title: The changes of hepatic sinusoidal microcirculation and effects of nitric oxide synthase inhibitor during sepsis.
abstract: OBJECTIVE
  Sepsis may cause changes in liver blood flow, which may result in liver injury. Microcirculation in organ undergoes moderate alteration during sepsis or septic shock. The changes in hepatic microcirculation corresponding to liver functions and the effects of nitric oxide synthase inhibitor on the liver during sepsis were studied.
  
  
  METHODS
  Sepsis was produced by CLP (cecal ligation and two-hole puncture). In part I, the leukocyte adherence, leukocyte rolling numbers, and velocity of sinusoidal microcirculation of liver were compared with in vivo microscopy among early septic, late septic and control rats. In part II, the rats were randomly divided into two groups after CLP procedure, group A was given L-NAME (NG-nitro-L-arginine-methylester hydrochloride), 10 mg/kg BW, and group B was given normal saline as a control. The hepatic microcirculation, measured with a Laser-Doppler Flowmeter, was performed at 0, 2, 4, 6, and 8 hours after the CLP procedure. Their liver functions were also examined and compared with the microcirculation.
  
  
  RESULTS
  The results showed that the adherent and rolling numbers of leukocytes in the sinusoidal capillary significantly increased in early and late septic rats; and the centralized velocity of flow significantly decreased in late septic rats. For rats without L-NAME, their sinusoidal flux of the liver increased 2 and 4 hours after CLP, and then decreased gradually. Their GOT levels progressively increased after CLP, but the albumin levels decreased. For rats with L-NAME (group A), their sinusoidal flux levels at 2, 4 and 6 hours after CLP were significantly lower than those in rats without L-NAME (group B), but their GOT levels were higher since the 4th hour after CLP.
  
  
  CONCLUSIONS
  Our conclusions are that hepatic microcirculation initially increased then decreased and the liver functions deteriorated gradually after sepsis was induced. These changes were aggravated when the nitric oxide synthesis was inhibited.
authors.affiliation: Department of Surgery, Chang Gung Memorial Hospital 199, Tung-Hwa N. Rd., Taipei, Taiwan.
authors.forename: Tsann-Long
authors.initials: TL
authors.lastname: Hwang
authors.forename: Mei-Ling
authors.initials: ML
authors.lastname: Han
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D017078:Laser-Doppler Flowmetry; D008099:Liver / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000503:physiopathology*; D008102:Liver Circulation / Q000187:drug effects* / Q000502:physiology*; D008297:Male; D008833:Microcirculation / Q000187:drug effects* / Q000503:physiopathology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors* / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000000981:diagnostic imaging / Q000503:physiopathology*; D014463:Ultrasonography
chemical_list: D004791:Enzyme Inhibitors; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester