2 b. A brown bitch, weighing about 25 lb., pulse 120, received gr. 1/6 subcutaneously. After 7 m., pulse 224 regular; after 9 m., pupils completely dilated and fixed; nose, mouth, and tongue quite dry. After 27 m. had lost much of her playfulness, and began prying slowly about room, now and then stumbling from unsteadiness of hind legs. After 1 h. continued in same state; consciousness unimpaired; was partially blind and went about cautiously, walked awkwardly, and hesitated to jump off a chair. Pulse between 300 and 400; respiration 22, regular. She now lay down for the first time, closed eyes, and dozed for 10 m.; then got up and walked about as before, smelling her way rather than seeing it. After 1 1/2 h., heart beating with noise and rapidity of a winnowing machine, about 400 times a minute, each beat distinctly perceptible through chest wall. Walked stiffly and clumsily; when placed upon a shifting ground, such as a cushioned chair, she reeled very much, and could hardly keep her footing, and when called she walked straight into the air, and tumbled down. Then when called again, she came in the direction of my voice, hesitatingly and with groping movement, as if advancing in the dark. After 3 h., pulse as before, strong, regular, 250; respirations 18, interrupted at intervals by a long – drawn sigh. After 5 h., pulse 200, quite regular and strong. After 5 1/2 h., mouth moistening. After 6 h., pulse still 200 to 190; mouth moist; had recovered some activity, and came up when called, but when placed on the table walked off into the air, and fell down. After 7 h. took food, had recovered activity and sight, and was quite frolicsome. (HARLEY, op. cit., 196, 199,.)
2. Wharton Jones, Meuriot, T. Harley and others state (though Nunneley denies it) that when applied to the web of the frog’s foot belladonna contracts the smaller arteries, producing at first acceleration of the circulation, followed after a time by complete stasis, beginning, according to Meuriot, in the veins and capillaries, the circulation always continuing in the artery some time after it has completely ceased in the vein. According to Harley, a moderate dose contracts the arteries, whilst a large dose dilates them; the contraction being due to stimulation, and the dilatation to exhaustion of the sympathetic system resulting from its previous over-stimulation. (RINGER, op. cit.)
3. To briefly sum up the probable action of A. (as ascertained mainly by experiments on animals) we find that: –
3 a. It tetanises the cord and heightens its reflex action.
3 b. It stimulates the respiratory centre, the inhibitory centre of the heart, the cardiac accelerator nerve or its centre, and the vaso-motor centre (so heightening arterial pressure).
3 c. It paralyses the terminations of the vagi, both in the heart and lungs; of the secretory nerves of the salivary, and perhaps also of the sweat-glands; and of the inhibitory fibres of the splanchnics.
3 d. Large doses slightly depress the functions of the afferent nerves.
It appears, then, that while it acts as a stimulant to a large part of the central nervous system, to many of the nerves it operates as a paralyser. (Ibid.)
4 a. In a frog the primary stimulation quickly passes off, and there follows gradually increasing weakness both of respiratory and voluntary movements, until these are entirely abolished. The nervous trunks cease to respond to stimulation, and the only sign of vitality is an occasional and hardly perceptible beat of the heart, and retention of irritability in the striated muscles. But if kept in this condition 4 or 5 d. the apparent death is succeeded by a state of spinal excitement. The forearms pass from a state of complete flaccidity to one of rigid tonic contraction. The respiratory movements reappeared, the cardiac action became stronger, and the posterior extremities extended. In this condition a touch on the skin caused violent tetanus, usually opisthotonic, lasting from 2 to 16 seconds, and succeeded by a series of clonic spasms. A little later still the convulsions change their character, and become prosthotonic. These symptoms are due to the action of the poison on the cord itself, for they continue independently in the parts connected with each segment of the cord when it has been divided
Fraser, who first observed these phenomena, considered the paralysis due entirely to the action of the drug on the extremities of the motor nerves, the cord being stimulated throughout. Ringer and Muirrell, however, have found that when the ends of the motor nerves in one leg are protected from the action of the poison by ligature of the artery, there is no difference between it and the poisoned leg. whereas on Fraser’s hypothesis it ought to be in a state of violent spasm. Brunton explains the facts by the theory of interference between nerve- vibrations. [ Ringer and Murrell consider paralysis and tetanus to be merely successive forms of spinal depression, and that with A. the latter is more slowly induced than the former.-EDS.]
4 b. The motor nerves of involuntary muscular fibre appear to be affected by A. and its congeners in a similar way to those of voluntary muscular fibre by curare – small doses of A. paralysing the former, and only large doses the latter, while the converse is the case with curare. These effects are usually supposed to be due to a definite paralytic action on the nerves themselves. There are difficulties, however, in the way of this hypothesis, and a more probable one, perhaps, is that these drugs disturb the relations between the nerves and the muscular fibres which they excite. On the idea of a specific action it seems hard to explain the results obtained by Szpilman and Luchsinger, who found that A. produced paralysis of the motor fibers of the vagi supplying the oesophagus only in those parts of it where involuntary fibre is present. Thus the oesophagus of the frog and the crop of birds consist of involuntary muscular fibre, and A. destroys the motor power of the vagus over them. the oesophagus of the dog and rabbit contains striated muscular fibre, and A. does not paralyse its motor nerves. That of the cat contains striated fibre in its upper three fourths and non-striated in its lower fourth; A. destroys the motor action of the vagus upon the upper part, but not upon the lower fourth. [ So stated by Brunton; but converse is needed to substantiate his position.- EDS.]
4 c. The action of A. on the excised heart of the frog illustrates the dependence of contradictory statements on differences in the temperature at which the observations were made. Thus Bowditch and Lulciani found that the contractions, both of the frog’s heart containing ganglia and of the apex alone, were rendered more powerful by A., while Gnauck, on the contrary, found that the contractions of the ventricle were diminished by it. Kronecker and Schapiro have found that these contradictory observations are both correct, but at different temperatures. When the temperature is low (7 to 8 C.) the ventricular contractions are enhanced by A., diminished by it when the temperature rises above 15 C.
4 d. A. paralyses the secreting fibres of the chorda tympani without affecting the vaso-dilator fibres, so that when the nerve is stimulated, either directly or reflexly, the flow of blood to the gland is increased, but no fluid exudes from the duct. That this absence of secretion is due to paralysis of secretory nerves and not of the secreting cells appears to be shown by the fact that at the time when the power of the chorda to induce secretion is completely paralysed, stimulation of the sympathetic will still induce secretion. A. probably has a similar action on many, if not all, glands, including the sweat, milk, and mucous glands, the pancreas, and the liver. It does not, however, prevent secretion in the intestine after division of the intestinal nerves. The secretion of urine is sometimes increased.
4 e. Small doses increase the movements of the intestines. This action is probably due to paralysis of the inhibitory fibres of the splanchnic, since stimulation of the fibres of the peripheral and of the cut splanchnic will cause arrest of movement in the unpoisoned, but not in the poisoned animal. Moderate doses completely arrest peristaltic movement, but the muscular fibres of the intestine retain their irritability. Local irritation causes a local contraction but no peristalsis. This is probably due to paralysis of the intestinal ganglia. Large doses stop the movements and paralyse the involuntary muscular fibres of the intestine, so that they only contract feebly or not at all when directly irritated.
4 f. A. greatly increases the tendency to epileptic convulsions in dogs, so that they can be produced by much slighter stimulation than usual, strychnine, absinthe, and cannabis having a similar, and bromide of potassium an opposite effect.
4 g. A. large number of drugs, more particularly A., curare, coniline, and nicotine, when injected into the circulation, have the power of completely destroying the inhibitory influence of the vagi so far as the rate of rhythm is concerned, so that when their fibres are stimulated the heart is not arrested, nor are its beats rendered slower, but they are, on the contrary, quickened. A. and its congeners, moreover, prevent any inhibition occurring when the venous sinus is stimulated, or when muscarine is applied directly to the heart. On the vagus centre, however, the drug acts as a stimulant, this being evidenced by slowing of the pulse disappearing after section of the nerves. (BRUNTON, Pharm and Theridion).
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.