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No modification, neither immediate nor late, was observed after the intravenous injection of high doses of the coenzymatic forms of thiamine and pyridoxine. On the contrary, after the injection of high doses of the coenzyme A, a sudden, conspicuous and brief (20-25") diminution of heart rate was observed. Such a phenomenon was much more marked and longer if, before the coenzyme A, a digitalic compound (desacetil-lanatoside C or digitoxin) was administered.

In the course of their experiments, the Authors did not observe any modifications in the rat electrocardiogram, induced by a 2,5 mg DCA-ajmaline intravenous injection, nor, in particular, any negative bathmotropic action due to it.

From the Authors' observations during this research, there emerges the fact that pindololo does not seem deprived of that cardiodepressive action, which is typical of all beta-blocking drugs.

The authors, having in a previous series of experiments observed that coenzyme A, administered intravenously in doses from 200 to 500 U.L., causes an immediate and transient decrease of the sinus rate, wanted to study to which part of the complex molecule of coenzyme A such effect is due. That's why they studied the action, intravenously, of pantothenic acid (200-400 mg/Kg), of cysteine (40-80 mg/Kg), of pantethein (40-100 mg/Kg) and of adenosine (4-10 mg/Kg). The results of the experiments demonstrate that the former bradycardia is due to adenosine, whereas the other substances have not this effect.

Electrocardiographic changes induced by Verapamil, drug inducing inhibition of transmembrane movement of calcium into cardiac cells and mobilization of intracellular Ca++, have been studied in 10 anesthetized rats. Authors observed that Verapamil has: 1) negative chronotropic action on SA node; sometimes appears a superior nodal rhythm; 2) inconstantly, negative dromotropic action with prolonged atrioventricular conduction and "period of Luciani-Wenckebach'; 3) effective antiarrhythmic action; 4) no protective action towards peripheric vascular epinephrine effects; 5) remarkable negative inotropic action, whose Authors consider indirect signs the electrocardiographic changes, which indicate severe coronary failure, and the death of 6 rats by acute pulmonary edema.

In these experiments in the rat was studied the action of nicotine, administered intravenously in doses from 20 to 900 gamma/Kg. It was seen that, after the injection of lower doses, in the first phase there is always a more or less conspicuous diminution of the heart rate and a light and fleeting rise of the time of a-v conduction; there follows, after 25-30', a phase in which there is, as already noted, a rise of the heart rate. After higher doses was observed always an increase of the heart rate. Extrasystoles due to the action of nicotine was not observed. Sometime were observed signs of subendocardial damage or of fleeting right bundle-branch block. After a dose of 300 gamma (900 gamma/Kg) was observed a conspicuous and brief inhibition of sinus node activity and of the a-v conduction.

Electrocardiographic changes induced by desacetil-lanatoside C and digitoxin, administered intravenously, have been studied in 25 anesthetized rats. No differences were observed between the actions of the two glucosides. Their negative chronotropic action can be effected with two mechanisms: one indirect, through vagal reflex, therefore immediate and, in general, brief; one direct, for direct action on the heart, which is gradual and long lasting. Their action on the a-v conduction is recorded by a rise in the duration of the P-Q tract, or, for higher doses, by blocking fenomena, which are brief and completely reversible. Signs of subendocardial damage are often observed, these too brief. The appearance of extrasystoles is rare.