title: The role of ITP-DAG regulatory cascade in the mechanism of cardioprotective effect of adaptation to stress.
abstract: OBJECTIVE
  To study the role of inositol-triphosphate-diacylglycerol (ITP-DAG) regulatory cascade in the development of adaptive stabilization of structures.
  
  
  METHODS
  Double-blind, randomized trial.
  
  
  METHODS
  Wistar male rats, 250 to 300 g.
  
  
  METHODS
  Adaptation to restrained stress. Investigation of adapted animals consisted of three main steps: first, alpha 1-adrenoreactivity of isolated heart from animals adapted to short term stress exposure were studied. Second, the state of a1-adrenoceptors and phospholipase C activity were estimated by biochemical methods. Third, the contractile function of heart and its in vivo resistance to acute anoxia were studied as well as the resistance of isolated heart to ischemia reperfusion injury. All these studies were performed 15 and 30 days following the onset of adaptation to immobilization stress.
  
  
  RESULTS
  It is known that in adaptation to repeated stress exposure, a phenomenon of adaptive stabilization of structures (PhASS) develops. This phenomenon manifests itself, in particular, in isolated hearts from adapted animals as well as nuclei and cytoplasmic organelles of cardiomyocytes that acquire quite a high resistance to a broad spectrum of damaging factors. The present study shows that the development of PhASS and its cardioprotective effects with respect to anoxia, ischemia and reperfusion are associated with an increase in positive inotropic effect of selective alpha-agonist phenylephrine and an activation of myocardial phospholipase C. In long term adaptation both these alterations disappear and the PhASS-induced cardioprotective effect disappears simultaneously. A hypothesis on the important role of ITP-DAG regulatory cascade in PhASS development is put forward.
  
  
  CONCLUSIONS
  ITP-DAG regulatory cascade plays an important role in the mechanism of cardioprotective effect of adaptation to repeated stress exposure, in particular in increased resistance of the heart to ischemia and subsequent reperfusion.
authors.affiliation: Institute of General Pathology and Pathological Physiology of the USSR AMS, Moscow.
authors.forename: F Z
authors.initials: FZ
authors.lastname: Meerson
authors.forename: Y N
authors.initials: YN
authors.lastname: Kopylov
authors.lastname: Golubeva LYu
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology*; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D004075:Diglycerides / Q000502:physiology*; D006321:Heart / Q000503:physiopathology*; D066298:In Vitro Techniques; D007295:Inositol Phosphates / Q000502:physiology*; D008297:Male; D009200:Myocardial Contraction; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism; D010656:Phenylephrine / Q000494:pharmacology; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D018340:Receptors, Adrenergic, alpha-1 / Q000378:metabolism; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000503:physiopathology*; D010738:Type C Phospholipases / Q000378:metabolism
chemical_list: D004075:Diglycerides; D007295:Inositol Phosphates; D018340:Receptors, Adrenergic, alpha-1; D010656:Phenylephrine; D010738:Type C Phospholipases