title: Ischemia-reperfusion-induced unmeasured anion generation and glycocalyx shedding: sevoflurane versus propofol anesthesia.
abstract: BACKGROUND
  Vascular leakage after ischemia-reperfusion (IR) is largely attributed to the destruction of the endothelial barrier and its associated negatively charged glycocalyx. In vitro, sevoflurane attenuates these changes. Therefore, we compared sevoflurane with propofol with regard to the protection of the glycocalyx and the release of negatively charged substances in vivo.
  
  
  METHODS
  After surgical preparation under midazolam-fentanyl, nine pigs each received either propofol or sevoflurane. Ischemia of 90 min was induced by a balloon catheter in the thoracic aorta. After 120 min of reperfusion, the anesthetics were changed back to midazolam-fentanyl. Five animals, each without aortic occlusion, served as time controls. Blood electrolyte parameters were measured, from which the strong ion gap (SIG) was calculated. Serum heparan sulfate concentrations and immunohistology served as a marker of glycocalyx destruction.
  
  
  RESULTS
  Immediately after reperfusion, SIG increased significantly only in the propofol group (+6.7 mEq/l versus baseline; p < .05), remaining stable in sevoflurane and both time-controlled groups. Initially, heparan sulfate concentration increased comparably in both experimental groups, but after 120 min, it became stable in sevoflurane-anesthetized animals, while increasing further in the propofol group (p < .05).
  
  
  CONCLUSIONS
  Unmeasured anions, predictive of negative outcome in previous studies, did not increase significantly in sevoflurane-anesthetized animals. Additionally, there was less heparan sulfate shedding over time, signaling less destruction of the glycocalyx. Therefore, in this in-vivo situation, sevoflurane proves to be superior to propofol in protecting the endothelium from IR injury.
authors.affiliation: Department of Anesthesiology, University Hospital, Ludwig-Maximilians University Munich, Munich, Germany. thorsten.annecke@med.uni-muenchen.de
authors.forename: Thorsten
authors.initials: T
authors.lastname: Annecke
authors.forename: Markus
authors.initials: M
authors.lastname: Rehm
authors.forename: Dirk
authors.initials: D
authors.lastname: Bruegger
authors.forename: Jens C
authors.initials: JC
authors.lastname: Kubitz
authors.forename: Gregor I
authors.initials: GI
authors.lastname: Kemming
authors.forename: Mechthild
authors.initials: M
authors.lastname: Stoeckelhuber
authors.forename: Mechthild
authors.initials: M
authors.lastname: Stoekelhuber
authors.forename: Bernhard F
authors.initials: BF
authors.lastname: Becker
authors.forename: Peter F
authors.initials: PF
authors.lastname: Conzen
mesh_terms: D000136:Acid-Base Equilibrium / Q000187:drug effects; D000777:Anesthetics / Q000494:pharmacology; D000818:Animals; D002199:Capillary Permeability / Q000187:drug effects; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000187:drug effects / Q000293:injuries; D005260:Female; D019276:Glycocalyx / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D006497:Heparan Sulfate / Q000378:metabolism; D008297:Male; D008738:Methyl Ethers / Q000494:pharmacology*; D015742:Propofol / Q000494:pharmacology*; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D000077149:Sevoflurane; D034421:Sus scrofa
chemical_list: D000777:Anesthetics; D006497:Heparan Sulfate; D008738:Methyl Ethers; D015742:Propofol; D000077149:Sevoflurane