title: Ischemic preconditioning attenuates portal venous plasma concentrations of purines following warm liver ischemia in man.
abstract: OBJECTIVE
  Degradation of adenine nucleotides to adenosine has been suggested to play a critical role in ischemic preconditioning (IPC). Thus, we questioned in patients undergoing partial hepatectomy whether (i) IPC will increase plasma purine catabolites and whether (ii) formation of purines in response to vascular clamping (Pringle maneuver) can be attenuated by prior IPC.
  
  
  METHODS
  75 patients were randomly assigned to three groups: group I underwent hepatectomy without vascular clamping; group II was subjected to the Pringle maneuver during resection, and group III was preconditioned (10 min ischemia and 10 min reperfusion) prior to the Pringle maneuver for resection. Central, portal venous and arterial plasma concentrations of adenosine, inosine, hypoxanthine and xanthine were determined by high-performance liquid chromatography.
  
  
  RESULTS
  Duration of the Pringle maneuver did not differ between patients with or without IPC. Surgery without vascular clamping had only a minor effect on plasma purine concentrations. After IPC, plasma concentrations of purines transiently increased. After the Pringle maneuver alone, purine plasma concentrations were most increased. This strong rise in plasma purines caused by the Pringle maneuver, however, was significantly attenuated by IPC. When portal venous minus arterial concentration difference was calculated for inosine or hypoxanthine, the respective differences became positive in patients subjected to the Pringle maneuver and were completely prevented by preconditioning.
  
  
  CONCLUSIONS
  These data demonstrate that (i) IPC increases formation of adenosine, and that (ii) the unwanted degradation of adenine nucleotides to purines caused by the Pringle maneuver can be attenuated by IPC. Because IPC also induces a decrease of portal venous minus arterial purine plasma concentration differences, IPC might possibly decrease disturbances in the energy metabolism in the intestine as well.
authors.affiliation: Clinic of Anesthesiology, Klinikum Grosshadern, Ludwig Maximilians University, Munich, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Choukèr
authors.forename: A
authors.initials: A
authors.lastname: Martignoni
authors.forename: R J
authors.initials: RJ
authors.lastname: Schauer
authors.forename: H G
authors.initials: HG
authors.lastname: Rau
authors.forename: A
authors.initials: A
authors.lastname: Volk
authors.forename: O
authors.initials: O
authors.lastname: Heizmann
authors.forename: M
authors.initials: M
authors.lastname: Dugas
authors.forename: K
authors.initials: K
authors.lastname: Messmer
authors.forename: K
authors.initials: K
authors.lastname: Peter
authors.forename: M
authors.initials: M
authors.lastname: Thiel
mesh_terms: D000241:Adenosine / Q000097:blood / Q000378:metabolism; D000410:Alanine Transaminase / Q000097:blood; D001219:Aspartate Aminotransferases / Q000097:blood; D002851:Chromatography, High Pressure Liquid; D003250:Constriction; D006488:Hemostasis, Surgical / Q000009:adverse effects / Q000379:methods; D006498:Hepatectomy / Q000379:methods; D006801:Humans; D019271:Hypoxanthine / Q000097:blood; D007511:Ischemia / Q000097:blood*; D019194:Ischemic Preconditioning; D019344:Lactic Acid / Q000097:blood; D008099:Liver / Q000098:blood supply* / Q000201:enzymology; D009994:Osmolar Concentration; D011169:Portal Vein; D011687:Purines / Q000097:blood*; D019820:Xanthine / Q000097:blood
chemical_list: D011687:Purines; D019820:Xanthine; D019271:Hypoxanthine; D019344:Lactic Acid; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D000241:Adenosine