title: Effect of nitric oxide synthase inhibition on hemoglobin-oxygen affinity and lipid peroxidation in rabbits during fever.
abstract: BACKGROUND
  Nitric oxide (NO) is one of the most important biologic messengers and takes part in the development of fever. It can influence on the body prooxidant-antioxidant balance by different ways including interaction with hemoglobin (Hb).
  
  
  METHODS
  The effects of nitric oxide synthesis inhibition on the febrile response, hemoglobin-oxygen affinity and parameters of lipid peroxidation were studied in rabbits with fever. The fever was induced by intravenous administration of lipopolysaccharide from Salmonella typhi (0.6 microg/kg). Mixed venous blood was taken before the administration and 60, 120 and 180 min after it. The following parameters were measured: half-saturation oxygen pressure (P(50)), concentrations of conjugated dienes, Schiff bases and alpha-tocopherol in plasma and red blood cells, and activity of catalase in red blood cells.
  
  
  RESULTS
  The intravenous administration of the nitric oxide synthase inhibitor (N(omega)-nitro-L-arginine; 5x10(-3) M) reduced the lipopolysaccharide-induced rise in body temperature. After 180 min the actual P(50) had decreased from 35.0+/-1.7 to 29.4+/-1.3 mm Hg. An increase in the lipid peroxidation parameters and a decrease of the antioxidant system indices were observed. The administration of L-arginine to prevent nitric oxide synthase inhibition was accompanied by a shift of the oxyhemoglobin dissociation curve rightwards, more marked activation of the free radical processes and a greater elevation of body temperature. The multiple regression analysis showed a close linear correlation between P(50) and conjugated dienes, Schiff bases, alpha-tocopherol and catalase.
  
  
  CONCLUSIONS
  These results suggest that the increased hemoglobin-oxygen affinity found after the inhibition of nitric oxide synthesis lowers the oxygen flow to tissues and its fraction utilized in free radical oxidations, which finally causes a reduction of the fever response to the lipopolysaccharide.
authors.affiliation: Department of Physiology, Grodno Medical Institute, Grodno, Belarus. zinchuk@ggmi.belpak.grodno.by
authors.forename: V
authors.initials: V
authors.lastname: Zinchuk
mesh_terms: D000818:Animals; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005334:Fever / Q000209:etiology / Q000378:metabolism*; D015227:Lipid Peroxidation; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D019335:Nitroarginine / Q000494:pharmacology; D010108:Oxyhemoglobins / Q000378:metabolism*; D011817:Rabbits
chemical_list: D004791:Enzyme Inhibitors; D008070:Lipopolysaccharides; D010108:Oxyhemoglobins; D019335:Nitroarginine; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase