Hce'moglobin{Sinia . — Asotcemia . — Etc. 44 1 



protection by interfering with the thoroughness of digestion and 

 absorption, by securing elimination from the portal veins and 

 liver, and by reducing the amount of albuminoids in the blood. 



A blood abnormally rich in albuminoids, as it is in the tran- 

 sient plethora induced by a short period of rest, in the well- 

 conditioned working horse, without any restriction of his diet, 

 may therefore be set down as one of the most important factors 

 in producing hsemoglobinsemia. Nor is this without approxi- 

 mate examples in human pathology. VonBamberger has shown 

 that " hsematogenous albuminuria" will occur in healthy indi- 

 viduals when there is an excess of albumen in the blood-plafsma, 

 as after a too free use of albuminous food, or after suppression 

 of the milk secretion (lyandois). A .similar result comes from 

 increase of blood pressure, as after drinking freely, or when, 

 under emotion or violent exertion, the heart's action is increased 

 in force and the blood is thrown with greater impetus into the 

 large renal arteries. Senator has found albuminous urine to 

 attend and follow, for several days, upon forced marches made by 

 young recruits. Here the muscular work is added to the in- 

 creased blood tension superinduced by the more active contrac- 

 tions of the heart. 



In this connection it is interesting to trace the changes in the 

 blood after transfusion. The dilatability of the capillaries 

 enables the system to accommodate itself to a very great increase 

 in the volume of blood An increase of 83 per cent, may be borne 

 without serious results, but above this limit there is increasing 

 risk and an increase of 150 per cent, entails immediate danger to 

 life. In the restoration of the blood to its normal condition, the 

 secretion of water sets in promptly leaving an excess of albumin- 

 oids and blood globules. The next change is in the albuminoids 

 which in two days are almost entirely transformed into urea. 

 This leaves the blood abnormally rich in globules (Panum, I,esser, 

 Worm-Miiller), the red globules break up much more .slowly and 

 may. still be in excess after the lapse of a month (T.scherjew). 



In this light, temporary plethora cannot of itself be accepted as 

 the main or essential cause of the disease. It must be admitted 

 to be a more constant and important factor than the mere ex- 

 posure to cold, but of itself it is inadequate to the production of 

 hsemogldbinsemia. In the absence of exertion the general 



