|
KMID : 0381219710030010001
|
|
Journal of RIMSK
1971 Volume.3 No. 1 p.1 ~ p.22
|
|
|
RESPONSE TO INJURY
|
|
|
|
|
Abstract
|
|
|
In a strict or traditional sense, this account will not be a review because of its incomplete list of references. The author in tented, however, to build up comprehensive image of our articles from 1942 up to date concerning systemic effects due to injury and also to include all the references which
are important and inevitable for our comprehension.
Since the Cuthbertson´s report that traumatic injuries cause a marked increase of nitrogen in the urine, it has been generally believed that the traumatic injuries enhance the catabolism of the body and this increased catabolism is caused by the activities of adrenal cortical hormones. Seyle (1940) presented a conception of the general adaptation syndrome and its in vivo mechanism. His presentation seems to be too hasty to build up the image of his schema. It lacks the details of the mode of action of cortical hormones on the target tissue and is also an oversimplified schematic unitary theory.
We started from the keen observation of individual systemic effect of injury and then investigated its in vivo mechanism of injury. and we did not hasten to postulate the results. Some response to injury did not run along the line of Selye´s schema.
The list of our works and the outline of the results were as follows.
1) In the hemorrhagic shock, the morphological shock signs such as simultaneous appearance of congestion and small hemorrhage in the liver, the lungs, the adrenal glands, the heart and the kidneys which were pointed out by Mallory et al. (1950) were masked by means of adrenalectomy.
2) The names of the blood-coagulation-accelerating agents that were confirmed by us are salt solutions(calcium chloride, sodium citricum, sodium oxalate, calcium lacticum); available organ extracts; adrenaline; monosaccharides solution (glucose, fructose, mannose, galactose, xylose); colloidal solution (casein, pepton, gelatin); hydraulic and high atmospheric pressure; acute hemorrhage and infusion of hemolized blood; fat ingestion; ACTH; hypoxia, electric shock; DOCA, and cholesterol; emulsion of steroid hormones (testosterone, estrogen, cortisone, theelin, androgen), traumatic shock (done by hammer in the legs); RES blocking agent (dextran, PVP, collargol, lithium carmine, indian ink); X-ray radiation.
The above mentioned agents were able to be classified into 3 groups according to their in vivo mode of action.
a) Most of them except X-ray, emulsion of steroid hormone, DOCA, hemolized blood, fat ingestion
induced increase of total cholesterol and phospholipids in the circulating blood which were liberated from the adrenal cortex, and these liberated lipids act on the thromboplastin generation of blood clotting process and cause shortening of blood clotting time(indirect agents).b) The accelerating action of hypoxia and electric shock were masked in hypophysectomized rabbits and carbon tetrachloride intoxicated rabbits respectively.
c) The accelerating action of emulsion of steroid hormones, hemolized blood, DOCA, cortisone, cholesterol, and fat ingestion: was direct effect on this thromboplastin generation (direct agents); it was not blocked by adrenalectomy, hypophysectomy, intoxication with carbon tetrachloride.
When the adrenals were stimulated by above mentioned indirect agents, sudanophilic substance, cholesterol, phospholipid and ascorbic acid diminished but the activity of alkaline phosphates and the amount of RNA in zona fasciculata markedly increased especially in stimulation with ACTH.
3) The acceleration of erythrocyte sedimentation rate due to burns, dermatitis (croton oil) and tuberculosis were corrected to normal rate by liver intoxication with carbon tetrachloride.
The rate of acceleration ran in parallel with the grade of changes of A/G ratio and increase of fibrinogen. These changes of plasma protein fraction following burns were due to increased synthesis and turn-over rate of albumin and decreased synthesis and turn-over rate of fibrinogen in the liver.
The activity of mitochondria and the increase of RNA in the liver cells were markedly prominent in burned rats.
4) The marked leucocytosis due to prednisolone ran in parallel with increase of nucleic acid in the circulating blood and it was inhibited in thoracic duct fistula rabbii in the absence of increase of nucleic acid.
The thoracic duct fluid from thoracic duct fistula rabbits contained strong active leucocytosis inducing substance.
From the above mentioned results we postulated that the leucocytosis inducing action of corticoids are due to the liberation of nucleic acids from lymphoid tissues, and nucleic acids act on bone marrow directly because sodium salts of nucleic acids are potent leucocytosis inducing substance.
5) The injury (formalin) induced marked increase of zymogen granules and amylase activity and RNA in the acinar cells, and increased incorporation rate of L-leucine-C14 into protein of pancreas acinar cells and salivary glands acinar cells.
These change due to injury were masked in the adrenalectomized rat.
6) The injury(formalin) induced increase of the number of atretic, developing and Graafian follicles and decrease of the number of normal developing and Graafian follicles in the normal rats, on the other hand, in adrenalectomized rats, formalin did not induce any noticeable effect on the number of follicles, and many intermediate stages of transformation of theca interna into interstitial gland were observed.
7) Injury induced marked regressive changes and also marked increase of mucin production both in gastric mucosa and rectum.
8) Injury affected profoundly the respiratory tract and brought forth regressive changes in the ciliated epithelium, goblet cells and mixed glands, and reduced mucous secretion due to the interference
of uptake of 35S(Na235SO4) into the goblet cells.
Summary:
Now it is evident that injury causes the increased synthesis of albumin fraction in the plasma protein, and increased synthesis of RNA in the liver cells, adrenal cortex, and pancreas acinar cells, and increased incorporation rate of amino acids into liver, pancreas and salivary glands tissue protein, and The mode of action of injury is not operable solely through the channel of hypophysis, but the necessity of adrenal glands is absolute in the in vivo mechanism of systemic effect due to injury.
|
|
|
KEYWORD
|
|
|
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|
|
|