a continuous flow right ventricular assist device (RVAD); and 4 had a pulsatile total artificial heart (TAH). Six other calves were histologic and immunohistochemical controls. In the LVAD group, the pulsatility index was significantly lower (0.28 +/- 0.07 LVAD vs 0.56 +/- 0.08 RVAD, vs 0.53 +/- 0.10 TAH; P < 0.01), and we observed severe periarteritis in all cases in the LVAD group. The number of angiotensin II type 1 receptor-positive cells and angiotensin converting enzyme-positive cells in periarterial areas was significantly higher in the LVAD group (angiotensin II type 1 receptor: 350 +/- 139 LVAD vs 8 +/- 6 RVAD, vs 3 +/- 2 TAH, vs 3 +/- 2 control; P < .001; angiotensin-converting enzyme: 325 +/- 59 LVAD vs 6 +/- 4 RVAD, vs 6 +/- 5 TAH, vs 3 +/- 1 control; P < .001).
  
  
  CONCLUSIONS
  The reduced pulsatility produced by a continuous flow LVAD implantation induced severe periarteritis in the kidneys. The local renin-angiotensin system was up-regulated in the inflammatory cells only in the continuous flow LVAD group.
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: Keiji
authors.initials: K
authors.lastname: Kamohara
authors.forename: Stephan
authors.initials: S
authors.lastname: Weber
authors.forename: Ryan S
authors.initials: RS
authors.lastname: Klatte
authors.forename: William A
authors.initials: WA
authors.lastname: Smith
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: D000804:Angiotensin II / Q000096:biosynthesis; D000818:Animals; D001167:Arteritis / Q000473:pathology / Q000503:physiopathology*; D002417:Cattle; D006439:Hemodynamics; D007150:Immunohistochemistry; D007668:Kidney / Q000098:blood supply* / Q000378:metabolism; D008297:Male; D009393:Nephritis / Q000473:pathology / Q000503:physiopathology*; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D011673:Pulsatile Flow; D011945:Receptors, Angiotensin / Q000378:metabolism; D012077:Renal Artery / Q000473:pathology* / Q000503:physiopathology*; D012084:Renin-Angiotensin System
chemical_list: D011945:Receptors, Angiotensin; D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A