The influence of hypoxia and metabolic inhibitors on the excitation process in atrioventricular node.
In small specimens prepared from the atrioventricular node of rabbits, the influence of hypoxia and metabolic inhibitors (Na-cyanide, 2.4 dinitrophenol, 2-desoxyglucose) on the av-node action potential was studied. The action potentials in these specimens proved to be of slow response type regardless of their origin, either the N or the NH-region of the node. 1. Following superfusion with O2-poor Tyrode solution, Vmax of the atrioventricular action potential gradually declined within 90 min and attained finally a new steady state. A mean decrease of 30.2 +/- 9.4% was obtained. Frequency a automatic impulse formation went down by almost the same amount within only 20 min. On return to an oxygenated Tyrode solution, or in the continued presence of O2 deficiency after an increase of the external glucose concentration from 11 mM to 33 mM, full recovery of these effects occurred. 2. After administration of Na-cyanide (1 X 10(-3) M), a similar Vmax decrease of 29.0 +/- 7.0% appeared. It took only 20 min for full development and was accompanied by a decrease reversible within 10-20 min on return to a cyanide-free medium. Poisoning the atrioventricular cell with 2.4 dinitrophenol (1 X 10(-3) M) led to the same result. Treatment with 2-desoxyglucose (3 X 10(-2) M) evoked a more pronounced Vmax diminution of 50%. 3. The inhibitor of K conductance, 4-aminopyridine (2 X 10(-3) M) did not remove the metabolically induced changes of Vmax of the atrioventricular action potential. After poisoning of oxydative phosphorylation, this compound caused in some cases evan a further reduction of Vmax. 4. The beta-adrenergic compound isoproterenol (9.2 X 10(-6) M) restored the hypoxia or cyanide-induced suppression of both Vmax and frequency of automatic impulse formation. The particularly pronounced response of Vmax led to an increase far exceeding the initial control values obtained under normal metabolic conditions of the atrioventricular cell.
D019297:2,4-Dinitrophenol; D000200:Action Potentials / Q000187:drug effects; D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000818:Animals; D001283:Atrioventricular Node / Q000187:drug effects / Q000503:physiopathology*; D001786:Blood Glucose / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D003847:Deoxyglucose / Q000494:pharmacology; D004140:Dinitrophenols / Q000494:pharmacology; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D011817:Rabbits; D012966:Sodium Cyanide / Q000494:pharmacology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
D001786:Blood Glucose; D004140:Dinitrophenols; D000255:Adenosine Triphosphate; D003847:Deoxyglucose; D000254:Sodium-Potassium-Exchanging ATPase; D012966:Sodium Cyanide; D019297:2,4-Dinitrophenol; D002118:Calcium