Glycogen and sugar are evidently of use in muscular contraction as they are always diminished in the vessels of contracting muscles (Sanderson), being converted into lactic acid (Bernard).
Forced muscular movements soon expel glycogen from the dog’s liver, passing it into the blood, and there the excess of glycogen dissolves the red blood globules. If glycogen is injected into the blood, achrodextrin and hæmaglobin appear in the urine (Landois).
Ammonia carbonate and asparagin, or glycin, with a carbhydrate diet produced in rabbits a considerable increase of glycogen (Rohmann).
Poisoning by arsenic, phosphorus or antimony destroys the glycogenic function of the liver, which then fails to respond even to diabetic puncture of the medulla.
There are important changes effected in the blood globules in passing through the liver. The leucocytes are increased, the hepatic veins containing 5 or even 10 times as many as the portal vein (Bernard, Lehmann, McDonald). Their ratio to the red globules is in the portal vein 1:524 and in the hepatic veins 1:136 (Hirt). The red globules undergo marked changes, having, in the hepatic veins, a smaller size, sharper outlines, less flattening in the disc, a habit of massing together irregularly in place of adhering in rouleaux, and they dissolve less readily in water.
REDUCTION OF ALBUMINOIDS.
A large proportion of the fibrine formers are changed in passing through the liver (Lehmann, Bernard), in man as much as 2,690 grammes daily (Brown Sequard), a fact which goes to account for the increase of fibrine in inflammation when the liver is inactive. The change consists mainly in deoxidation and reduction into simpler compounds which can be more readily dissolved and eliminated. Arrest of the liver functions in fever is therefore liable to throw into the blood, products that are little soluble and often poisonous. The end product is largely urea, and this Cyon always found in excess in the hepatic veins of dogs (in the portal veins 0.08 grammes, and in the hepatic veins 0.14 to 0.17 grammes). In man hepatic disorder is at once marked by the lessening or disappearance of urea from the urine, and the increase of the less oxidized uric acid (Parkes). In acute atrophy of the liver, urea disappears from the urine, being replaced by the less oxidized leucin and tyrosin (Frerichs, Murchison). In birds urea is replaced by uric acid and this is always found in the liver.
The increase of urea and allied products bears a direct relation to the activity of the hepatic circulation. Stimulation of the liver by electric current sent through the abdominal walls largely increased the secretion of urea (Sigrist, Stolnikow, Schröder and Salomon). Murchison, Perrin and Bruardel had a great increase of urea by stimulating the circulation in the liver. Certain agents ingested are transformed into urea, among which may be named glycocolle, brucin, asparagin, sarcine, alanine, and ammonia muriate.
Any degeneration of the hepatic cells which impairs or arrests their functions lessens the production of urea. In fevers therefore and in hepatic degenerations the extent of the functional or structural derangement may be to a large extent gauged by the diminution of urea. A simple hyperæmia, without as yet any serious impairment of structure or function, may be attended by a marked increase of urea, whereas any destruction of the liver cells, or any serious modification which interferes with the normal function, brings about a decided decrease. A hepatic disorder accompanied by suppression of urine is always a grave disorder. On the contrary a free secretion of urine during liver disease is a favorable symptom.
There is reason to believe that red blood globules are destroyed in the healthy liver, producing bilirubin and urea (Landois). In diseased states this becomes excessive, and the resulting coloring matter is often modified, giving the strong tints, seen in the urine in fever and certain hepatic disorders.