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).
THE LIVER AS A DESTINATION AND DESTROYER OF POISONS.
The liver in the mature animal, being the one destination of the blood carried in the portal vein, necessarily becomes the recipient of all medicinal and poisonous agents absorbed by the capillaries and venous radicals of the stomach and intestines. This organ retains and lays up for a time the heavier metals, such as the salts of copper and iron, the iodides and bromides, the vegetable alkaloids such as nicotine, quinine, morphia, and curare, the toxic elements of the bile, the ptomaines and toxins produced by gastric and intestinal fermentations, indol, phenol, etc. Some agents it transforms, as peptones (which it renders non-poisonous), casein, the carbonate of ammonia and its salts with vegetable acids, also indol and phenol, which it combines with sulphuric acid as indyxol and phenyl sulphate, thus rendering them much less toxic. The destructions or new combinations established in the cases of the ptomaines and toxins may explain why such agents are usually much less poisonous when taken by the stomach than when generated in tissues or blood, or when injected hypodermically. Another interesting fact in connection with the ingestion of these bacteridian products (ptomaines and albumoses) is that, when the liver functions are normal as evidenced by the production of glycogen, the toxins are largely destroyed, and they fail to produce poisoning, whereas with a functionally deranged liver and no production of glycogen, they retain their potency, almost as if injected subcutem.
FUNCTIONAL DISORDERS OF THE LIVER.
MELLITURIA, GLYCOSURIA, DIABETES MELLITUS, SACCHARINE URINE.
Source of glucose in food. Glycogen: Its use: Enlarged liver means more glycogen. Glycosuric centre in medulla. Other glycosuric nerve centres. Reflex action, action of drugs and poisons, phlorizin. Disease of lungs or pancreas. Removal of pancreas in dogs. Removal of thyroid. Diseased, liver, fatty, fibroid, hypertrophy, congestion. Extreme fatty change arrests glycogenesis. In solipeds: 3 cases with liver hypertrophy; 1 case with adenitis; 6 cases with emaciation; 2 cases with hæmoglobinuria. Symptoms: Emaciation, debility, langor, fatigue, breathlessness, hollow flanks, unthrifty skin, ardent thirst, polyuria, urine saccharine, of high density. Diagnosis by analysis of urine, sweet taste, Fehling’s test, Trommer’s test, fermentation test. Prognosis: Grave, diet being carbonaceous, when functional resulting from curable disease is hopeful. Treatment: In poisoning cases, antidotes and eliminants, in curable disorders treat these, in more inveterate cholagogues, antiseptics, codeine, opium, croton chloral, strychnia, phosphoric acid, iodoform, ergot, skim milk or buttermilk, good hygiene, open air, shelter, carminatives, bitters, mineral acids, treat complications.
Grape sugar (glucose, C6H12O6) is undoubtedly formed in the stomach and intestines by the action of saliva and pancreatic juice on starch (C6H10O5), and glucose and laevulose (C6H12O6) are also derived from the transformation of cane sugar (C12H12O11). These sugars are absorbed, transformed into glycogen in the liver and passed into the circulation, where they serve to maintain animal heat through their decomposition into carbonic acid and water. They further assist in nutrition and growth, and if their metamorphosis is imperfect they pass out of the system in the urine, producing a temporary glycosuria. As shown above glycogen is produced in the liver cells, and stored up there, in greatest abundance during digestion of starchy and saccharine food, but it is also formed in animals kept on a purely albuminous diet, (flesh), and in the fœtal calf and unhatched chick to which neither starch nor sugar has been furnished as food. It is produced during the decomposition of albuminoids, along with the other end products, leucin, tyrosin and urea. None of these last three is found in the portal vein nor bile ducts, but all four are found in the liver cells, and in the hepatic veins.
In health a physiological balance is maintained by the oxidation of the glucose, mainly in the lungs, so that in the blood of the pulmonary veins no sugar is found. There is an exception to this observable after a full meal, rich in starch and sugar, which produces such an excess of glycogen that a portion is carried to the kidneys and expelled by them causing temporary glycosuria.