The secretion of bile is but a small part of the function of the liver,
and that is by no means a purely eliminating process. Man secretes in
twenty-four hours about 10 parts per 1,000 of body weight, the dog 14 to
15, the cat 15 to 20, the sheep 25, the rabbit 130, the Guinea-pig 170,
the goose 12 (Cadeac), the horse 12 (Colin). But the amount varies
largely; Scott found that a dog yielded 21, and Kölliker that another
yielded 36 per 1,000 of the body weight.
Only about one-fourth of the biliary acids (Bischoff, Voigt), and
one-eighth of the sulphur (Bidder and Schmidt) of the bile can be found
in the fæces. Most of the bile is re-absorbed from the intestine and
secreted anew, so that, in the course of twenty-four hours, the material
secreted serves the same purpose again and again. During this repetition
of secretion and absorption, it becomes little by little metamorphosed
into other products, which are eliminated by the lungs and kidneys
(Parkes, Murchison).
The functions of the bile so far as known are:
_a._ The solution of alimentary matters, and especially of fat, in the
intestine, and the hastening of endosmosis, of fats and peptones;
_b._ The stimulation of peristalsis in the bowel;
_c._ Antisepsis and deodorization of the contents of the bowels;
_d._ The determination of the formation of glycogen;
_e._ The excretion of bile coloring matter, bile acids and cholesterine.
In regard to the glycogenic action it may be said that in cats, the bile
ducts of which have been tied, no glycogen was formed, even when the
diabetic puncture of the brain was made (Legg). Clinical observation
seems to throw some doubt on the formation of bile coloring matter apart
from the liver. In diseased liver with suspended secretion of bile (waxy
and fatty degeneration, cancer, cirrhosis) the bile pigment was found in
neither blood nor urine (Frerichs, Murchison, Haspell, Budd). Even after
extirpation of the liver in frogs, neither biliary acid nor pigment
could be found in the blood (Müller, Lehmann, Moleschott). These results
must, however, be qualified by the observations of Hammersten who found
bilirubin as a normal constituent of blood serum in the horse, and by
Virchow’s discovery that hæmatoidin (now held to be identical with
bilirubin) is constantly found in old blood extravasations into the
tissues.
The origin of the bile coloring matters may be traced in part to
destruction of red globules in the liver. Quincke has shown that in the
hepatic capillaries in post-embryonic life the leucocytes englobe and
destroy the old and worn out red blood corpuscles which thus become a
source of bile coloring matter. Such destruction is specially likely to
occur in badly maintained conditions of the blood, and in hepatitis or
other liver disease in which the white cells accumulate in the hepatic
capillaries, and when the blood current is retarded. Hence the liability
to jaundice in such conditions. The formation of new red blood
corpuscles has been observed in the protoplasmic cells of the liver in
the embryo, but this has not been established for post-embryonic life
(Neumann, Lowit).
The two common coloring matters of the bile are =bilirubin= which
colors the yellow bile of man, omnivora, and carnivora and
=biliverdin= which tints the dark green bile of herbivora. =Bilirubin=
(C_{32}H_{36}N_{4}O_{6}) forms transparent fox red clinorhombic
prisms. It is insoluble in water but soluble in chloroform, and may
thus be separated from the biliverdin which is insoluble in
chloroform. United as a second basic acid with alkalies it is soluble
in water. It is easily obtained from the red gall-stones of man or ox,
and is chemically identical with hæmatoidin. =Biliverdin=
(C_{32}H_{36}N_{4}O_{8}) is an oxidized derivative of bilirubin and is
insoluble in chloroform, slightly soluble in ether and freely soluble
in water. In addition to its presence in bile it has been found in the
placenta of the bitch. The =test= for bile coloring matter is made by
placing a drop of the suspected liquid on a white porcelain plate and
adding a drop of impure, brown, nitric acid (nitric and nitrous
acids). If bile is present there is produced a beautiful play of
colors passing from the green of biliverdin, through blue, violet,
red, and ending in yellow.
With regard to the formation of bile pigments in morbid conditions it
may be noted, that agents which dissolve the red blood globules (such as
bile acids or water), when injected into the veins determine the
appearance of bile pigment in the urine (Frerichs, Kuhne). When we
consider that an animal (dog) secretes ¹⁄₅₀ of its body weight daily of
bile, and that nearly all of this is re-absorbed from the intestines, we
can realize this as an important source of bile and urinary pigments.
Of the =bile acids=, =taurocholic= is the most abundant in the bile of
man, birds, and of many mammals and amphibians, while =glycocholic acid=
is the more plentiful in the ox and pig. It is absent in sucklings. The
taurocholic acid has been found to prove most destructive to red blood
corpuscles, and in strong solution is distinctly antiseptic, checking
the development of bacteria, of the alcoholic and lactic fermentations
and of the tryptic and diastatic action of pancreatic juice.
These are conjugate acids, formed by the union of cholic acid with
taurin and glycin respectively, and they are found almost exclusively,
in combination with soda in the bile. They are found in the liver and do
not accumulate in the blood when the liver has been removed. They
increase under an albuminous diet.
The =test for bile acid=, is to take the suspected liquid from which all
albumen has been precipitated, add a few drops of solution of cane
sugar, shake into a froth, and pour sulphuric acid, drop by drop, down
the side of the test tube. A _reddish purple_ color appears in the
froth, and shows two absorption bands at E and F. Any albumen left in
the liquid will give the same color, but only one absorption band.
The =secretion of bile= is more abundant on animal than on vegetable
food, and on albuminous than fatty. It ceases during hunger, but is
increased by ingestion of water. Its solids are most abundant one hour
after feeding. It increases under a copious and rapid blood supply, but
is arrested by diminished blood flow, even under increased pressure (in
ligature of the vena cava in front of the diaphragm). Vigorous exertion,
drawing off blood to the muscles of the trunk, diminishes the secretion
of bile, while transfusion of blood, up to a given grade of blood
pressure increases it. Nervous conditions, which cause contraction of
the portal vessels, increase the secretion by forcing more blood through
the liver. Such are strychnia or other stimulation of the valve of
Vieussens, of the inferior cervical ganglion, of the hepatic or
splanchnic nerves, or of the spinal cord. Fever causes its arrest.
The =secretion of bile= is further stimulated by the following :
_a._ The ingestion of bile into the stomach and abdomen. This being
absorbed and carried to the liver greatly increases the biliary
secretion. It is not necessary that the bile shall be a product of the
same genus of animal, the bile of the ox is an active stimulant of the
liver of the dog.
_b._ Of medicinal agents the following increase and liquefy the bile:
olive oil in large doses, phosphate of soda, salol, and salicylate of
soda.
_c._ The following not only increase the bile, but through their
purgative operation, expel it from the bowels: calomel, mercuric
chloride, colocynth, aloes, jalap, rhubarb, podophyllin, and cold rectal
injections. These accordingly lessen the secretion later, by removing
the stimulus of the absorbed bile.
_d._ The following are comparatively mild biliary stimulants: benzoic
acid, benzoate of soda, oil of turpentine, terpene, terpinol, and
euonymus, and still less active are alkaline bicarbonates, bromides,
sulphates and chlorides, arsenic and ether.
=Secretion of bile is lessened= by: starvation, a too fatty dietary,
alkaline iodides, atropia, strychina, hepatic degenerations, (fatty,
cirrhosis), catarrh of the bile ducts, diseases of the liver, gall duct,
or duodenum which interfere with the discharge of bile, the antisepsis
of the bowels, or the reabsorption of bile. This work virtually moves in
a vicious circle, as the action of septic ferments in the duodenum
hinders the reabsorption of bile and of the food products which go to
the production of bile, and in its turn the withholding of bile from the
intestine removes the normal antiseptic (the bile acids) and favors
septic fermentation and the inhibition of duodenal digestion and
absorption. Another factor is found in the ptomaines and toxins absorbed
from the alimentary canal and arrested in the liver. These debilitate
the liver cells, impair the liver functions and lay the gland open to
bacteridian infection. The bile in such a case is transformed into a
pale or yellow, viscid liquid, with more or less dark colored granular
debris, and this proves a favorable culture ground for bacteria
especially the _golden staphylococcus_ and the _bacterium coli commune_.
With septic condition of the liver the usual result of ligature of the
bile duct is a peri- and intralobular sclerosis and the formation of
minute biliary abscesses. In the absence of sepsis, ligature of the
biliary duct, produces—not abscess but—necrobiosis, preceded by
interlobular connective tissue hyperplasia, and granular or fatty
degeneration of the hepatic cells. (Charcot, Legg, Lahousse, Dupre).