7b. Experiments with fractions of a milligramme constantly showed a more or less considerable acceleration of the beat of the heart (10 to 30 in morning). In some cases the acceleration diminished and the heart recovered itself fully, but it mostly formed the first stage of a series of manifestations, gradually more and more approximating the picture of poisoning with larger doses, as already shown. After the acceleration had lasted about 10 morning with perfect regularity of the heart’s motion the already described spasms set in, but far more decided and outspoken than with larger doses. Auricles and ventricles equally take part in these spasms set in, but far more decided and outspoken that the larger doses. Auricles and ventricles equally take part in these spasms, which always set in suddenly and without preceding irregularities in the beat of the heart. The chief event in the rhythmic beat of the heart, the alternation of systole and diastole at regular intervals, has ceased, and it is nearly impossible to describe the ensuing phenomena. The muscle labours in vain to expel its contents-it throws them as it were, from one corner of the heart to another-and thus a systole, limited to small spaces, rolls in vermicular motion over the whole heart. A stage of exhaustion follows this second stage of spasm gradually, but in longer time, passing over into a cessation of the heart-beats.
7c. “We must also” (writes Boehm) “examine in what relation this poison stands to the vagus and the inhibitory centre. Our experiments were made in the usual way, by dividing the exposed nerve, testing its excitability, and then poisoning the animal. The excitation after the poisoning produces yet for some time an evident retardation, but not a cessation of the heart’s motion, and finally all the influence of the vagus on the number of the heart’s beats ceases. If we irritate mechanically of by electricity the heart which has ceased to beat under the action of aconitine, we usually see no effect by applying the irritation at the apex of the ventricles, whereas an irritation at the auricles frequently produces rhythmical contractions of auricles and ventricles.
7d. “Poisoning by aconitine may therefore be divided in its action on the heart into three stages-1, a stage of acceleration of the beats of the heart; 2, a stage of spasms of the heart; 3, a stage of cessation of movement in the heart.
7e. “We did not know till now any poison which produced with certainty a direct acceleration of the beat of the heart in frogs. Atropine from which we might expect such an effect a priori, and which really shows it in mammalia in a high degree, leaves the number of heart’s beats unaltered in the frog. It seems, therefore, that the diminution of resistance solely, the so called paralysis of inhibitory centra, is not by itself able to increase the number of the pulsations. It rather seems that in the frog its still needs a direct irritation of the excito-motor centres to effect an acceleration; and this is probably what caused the acceleration in the first stage of aconitine poisoning.
7f. “Experiments prove, furthermore, that aconitine gradually diminishes down to zero the excitability of the inhibitory nervous system. This diminution may contribute to the occurrence of the acceleration in the first stage, but is, I believe, of more importance to the second stage, left evening the occurrence of the spasmodic peristaltic cardiac movements. The cause of the rhythm of the heart’s movements is now generally supposed to stand in forces which arise in the so-called inhibitory centres, and as it were oppose themselves, as though they were obstacles to be overcome, to the motorial impulses which are continually proceeding from the automatic motor centres. In order to overpower them, the latter must acquire a certain potential energy, which, when the obstacles are overcome, passes over into vital force. After each movement some time passes till the necessary sum of potential energy is again accumulated, and thus arise the regular pauses between the beats of the heart and the rhythm. The number of beats, therefore, in a given time depends on the amount of the elastic spasms of aconitine. The motor impulses fail to be garnered up to a certain degree, and they are not restrained by a sufficiently strong resisting power, but let loose these irregular movements. Even a very strong irritation of the excito-motor centres would not suffice to produce these spasms, because, according to the above theory, the resistance emanating from the inhibitory centres must cause a cessation of the motion after each overpowering of it. The irritation of the excito-motor centres is necessary for the rapid succession of motor impulses, but a paralysis of the inhibitory organs is necessary for the spasms; and this we witness perfectly in this stage of the action of aconitine.
7g. “It may be asked, why then does not such a state produce tetanus of the heart, as all conditions for it are present But there is an important obstacle to a lasting tetanic systole in this case. The excitation of the motor centres, which, as we are as yet bound to believe, lie scattered in various parts of the heart, must take place with a certain simultaneousness in order to produce a regular cardiac contraction. Aconitine abolishes such regularity, for we see in the spasms caused by it the different parts of the heart contracting one after another without regular succession or co-ordination. Thus the heart never contracts in total, the blood is pushed from the most contracted parts to those less so, producing here and there a transient systole.
7h. “We wish to draw attention to a remarkable consonance between the action of higher degrees of heat and that of aconitine. Cyon found that the heart, when exposed to gradually higher and higher temperatures, is retarded at first in its pulsations, and then accelerated. After reaching their acme, the beats become irregular, and symptoms set in similar to aconitine spasms, and finally the heart stands still in diastole. When Cyon, before the warming process, paralysed by curare the ends of the vagus, the primary retardation failed to appear, acceleration immediately set in, followed by spasms and cessation. The action of higher temperatures on the heart, preceded by poisoning with curare, exactly corresponds with the symptoms of poisoning by aconitine; and we must consider both as an irritation of the excitomotor heart centres combined with a paralysis of the inhibitory nervous system, and of some, as yet unknown, regulating mechanism.
7i. ” The cessation of motion of the heart in diastole in the third stage of poisoning by aconitine is clearly a cessation from weariness. The heart shows all the characters of an organ semi-paralysed and wearied out by excess of activity and irritation, which may still by strong stimuli be spurred to transient activity, but which, left to itself, gradually entirely loses its vital qualities.
7j. “We consider also of important the change which the striped muscular substance, apart from the nerve centres situated on it, undergoes under the action of the poison. This presumption is confirmed by the fact that the auricles, which have, as is well known, no striped muscles, cannot be brought fully to a cessation by aconitine; they still beat, though weakly, for hours after the death of the remainder of the heart. As aconitine shows a very severe action on all other striped muscles, we must suppose a complication of two actions on the heart, and it is probable that we have to consider the latter action as the most important cause of the cessation of motion in the ventricles by aconitine. That the impulses for rhythmical motion emanating from the motor centra have not ceased, and consequently that their cessation cannot be the cause of the cessation of movement in the ventricles, is proved by the continuance of rhythmical motion in the auricles, which, if our explanation of the action of aconitine be correct, are not accessible to the action of this poison on the striped muscular substance.” (BOEHM, Ueber Herzgifte.).
Hughes was a great writer and a scholar. He actively cooperated with Dr. T.F. Allen to compile his 'Encyclopedia' and rendered immeasurable aid to Dr. Dudgeon in translating Hahnemann's 'Materia Medica Pura' into English. In 1889 he was appointed an Editor of the 'British Homoeopathic Journal' and continued in that capacity until his demise. In 1876, Dr. Hughes was appointed as the Permanent Secretary of the Organization of the International Congress of Homoeopathy Physicians in Philadelphia. He also presided over the International Congress in London.