title: Interaction between Kupffer cells and platelets in the early period of hepatic ischemia-reperfusion injury--an in vivo study.
abstract: BACKGROUND
  Hepatic ischemia-reperfusion (I/R) leads to activation of Kupffer cells (KCs). The activated KCs cause platelet and leukocyte adhesion to the sinusoidal endothelium. Previously, we reported that platelet-endothelium interactions occur earlier than leukocyte responses. The aim of this study was to evaluate the interaction between platelets and KCs in the hepatic microcirculation after I/R.
  
  
  METHODS
  Sprague-Dawley rats were divided into three groups: the no-ischemia group (control group; n = 6); the 20-min ischemia group (I/R group; n = 6); and the 20-min ischemia + anti-rat platelet serum group (APS group; n = 6). KCs were labeled using the liposome entrapment method. The number of adherent platelets was observed for up to 120 min after reperfusion by intravital microscopy. To investigate the effects of platelets on I/R injury, rats were injected intravenously with rabbit APS for platelet depletion.
  
  
  RESULTS
  In the I/R group, the number of adherent platelets increased significantly after I/R. More than 50% of the adherent platelets adhered to KCs. Electron microscopy indicated that the platelets attached to the KCs after hepatic ischemia. The histologic findings indicated liver damage and apoptosis of hepatocytes in zone 1. In the I/R group, but not in the control and APS groups, serum ALT increased immediately after reperfusion.
  
  
  CONCLUSIONS
  We succeeded in visualizing the dynamics of both KCs and platelets in the hepatic sinusoids. Liver ischemia induced the adhesion of platelets to KCs in the early period, which could play a key role in reperfusion injury of the liver.
authors.affiliation: Department of Surgery, Doctoral Program in Clinical Science, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan.
authors.forename: Takafumi
authors.initials: T
authors.lastname: Tamura
authors.forename: Tadashi
authors.initials: T
authors.lastname: Kondo
authors.forename: Sugiru
authors.initials: S
authors.lastname: Pak
authors.forename: Yoritaka
authors.initials: Y
authors.lastname: Nakano
authors.forename: Soichiro
authors.initials: S
authors.lastname: Murata
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Fukunaga
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Ohkohchi
mesh_terms: D061354:Acinar Cells / Q000166:cytology / Q000502:physiology / Q000648:ultrastructure; D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001792:Blood Platelets / Q000166:cytology* / Q000502:physiology / Q000648:ultrastructure; D002450:Cell Communication / Q000502:physiology*; D007728:Kupffer Cells / Q000166:cytology* / Q000502:physiology / Q000648:ultrastructure; D008081:Liposomes / Q000378:metabolism; D008107:Liver Diseases / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D008833:Microcirculation / Q000502:physiology; D046529:Microscopy, Electron, Transmission; D010973:Platelet Adhesiveness / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000473:pathology* / Q000503:physiopathology
chemical_list: D008081:Liposomes; D000410:Alanine Transaminase