title: Effect of pneumoperitoneum on renal tissue oxygenation and blood flow in a rat model.
abstract: OBJECTIVE
  To determine the correlation between the renal blood flow (RBF) and tissue oxygenation (PO(2)) at varying intra-abdominal pressures (IAPs) and to compare the effects on renal blood flow from carbon dioxide-induced pneumoperitoneum.
  
  
  METHODS
  Carbon dioxide pneumoperitoneum was established in Sprague-Dawley rats (n = 6). Licox oxygen/temperature tissue probes were laparoscopically inserted into the renal parenchyma, with the renal PO(2) and RBF recorded every 30 seconds while the IAP was gradually increased. Microprobes measuring the RBF, mean arterial pressures and serum pH were placed into the parenchyma to compare the effects of carbon dioxide pneumoperitoneum (n = 7) with that of open surgery (n = 6) and medical air pneumoperitoneum (n = 6).
  
  
  RESULTS
  Renal PO(2) was inversely related to the IAP (P < .001). Despite the reduction in IAP, the renal PO(2) in the recovery phase was lower than at baseline (P = .045). The renal PO(2) and RBF changed in a virtually identical pattern at varying levels of IAP (P > .05). The RBF significantly declined with a pneumoperitoneal pressure of 15 and 20 mm Hg (P = .022), regardless of the gas used to create the pneumoperitoneum. A partial reversal of the RBF occurred with a decrease of the IAP. The RBF in the open surgical arm remained unchanged. Although both the serum pH and the mean arterial pressure were inversely proportional to the IAP (P < .001), the mean arterial pressure was depressed to the greatest extent in the medical air group (P = .02).
  
  
  CONCLUSIONS
  These results have demonstrated that elevated IAP secondary to pneumoperitoneum causes significant renal hypoxia and decreased RBF. Additionally, this experiment has demonstrated the use of the Licox probes in monitoring the renal PO(2) and established a novel method for evaluating the effects of IAP on the kidney.
authors.affiliation: Department of Surgery, Division of Urology, Keenan Research Institute, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada.
authors.forename: Joshua D
authors.initials: JD
authors.lastname: Wiesenthal
authors.forename: Luke M
authors.initials: LM
authors.lastname: Fazio
authors.forename: Alexandra E
authors.initials: AE
authors.lastname: Perks
authors.forename: Brian D M
authors.initials: BD
authors.lastname: Blew
authors.forename: David
authors.initials: D
authors.lastname: Mazer
authors.forename: Greg
authors.initials: G
authors.lastname: Hare
authors.forename: R John D'A
authors.initials: RJ
authors.lastname: Honey
authors.forename: Kenneth T
authors.initials: KT
authors.lastname: Pace
mesh_terms: D000818:Animals; D002245:Carbon Dioxide / Q000737:chemistry; D004195:Disease Models, Animal; D005740:Gases; D006801:Humans; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000378:metabolism; D007668:Kidney / Q000098:blood supply* / Q000378:metabolism*; D010535:Laparoscopy / Q000379:methods; D010100:Oxygen / Q000737:chemistry / Q000378:metabolism; D011027:Pneumoperitoneum / Q000378:metabolism / Q000473:pathology*; D011312:Pressure; D051381:Rats; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation
chemical_list: D005740:Gases; D002245:Carbon Dioxide; D010100:Oxygen