Experimental action of triphosphoric thiamine on the heart

Abstract

The action of the triphosphoric derivative of Vit. (TPT) has been studied taking as a base the alterations which take place in the cardiac rhythm in cases of Vit. B1 deficiency and on the grave metabolic alterations produced in those cases as a consequence — primarily — of the accumulation of piruvic acid in the organism as a result of decarboxylation.

There are many works on the action of cocarboxylase or diphosphoric thiamine (DPT) on the heart, but very few on the action of TPT.

VELLUZ, AMIARD and BARTOS maintain, with other authors, that TPT also has cocarboxylic action, while DE LA FUENTE and BEGUE and, on the other hand, KIESSLING denie it.

Nevertheless there are series of works marking its protective action over the myocardium experimentally depressed with some ions (K, Ca and Ba) or electrically.

We have proceded to the comparative study of the three phosphoric derivatives of thiamine, presenting in this paper the results obtained with TPT on the heart of the frog, Straub’s technique, on «in situ» heart of cat and on a heartlung preparation of dog.

On the frog’s heart we have found negative inotropic effect, greater the higher the concentration used, which has oscillated between 10-c-10~3. At lower concentrations there is no valuable effect. At a 10-i concentration we have seen that it protects the heart against the action of an excess of Ca (fig. 2) preventing also the systolic failure. A similar effect is seen against the Ba ion (fig. 3). There is no protection against the action of the K ion.

The action of TPT over a heart subjected to an induction current has been studied and we have seen that the time of heart failure which appears upon ending the electric stimulus is not lowered, but on the other hand, the recovery is more energetic, as can be seen by the systolic amplitude (fig. 4).

On the heart of the cat, the arterial pressure, the ventricular beat and the duration of the electric stimulus has been recorded. It has been made to fibrillate by subjecting it to the action of an induced current and it has been observed that 10 minutes, or more, after injecting 10 mg. of TPT/Kg. of weight intravenously or intracardialy, an electric stimulus of the same time of duration produces a ventricular fibrillation which last less than on the previous control experiment (fig. 6); or even mates a fibrillation reversible while on the control it was irreversible and from which the animal had to be reanimated with manual compression, adrenaline and massage (fig. 5).

As the cat’s heart is very resistant to fibrillation, with the purpose of making the experiment more aplicable to human clinic, we have studied the action of TPT on the heart of the dog, whose fibrillation is provoked easily and is practically irriversible. With the purpose of avoiding interferences in the metabolism of TPT in the cardiac muscle, we have used the cardio pulmonary preparation.

The results are more difficult to evaluate than on the heart of the cat, because we are dealing with differences in time of 1 second between a positive and a negative result; but based on statistics we can affirm that addition of 10 mg. of TPT/Kg. of weight lowers the appearance of ventricular fibrillations, as 2, 3 or 4 electric stimuli with induced current of 1 second duration are tolerated (fig. 7), a 2 seconds stimulus being necessary for provoking fibrillation, while on the control dogs series, this appeared with a 1 second stimulus (sometimes two were needed).