Physiological Action.—Phosphorus being a constituent of most tissues, it exerts a stimulating influence, when ad ministered in small doses, upon their nu trition. This is particularly marked as regards the nervous and osseous systems. When, however, it is administered in toxic doses, it gives rise to changes in the metabolism which Mtinzer (Dent. Archiv f. klin. Med., B. 52, H. 3, 4, '94) summarizes as follows, after an analysis of 15 cases of acute poisoning: During the first two or three days after the poison is swallowed there is a marked diminution in the total amount of nitro gen present in the urine, attributed not to the specific action of the phosphorus, but to the persistent vomiting and con sequent state of starvation. On the sec ond or third day after the poison is taken a marked increase in the excre tion of nitrogen takes place, attributable to excessive destruction of tissue-pro teids caused by the phosphorus. Usually death quickly occurs as soon as the amount of nitrogen has become very great; but in many cases there is a dim inution both in nitrogen and of the quantity of urine excreted during the last hours of life. As regards the per centage of urea, if it is below S5 to 90 per cent. of the total amount of nitro gen excreted, disease of the liver, of such a kind as to interfere with its urea-form ing function, is thereby indicated, the absent urea being replaced by excess of ammonia, which ought to have been converted into urea. But in some of the cases observed the quantity of urea ex creted, after having been reduced very low, was subsequently increased three fold, although the condition of the liver was progressively becoming worse. The view taken is that the excess of am monia is solely due to development of acid products in the tissues, caused by the toxic action of the phosphorus, and not to arrest of the urea-forming func tion of the liver. In addition to the in crease in ammonia there is excess of uric acid excreted in cases of acute phos phorus poisoning during the stage of rapid proteid metabolism, and also of nitrogenous extractives. Miinzer failed, with one exception, to find peptones in the urine.
The chlorides of the urine are rapidly diminished after the acute toxic effects of phosphorus develop. The excretion of phosphoric acid is increased during the first few days; afterward it pro gressively diminishes until death.
The excretion of sulphuric acid, upon the whole, runs the same course as that of phosphoric acid; ether sulphates are increased. No fatty acids—tyrosin, leucin—nor sarcolactic acid were found, nor any diamines. Chemical analysis of the brain-substance showed an in creased percentage, and of the liver a decreased percentage, of phosphoric acid.
While phosphoretted hydrogen gives rise to the same toxic effects as those of phosphorus, red phosphorus is not poisonous; consequently the cause of the toxic quality of white phosphorus must lie in the production of phosphoretted hydrogen when in contact with living tissues. In other words, when white phosphorus is introduced into the di gestive tract phosphoretted hydrogen is given off, which, being easily absorbed, passes into the blood and gives rise to disturbances which prevent hmmatosis This pathogenesis being granted, a new method of treatment is to be followed, which consists in acting against the for mation and absorption of phosphoretted hydrogen. J. Noe (Le Bull. Meld., Apr. 21, '95).
The physiological action of phos phorus in chronic poisoning was out lined in the section on diseases of the jaws (NECROSIS, PATHOLOGY).
Experiments conducted upon dogs who were poisoned by gradually increasing doses of phosphorus, given hypodermic ally in oil. Immediately after death the nervous tissues were fixed in cor rosive-sublimate solutions and stained by Nissl's methods and its modifications and with Biondi-Heidenhain solutions.
In three dogs poisoned by phosphorus. varied and diffuse changes of the cellu lar elements of the nervous system and of their elementary constituents were found. The changes in the spinal cord increased gradually from the anterior to the posterior roots.
The anatorno-pathological process con sisted in a primary degeneration of the co•tico-medullary cells, of those of the cerebellum and of the spinal ganglia with a varying amount of participation of the chromophilic substance of the dendrites. No changes were observed in the neuroglia nor in the blood-vessels. Enrico Rossi (Riv. di Patol. Nerv. e Alent., vol. ii, p. 535, 'DS).
Poisoning by Phosphorus.—Poisoning by phosphorus may be acute or chronic.