title: [Change of cardiac ino- and chronotropic functions in stressed animals with blockade of different NO-synthases].
abstract: OBJECTIVE
  To investigate the effect of long-term immobilization-painful stress on ino- and chronotropic functions of the heart with inhibition of various NO-synthases.
  
  
  METHODS
  30 female albino rats were taken. Blockers of NO-system were: aminoguanidine (50 mg/kg), (50 mg/kg) and NG-nitro-L-arginine methyl ester (10 mg/kg). Stress was modeled by suspending the animals for cervical dorsal skin fold for 24 hours. The functional reserves of the heart were studied using adrenoreactivity and isometric load tests.
  
  
  RESULTS
  experiments showed that painful stress leads to a decrease of cardiac ino- and chronotropic functions which is observed in the reduction of increment dp/dt+, dp/dt-, LVP and HR during load tests in comparison to control group of intact animals. Selective blockade of nNOS with 7-Nitroindazole causes even greater decrease an increment indices of myocardial contractility and LVP in stressed animals during load tests. The most pronounced inhibition of inotropic function of the stressed animal's heart observed in the non-selective inhibition of NO-synthases by L-NAME. Administration of aminoguanidine to animals (inducible NOS blocker) before and after stress causes an increase of inotropic reserve of the heart, resulting in increased increment of myocardial contractility and relaxation findings, left ventricular pressure and heart rate during load tests,
  
  
  CONCLUSIONS
  NO-ergic system plays a significant role in limiting of the negative stress effects on the contractile function of the heart.
authors: I N
authors: IN
authors: Tiurenkov
authors: V N
authors: VN
authors: Perfilova
authors: N V
authors: NV
authors: Sadikova
mesh_terms: D000818:Animals; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005260:Female; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006339:Heart Rate; D007191:Indazoles / Q000494:pharmacology; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000201:enzymology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors* / Q000378:metabolism; D051381:Rats; D012149:Restraint, Physical; D013312:Stress, Physiological; D013315:Stress, Psychological / Q000201:enzymology / Q000503:physiopathology*
chemical_list: D004791:Enzyme Inhibitors; D007191:Indazoles; D019001:Nitric Oxide Synthase; C080122:7-nitroindazole; D019331:NG-Nitroarginine Methyl Ester