title: Portal Hyperperfusion after Extended Hepatectomy Does Not Induce a Hepatic Arterial Buffer Response (HABR) but Impairs Mitochondrial Redox State and Hepatocellular Oxygenation.
abstract: OBJECTIVE
  Portal hyperperfusion after extended hepatectomy or small-for-size liver transplantation may induce organ dysfunction and failure. The underlying mechanisms, however, are still not completely understood. Herein, we analysed whether hepatectomy-associated portal hyperperfusion induces a hepatic arterial buffer response, i.e., an adaptive hepatic arterial constriction, which may cause hepatocellular hypoxia and organ dysfunction.
  
  
  METHODS
  Sprague-Dawley rats underwent 30%, 70% and 90% hepatectomy. Baseline measurements before hepatectomy served as controls. Hepatic arterial and portal venous flows were analysed by ultrasonic flow measurement. Microvascular blood flow and mitochondrial redox state were determined by intravital fluorescence microscopy. Hepatic tissue pO2 was analysed by polarographic techniques. Hepatic function and integrity were studied by bromosulfophthalein bile excretion and liver histology.
  
  
  RESULTS
  Portal blood flow was 2- to 4-fold increased after 70% and 90% hepatectomy. This, however, did not provoke a hepatic arterial buffer response. Nonetheless, portal hyperperfusion and constant hepatic arterial blood flow were associated with a reduced mitochondrial redox state and a decreased hepatic tissue pO2 after 70% and 90% hepatectomy. Microvascular blood flow increased significantly after hepatectomy and functional sinusoidal density was found only slightly reduced. Major hepatectomy further induced a 2- to 3-fold increase of bile flow. This was associated with a 2-fold increase of bromosulfophthalein excretion.
  
  
  CONCLUSIONS
  Portal hyperperfusion after extended hepatectomy does not induce a hepatic arterial buffer response but reduces mitochondrial redox state and hepatocellular oxygenation. This is not due to a deterioration of microvascular perfusion, but rather due to a relative hypermetabolism of the remnant liver after major resection.
authors.affiliation: Department of General-, Visceral-, Vascular- and Pediatric Surgery, University of Saarland, Homburg/Saar, Germany.
authors.forename: Stefan
authors.initials: S
authors.lastname: Dold
authors.affiliation: Department of General-, Visceral-, Vascular- and Pediatric Surgery, University of Saarland, Homburg/Saar, Germany.
authors.forename: Sven
authors.initials: S
authors.lastname: Richter
authors.affiliation: Department of General-, Visceral-, Vascular- and Pediatric Surgery, University of Saarland, Homburg/Saar, Germany.
authors.forename: Otto
authors.initials: O
authors.lastname: Kollmar
authors.affiliation: Department of General-, Visceral-, Vascular- and Pediatric Surgery, University of Saarland, Homburg/Saar, Germany.
authors.forename: Maximilian
authors.initials: M
authors.lastname: von Heesen
authors.affiliation: Institute for Clinical & Experimental Surgery, University of Saarland, Homburg/Saar, Germany.
authors.forename: Claudia
authors.initials: C
authors.lastname: Scheuer
authors.affiliation: Institute for Clinical & Experimental Surgery, University of Saarland, Homburg/Saar, Germany.
authors.forename: Matthias W
authors.initials: MW
authors.lastname: Laschke
authors.affiliation: Institute for Experimental Surgery, University of Rostock, Rostock, Germany.
authors.forename: Brigitte
authors.initials: B
authors.lastname: Vollmar
authors.affiliation: Department of General-, Visceral-, Vascular- and Pediatric Surgery, University of Saarland, Homburg/Saar, Germany.
authors.forename: Martin K
authors.initials: MK
authors.lastname: Schilling
authors.affiliation: Institute for Clinical & Experimental Surgery, University of Saarland, Homburg/Saar, Germany.
authors.forename: Michael D
authors.initials: MD
authors.lastname: Menger
mesh_terms: D000818:Animals; D005260:Female; D006498:Hepatectomy; D006499:Hepatic Artery / Q000502:physiology; D008099:Liver / Q000098:blood supply* / Q000378:metabolism / Q000601:surgery; D008297:Male; D008928:Mitochondria / Q000378:metabolism*; D010084:Oxidation-Reduction; D010100:Oxygen / Q000378:metabolism*; D011169:Portal Vein / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D010100:Oxygen