title: Nitric oxide synthases are involved in the modulation of cardiovascular adaptation in hemorrhaged rats.
abstract: OBJECTIVE
  Nitric oxide has been implicated in the cardiovascular adaptation to hemorrhagic shock. Our aim was to study the potential role of nitric oxide synthases (NOS) in the cardiovascular response in hemorrhagic hypotension produced experimentally in anesthetized rats.
  
  
  METHODS
  Groups of animals (n = 14, per group): (a) normotensive; (b) hypovolemic (20% blood loss); (c) normotensive and pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME); (d) hypovolemic and pretreatment with L-NAME.
  
  
  RESULTS
  L-NAME restored the hypotension induced by hemorrhage. Blood loss decreased heart rate in the first stage increasing at 60 and 120 min. L-NAME blunted this effect. Right atria and left ventricle histochemical NOS activities increased at 60 and 120 min (atria 8% and 24%, respectively; ventricle 21% and 45%, respectively). This activity increased 17% in smooth muscle at 120 min. Heart endothelial NOS protein levels increased in heart at 60 min being attenuated at 120 min. Inducible NOS protein levels raised significantly in right atria, left ventricle and aorta at 120 min.
  
  
  CONCLUSIONS
  Hemorrhagic shock induced a time-dependent and specific NOS activation modulating cardiovascular function. The inhibition of nitric oxide system appears to prevent the acceleration of heart rate during late phases after acute hypovolemic state induced by blood loss.
authors.affiliation: Department of Physiology, School of Pharmacy and Biochemistry, University of Buenos Aires, IQUIMEFA-CONICET, Junin 956 C1113AAD Buenos Aires, Argentina. abalasz@ffyb.uba.ar
authors.forename: Ana M
authors.initials: AM
authors.lastname: Balaszczuk
authors.forename: Noelia D
authors.initials: ND
authors.lastname: Arreche
authors.forename: Myriam
authors.initials: M
authors.lastname: Mc Laughlin
authors.forename: Cristina
authors.initials: C
authors.lastname: Arranz
authors.forename: Andrea L
authors.initials: AL
authors.lastname: Fellet
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000201:enzymology* / Q000473:pathology; D001794:Blood Pressure; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006321:Heart / Q000187:drug effects; D006339:Heart Rate; D006439:Hemodynamics; D006470:Hemorrhage / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology; D020896:Hypovolemia / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D004791:Enzyme Inhibitors; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496318:Nos2 protein, rat; D019331:NG-Nitroarginine Methyl Ester