title: Cytokine induction by LVAD in the canine kidney.
abstract: BACKGROUND
  The outcome of left ventricular assist device (LVAD) support is reported to be associated with proinflammatory cytokines. We investigated the effect of LVAD support on renal function and the resultant cytokine induction.
  
  
  METHODS
  A prospective experimental study was performed using 15 mongrel dogs weighing 14 to 36 kg. LVAD was introduced in nine dogs (LVAD group) and the remaining six dogs were managed without LVAD support (control group). All animals were observed for six hours after thoracotomy. Renal regional blood flow was measured, and albumin-creatinine ratio (ACR) and N-acetyl-beta-D-glucoseaminidase index (NAGI) were evaluated as parameters of glomerular and tubular function, respectively. Tumor necrosis factor alpha (TNF-alpha) concentrations in the blood and homogenate of renal tissues were measured and immunohistological examination of renal tissues was conducted by means of anti-nuclear factor kappa B (NF-kappa B), TNF-alpha and interleukin 1 beta (IL- 1 beta) antibodies.
  
  
  RESULTS
  In the LVAD group, the renal cortex-medullar blood flow ratio significantly (p<0.05) decreased, and ACR was significantly (p<0.05) higher than in the control group, indicating glomerular insufficiency. There were no significant differences in NAGI and TNF-alpha levels in the blood and renal tissues between the two groups. Immunohistological examination of renal tissues demonstrated an accumulation of NF-kappa B, TNF-alpha, and IL-1 beta in the LVAD group.
  
  
  CONCLUSIONS
  An LVAD alters renal regional blood flow and induces a small amount of cytokines. We speculate that if an LVAD is introduced during systemic inflammatory response syndrome, the LVAD will induce a second attack resulting in multiorgan failure. For successful LVAD support, the appropriate selection of time periods is essential.
authors.affiliation: Second Department of Surgery, Gunma University School of Medicine, Maebashi, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Yamagishi
authors.forename: K
authors.initials: K
authors.lastname: Oshima
authors.forename: Y
authors.initials: Y
authors.lastname: Hasegawa
authors.forename: J
authors.initials: J
authors.lastname: Mohara
authors.forename: T
authors.initials: T
authors.lastname: Kanda
authors.forename: S
authors.initials: S
authors.lastname: Ishikawa
authors.forename: Y
authors.initials: Y
authors.lastname: Morishita
mesh_terms: D000118:Acetylglucosaminidase / Q000652:urine; D000818:Animals; D002302:Cardiac Output; D016207:Cytokines / Q000378:metabolism*; D004285:Dogs; D006353:Heart-Assist Devices; D007150:Immunohistochemistry; D007375:Interleukin-1 / Q000276:immunology; D007668:Kidney / Q000098:blood supply* / Q000276:immunology*; D023421:Models, Animal; D016328:NF-kappa B / Q000276:immunology; D019990:Perioperative Care; D011446:Prospective Studies; D012039:Regional Blood Flow; D013908:Thoracotomy; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016207:Cytokines; D007375:Interleukin-1; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D000118:Acetylglucosaminidase