Abstract
The chronotropic and inotropic activity and the content of sodium and potassium of isolated rabbit atria have been determined in the presence of pyridoxal (PYR) either alone or in combination with deoxypyridoxine (DES), glycine, quinidine or Ambonestyl.
The conclusions that may be drawn from these experiments are that:
Pyridoxal combined with deoxypyridoxine in a 1:2 molar ratio significantly increases atrial frequency.
Quinidine and Ambonestyl both decrease atrial frequency; these actions are not altered by the addition of pyridoxal.
Pyridoxal significantly increases the amplitude of atrial contraction for periods of 60 to 75 minutes after exposure to the compound.
Pyridoxal, 1 x 10-3 M, plus either deoxypyridoxine or glycine produce a late depression of contraction, an effect caused by none of these compounds alone.
Quinidine depresses contraction, an effect which appears to be antagonized by pyridoxal for the first 60 minutes.
Ambonestyl increases contractile amplitude, an effect which is enhanced by pyridoxal early and depressed late in the experiment.
Pyridoxal causes a loss of tissue potassium and a gain in tissue sodium.
Ambonestyl produces no changes in the tissue content of sodium and potassium but does enhance the potassium loss while not significantly changing the sodium gain produced by pyridoxal.
Quinidine produces no changes in the tissue content of sodium and potassium and these actions are not altered by the addition of pyridoxal.
The positive inotropic effects of these agents are associated with either a loss of potassium, a gain of sodium or no net change in the tissue content of these ions.
Pyridoxal produces atrial contracture which is related to the alteration of electrolytes in the tissue.
Footnotes
- Received July 6, 1959.
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