title: Both ischemic and pharmacological preconditioning decrease hepatic leukocyte/endothelial cell interactions.
abstract: BACKGROUND
  Ischemic preconditioning has been shown to protect some tissues from ischemia/reperfusion (I/R) injury. Adenosine is believed to play an important role by attenuating leukocyte-endothelial cell adhesive interactions. Dipyridamole increases adenosine bioavailability. The purpose of this study was to evaluate the effects of mechanical (MPC) and pharmacological preconditioning (PPC) on leukocyte endothelial cell interaction in hepatic I/R injury.
  
  
  METHODS
  C57BL6 mice were subjected to 30 min of ischemia to the left lobe of the liver. Groups tested at 30 min, 2, 5, 12, and 24 hr of reperfusion had 1) sham laparotomy (n = 10, 2) I/R (n = 25), 3) ischemic preconditioning with 5 min of ischemia and 10 min reperfusion before I/R (n = 25), and 4) (PPC) with dipyridamole (n = 25). Intravital microscopic examination was used to assess leukocyte/endothelial cell adhesion. Blood was drawn for leukocyte counts and liver function tests.
  
  
  RESULTS
  A significant decrease in leukocyte rolling was observed at 30-min and 5-hr reperfusion intervals in the PPC and ischemic preconditioning groups compared with the I/R group. A significant decrease in leukocyte saltation was also observed in the PPC and MPC groups at 2, 5, and 12 hr of reperfusion when compared with the I/R group. aspartate aminotransferase was significantly decreased in the 5-hr preconditioning groups. There was not a significant decrease in the white blood cell count because of PPC or MPC vs. I/R CONCLUSIONS: Preconditioning decreases endothelial/ leukocyte interaction and reduces liver damage as measured by aspartate aminotransferase. These data prove that IPC and PPC provide some degree of hepatic protection in I/R injury.
authors.affiliation: Department of Surgery, Louisiana State University Medical Center, Shreveport 71130, USA.
authors.forename: J G
authors.initials: JG
authors.lastname: Howell
authors.forename: G B
authors.initials: GB
authors.lastname: Zibari
authors.forename: M F
authors.initials: MF
authors.lastname: Brown
authors.forename: D L
authors.initials: DL
authors.lastname: Burney
authors.forename: D E
authors.initials: DE
authors.lastname: Sawaya
authors.forename: J G
authors.initials: JG
authors.lastname: Olinde
authors.forename: D N
authors.initials: DN
authors.lastname: Granger
authors.forename: J C
authors.initials: JC
authors.lastname: McDonald
mesh_terms: D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D002448:Cell Adhesion; D004176:Dipyridamole / Q000627:therapeutic use; D004730:Endothelium, Vascular / Q000166:cytology*; D019194:Ischemic Preconditioning; D007958:Leukocyte Count / Q000187:drug effects; D007962:Leukocytes / Q000166:cytology*; D008099:Liver / Q000098:blood supply* / Q000166:cytology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D015427:Reperfusion Injury / Q000517:prevention & control
chemical_list: D010975:Platelet Aggregation Inhibitors; D004176:Dipyridamole; D001219:Aspartate Aminotransferases