Abstract
Propylene glycol, benzyl alcohol, quinidine, and procainamide were tested on the isolated rabbit atria and the isolated rabbit heart, for their effects on contractile force, spontaneous rate of contraction and coronary flow. All four drugs decreased the contractile force of isolated atria. Quinidine decreased the spontaneous rate in all doses tested. However procainamide at low doses decreased the rate at low doses but increased it at high doses. In contrast, propylene glycol and benzyl alcohol did not affect the spontaneous rate of contraction. On the isolated heart the ventricular contractile force was depressed by quinidine, procainamide, and benzyl alcohol, but propylene glycol showed a markedly positive inotropic effect. The negative inotropic effect of both quinidine and procainamide on isolated atria and isolated rabbit heart would seem likely to be elicited by the same mechanism, as shown by the regression coefficient of the slope. However, propylene glycol and benzyl alcohol showed different slopes in the isolated rabbit atria, which suggests that their depressor effects on atrial contractility are mediated by different mechanisms. The analysis of the affinity (pD′2) and relative responsiveness (ρ) give the following order of potency for depressing the ventricular contractility: quinidine > procainamide > benzyl alcohol. On the other hand, there was no strong correlation between contractile force, spontaneous rate, and coronary flow. These three physiological variables seem to be independent for the drugs tested.
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