title: Exaggerated liver injury induced by ischemia-reperfusion in spontaneously hypertensive rats.
abstract: BACKGROUND
  The functions of polymorphonuclear leukocytes (PMNs), which play a critical role in organ damage, are primed in patients with essential hypertension and spontaneously hypertensive rats (SHR). Hepatic ischemia-reperfusion (I/R) injury is shown to be caused and aggravated by the PMNs. We examined whether the hepatic I/R injury was exaggerated in SHR.
  
  
  METHODS
  The portal vein and artery were partially occluded for 60 min. Blood samples were obtained to determine the degree of liver damage during 48 h after reperfusion.
  
  
  RESULTS
  The increase in serum transaminase concentration and hepatic myeloperoxidase content, which reflects the number of PMNs in liver tissue, in SHR were significantly greater than those of their control rats, Wistar-Kyoto rat (WKY). However, the elevations in hepatic transaminases induced by I/R did not differ between other hypertensive animal models (N-nitro-L-arginine methyl ester [L-NAME]-treated and deoxycorticosterone acetate [DOCA]/salt-treated rats) and their controls.
  
  
  CONCLUSIONS
  These results suggest that the elevated PMNs, but not high blood pressure per se, contributes to the exaggerated hepatic I/R injury in SHR.
authors.affiliation: Department of Clinical Pharmacology, Jichi Medical School, Tochigi, Japan.
authors.forename: Masami
authors.initials: M
authors.lastname: Ohmori
authors.forename: Nobutaka
authors.initials: N
authors.lastname: Araki
authors.forename: Ken-ichi
authors.initials: K
authors.lastname: Harada
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Sudoh
authors.forename: Koh-ichi
authors.initials: K
authors.lastname: Sugimoto
authors.forename: Akio
authors.initials: A
authors.lastname: Fujimura
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D003900:Desoxycorticosterone / Q000008:administration & dosage; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006973:Hypertension / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D008099:Liver / Q000098:blood supply / Q000503:physiopathology; D008107:Liver Diseases / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009504:Neutrophils / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D015415:Biomarkers; D004791:Enzyme Inhibitors; D014409:Tumor Necrosis Factor-alpha; D003900:Desoxycorticosterone; D009195:Peroxidase; D019001:Nitric Oxide Synthase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D019331:NG-Nitroarginine Methyl Ester