[Heart function and the mechanisms of its regulation in modelling adaptation to hypoxia by 2,4-dinitrophenol administration].
Energy deficiency caused by 2,4-dinitrophenol (2,4-DNP), stimulates cardiac activity, increases noradrenaline (NA) content in the heart, but decreases the latter's adrenoreactivity. The removal of stellate ganglia reduces myocardial hyperfunction and prevents the rise of the cardiac NA content. Increasing the dose of 2,4-DNP inhibits cardiac activity and reduces cardiac NA and myocardial adrenoreactivity. Prolonged 2,4-DNP administration increases resistance to hypoxia in rats. Ten-day exposure to 2,4-DNP enhances the stability of the cardiac NA level and myocardial adrenoreactivity. By day 20, the reserve potential of myocardial contractility is enhanced, but the adaptive changes in the myocardial neuronic apparatus disappear. When circulation is stimulated, adaptive changes in sympathetic neurons and the myocardium develop and disappear after a certain pattern under the effect of energy deficiency.
D000222:Adaptation, Physiological / Q000187:drug effects*; D000818:Animals; D004295:Dihydroxyphenylalanine / Q000032:analysis; D004140:Dinitrophenols / Q000494:pharmacology*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004734:Energy Metabolism / Q000187:drug effects; D004837:Epinephrine / Q000032:analysis; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D009206:Myocardium / Q000032:analysis; D011817:Rabbits; D051381:Rats; D013997:Time Factors
D004140:Dinitrophenols; D004295:Dihydroxyphenylalanine; D004837:Epinephrine
Funktsiia serdtsa i nekotorye mekhanizmy ee reguliatsii pri modelirovanii adaptatsii k gipoksii vvedeniem 2,4-dinitrofenola.