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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).
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.
A small amount of glycogen is also produced habitually by the
white blood cells and stored up in them, but this is insufficient to
determine its appreciable elimination by the kidneys.
In cases of persistent glycosuria the fault may be held to consist in
one of three functional derangements:
1st. The failure of the liver to transform the alimentary sugar into
glycogen.
or 2d. The excessive production of glycogen in the liver.
or 3d. The arrest of the destructive oxidation of sugar in the lungs
and tissues.
In a diabetic patient who died suddenly of apoplexy Bernard found
that the liver was enlarged, comparing with the average as 25:14
while the contained sugar bore the ratio of 37.5:22. This enlargement
coming from malaria or other poison, such as alcohol, ether (Harley),
arsenic, quinia (Aitken), ammonia, chloroform, or phosphoric acid
(Murchison), is an established condition of glycosuria. A rich and
abundant food (starchy and saccharine especially), or an unusually
active hepatic circulation acts in the same way.
Bernard as early as 1849 showed that the glycogenic function of
the liver was greatly increased and glycosuria determined by pricking
the floor of the fourth ventricle in the median line just in front of the
calamus scriptorius and near the root of the vagus nerve, or a few
millimeters in front of this.
It follows that irritation of this part of the medulla however
produced, whether from local disease, or by reflex action from some
distant organ in a state of irritation, may serve as the starting point
of diabetes in particular instances. That the cause may be a reflex
stimulus is shown by the suspension of the glycogenic function after
section of the vagus nerves, and its reappearance when the central
end of the cut vagus is galvanized, or, the floor of the fourth ventricle
is irritated, the direct or efferent excitation being transmitted
through the sympathetic nerve (Bernard). I can cite a case of
glycosuria in a man supervening on a severe blow on the head from a
falling ledger. Brain injuries which suspend animal functions, but
not the nutritive ones, such as apoplexy, concussion of the brain or
curare poisoning are liable to induce diabetes.
Traumatic injuries to other parts of the nervous system induce
glycosuria. Thus traumatism of the optic thalami; of the cerebral
lobes or peduncles; of the pons; of the cerebellum or of its middle or
posterior peduncles; transverse section of the medulla or of the
spinal cord opposite the second dorsal vertebra; traumatism of the
superior or inferior cervical ganglion or the first thoracic (Eckhard);
of the sympathetic twig which accompanies the vertebral artery
(Pavy); of the brachial plexus; of the solar plexus (Munck, Klebs); or
of the sciatic nerve (Schiff).
The explanation of these facts may be sought in a reflex action
established by the conveyances of irritation to the true glycogenic
centres in the brain and the transference of the efferent nervous
impulse through the sympathetic nerve to the liver. It will be borne
in mind that in the case of section of the vagus nerve electric
stimulation of its detached peripheral part has no glycogenic effect
on the liver, while galvanizing the central portion determines
glycosuria.
In the case of glycosuria through stimulation of the sympathetic
nerve or its ganglia the action may be concluded to be direct.
Strangely enough, irritation of the sympathetic between the tenth
and twelfth ribs or the splanchnic nerves fails to produce glycosuria,
though the hepatic branches of the sympathetic pass through them.
In ordinary cases of reflex glycosuria it may be assumed that the
existence of irritation at the peripheral ends of the vagus and of some
other nerves, leads to an apparent glycogenic influence passing
through these to the brain, and of the distribution of the efferent
impulse through the upper portion of the spinal cord, as far as the
fourth dorsal vertebra in the rabbit (Cyon, Aladoff, Schiff), and
through the sympathetic nerve to the liver. This may account for the
appearance of the disorder as a sequel of disease in any part to which
the vagus in particular is distributed, and notably in the lungs. A
number of poisons (malarial, alcoholic, ether, carbon monoxide,
amyl nitrate, curare, or the nitro-propionic acid, methyl delphinin,
morphia, chloral hydrate, arsenic, quinia, ammonia, chloroform,
phosphoric acid, and phlorizin) produce glycosuria.
The intravenous injection of dilute saline solutions, or frequent
blood letting materially increases the sugar, probably by causing
solution of the red globules. Phlorizin is the most potent of all these
agents. Whether given hypodermically or by the stomach it causes in
three hours a marked production of glucose which continues to be
eliminated for a period of thirty-six hours. The urine may become
charged with glucose to the extent of from 6 to 13 per cent., and
without any rise in the body temperature. This artificial glycosuria
may be kept up indefinitely by the continued administration of
phlorizin, and even in the fasting animal, or one on an exclusively
albuminous diet, as well as in those on an aliment rich in saccharine
or hydro-carbonaceous matter. In the frog it produces diabetes even
after the extirpation of the liver showing that it stimulates other
sources of sugar production beside the hepatic or that it inhibits the
transformation of sugar derived from the alimentary canal and other
sources.
Another suggestive source of mellituria is disease of the lungs, or
any condition which interferes with the due æration of the blood and
oxidation of the alimentary or hepatic sugar. But it cannot be
assumed that the rôle is altogether or mainly chemical. The thoracic
organs being supplied by branches of the vagus and sympathetic
nerves there is the obvious suggestion of a reflex action through the
diabetic centers in the brain. The frequent complication of diabetes
with lung diseases (inflammatory, tubercular, syphilitic, and
otherwise) is abundantly proved, whether it is to be explained on the
above hypothesis or through other unknown changes in the blood.
Diabetes has been repeatedly found in connection with disease of
the pancreas, and the complete extirpation of the pancreas in dogs
gives rise to glycosuria (Mering and Minkowski, Thiroloix,
Lancereaux, Lepine). If a small portion of the pancreas remains
glycosuria does not supervene. It has been suggested that the
pancreas has a double function, and beside its secretion, produces a
glycolytic ferment which passing into the portal blood determines
the formation of glycogen in the liver. Arrest of the pancreatic
secretions does not cause glycosuria, so it has been suggested that
the glycogenic enzyme is a product of the connective tissue cells of
the pancreas. Functional as well as structural disease of the pancreas
can be conceived of as inhibiting the production of this ferment and
the consequent elaboration of glycogen. Chauveau and Kauffmann
deduce from their observations that the action is a reflex one
established through the glycogenic centres in the medulla. Pancreatic
glycosuria is especially fatal (Harley).
Finally extirpation of the thyroid body in dogs has been followed
by glycosuria (Falkenberg). This suggests a systematic examination
of the urine in all cases of goitre, with extensive glandular changes.
Apart from experimental cases diabetes in the lower animals has
been observed to be nearly always associated with diseased liver.
Fatty degeneration has been the most frequent lesion, but cirrhosis,
hypertrophy and congestion were present in other cases. In a
number of cases as the fatty degeneration reached an extreme
degree, the sugar disappeared from the urine, the hepatic cells being
no longer functionally active, and death speedily followed. The same
has been observed in the fatty degeneration attendant on poisoning
by arsenic or phosphorus.
GLYCOSURIA IN SOLIPEDS.
Heiss records two cases of this disease in heavy Belgian horses ten
and eleven years old, the urine of which showed a percentage of 3.75
of grape sugar, and which died in two months in a state of
marasmus. The liver was enlarged and of a clay yellow color.
Dieckerhoff reports one fatal case in which there were also yellow
discoloration, congestion and hypertrophy of the liver. No lesion
could be found in the pancreas nor nervous system. Perosino records
a case in a horse suffering from contagious adenitis, which may be
supposed to have been connected with the action of the toxins or the
imperfectly oxidized albuminoids on the nerve centres or liver.
Delprato relates six cases in the same stable in overworked, half
starved and emaciated horses. Rueff and Mouquet each contributes a
case occurring in paraplegia attendant on hæmoglobinuria and in
which the amounts of sugar were respectively 5.85 and 1.01 per cent.
These latter cases are manifestly complicated ones in which the
reflex irritation (or inhibition of glycogenesis) is transmitted from
the diseased or poisoned brain to the already disordered liver.
Symptoms. There is a profound interference with nutrition, a
rapid loss of flesh and weight, of spirit and energy and an extreme
muscular weakness in spite of an excessive appetite. The subject is
fatigued and breathless under the slightest exertion, the flanks are
retracted and hollow, and the hair dry, rigid and lifeless. Appetite is
poor and fastidious, but an intense and consuming thirst is usually
present, the animal drinking deeply at every opportunity, and
passing urine with corresponding frequency and abundance. The
urine is clear, yellow, neutral, and saccharine, the sugar varying from
1 to 12 per cent. (3.6 on an average). Notwithstanding the amount
passed (55 litres per day, Cadeac) the density usually exceeds the
normal (1052 and upward), normal being 1040 to 1050. There may
or may not be hyperthermia, and in exceptional cases appetite has
been retained to the last. Cataract and corneal ulceration are
sometimes observed as in man.
Diagnosis. Presumption may arise from the above mentioned
symptoms, and especially the bulimia, the polydipsia, the polyuria,
the rapidly advancing emaciation, weakness, and prostration and the
ocular troubles, but conclusive evidence is only found in the presence
of glucose permanently in the urine.
Tests for Sugar in the Urine. For one who can go through it the
touching of the tip of the tongue with a drop of the suspected urine
will give a prompt and reliable test.
Fehling’s cupric test is the next best for simplicity and availability.
Dissolve 34.639 grammes (1⅕ oz.) pure cupric sulphate in 200 cubic
centimeters of distilled water: 173 grammes (6 ozs.) of pure neutral
sodio-potassic tartrate and 80 grammes of potassium hydrate in 500
cubic centimetres of distilled water. Add the copper solution slowly
to the potassium one and dilute the clear mixture to one litre. One
cubic centimeter of this fluid will be discolorized by 0.005 gramme of
sugar; or 200 grains will be discolorized by 1 grain of sugar.
Trommer’s test is even simpler for a mere qualitative test. Pour the
suspected urine, freed from albumen, into a test tube and add a
solution of caustic potassa or soda until distinctly alkaline. Should
this throw down earthy phosphates or carbonates filter these out.
Then add drop by drop a solution of pure cupric sulphate in distilled
water (3.5:100) so long as it throws down a yellowish red precipitate
of oxide of copper. When the supernatent liquid remains clear and
assumes a distinctly bluish tint, the sugar has all been precipitated.
The amount of precipitate is a criterion of the quantity of sugar,
which may be otherwise estimated by the amount of copper salt
used.
The fermentation test is made by adding a teaspoonful of liquid
yeast to four ounces of the suspected urine, stopping the flask lightly
and placing it in a temperature of 60° to 80° F. for 12 to 24 hours
when the sugar will have been converted into alcohol and dioxide of
carbon. The loss of weight will indicate the amount of sugar, as also
will the lowering of the specific gravity. If before testing the urine
was 1060, and after 1035, it contained 15 grains of sugar to the fluid
ounce.
Prognosis. This is always rendered more grave in the horse than in
man, because of the impossibility of putting him on a purely
albuminous diet. The great tendency is to a rapidly fatal issue,
especially in cases of irremediable structural lesions in the brain and
liver. Where the disorder is largely functional, as in connection with
hæmoglobinuria or as the result of poisons ingested the prospect of
recovery is often good.
Treatment. In cases due to poisoning the use of antidotes and
eliminating agents will be effectual, and in transient and curable
diseases like pulmonary disorder, hæmoglobinuria and paralysis the
appropriate treatment will restore. In the more inveterate or
constitutional cases all treatment is liable to prove ineffectual. At the
outset some apparent amelioration may be obtained from salicylic
acid, salicylate of soda, bicarbonate, acetate, citrate, sulphate or
chloride of soda, nitro-muriatic acid and other cholagogues. Blisters
to the perichondrium may also be employed. Later, when
degeneration of the liver has reached an extreme point, these will be
of no avail. Cadeac recommends acetanilid, antipyrine, and benzo-
naphthol largely on their antiseptic merits, and Jong claims a
recovery in a horse under daily doses of 12 grains of codeine. Opium
has long been employed in man with partially good results, and
croton chloral, strychnia, phosphoric acid, iodoform and ergot are
recommended in different cases.
One of the most beneficial agents is skim milk or buttermilk as an
exclusive diet, and this may be to a large extent adopted for the
horse. Under its use the sugar may entirely disappear, and though
rheumatoid pains in the joints may be brought on, these usually
subside on withdrawing the source of lactic acid. They may further be
met by the use of salicylates. The greatest care should be taken of the
general health, an open air life, with protection against colds and
storms, and a healthy condition of bowels, kidneys and skin being
particularly important.
The impaired digestion and assimilation usually demand
carminatives, stomachics, bitters, and mineral acids, particularly the
nitro-muriatic. With the same intent a fair amount of exercise short
of absolute fatigue should be secured. But each case will require a
special study and treatment consonant to its special attendant
lesions, its causative functional disorders, and its stage. One case
may demand attention to bacteridian poisoning, one to a better
regimen and diet, one to liver disease, and one to disease of the
brain, etc. After this treatment specially directed to the abnormal
function or structure, would come the more specific treatment for
mellituria which would be more or less applicable to the general
glycolytic disorder.
GLYCOSURIA IN CATTLE.