Adrenalinemia

ADRENALINEMIA, the content of adrenaline in the blood. The question of the normal content of adrenaline in the blood (physiological adrenalinemia), as well as pathological hyper- and hypoadrenalinemia, are even at present among the most controversial questions in endocrinology. Numerous chemical methods for determining adrenaline do not give sufficiently accurate results. Biological methods, based on the property of adrenaline to raise blood pressure, cause pupil dilation, hyperglycemia, and enhance contractions of the isolated uterus, hardly have advantages over chemical methods, as they lack sufficient sensitivity and specificity. One must therefore judge the content of adrenaline in the blood of an experimental animal only indirectly, by determining adrenaline in the blood of the adrenal veins. Since in the blood flowing from the adrenal glands the concentration of adrenaline is incomparably greater than it would be possible in the rest of the blood, the errors of the determination methods affect the research results to a lesser degree. Despite this, the figures of various authors still diverge. On average, based on these determinations, it can be considered that normally in 1 cubic cm of blood from the adrenal vein there is contained about 0.0005 mg of adrenaline (Ehrmann, O'Connor and others). Biedl, however, considers this figure too low. Trendelenburg gives somewhat larger figures, on average, 0.00125 mg in 1 cubic cm of blood from the adrenal vein. According to this author, per minute, about 1.2 cubic cm of blood flows from the adrenal glands of a cat, which gives a daily production of adrenaline by the cat of about 5 mg. According to Neumann's data, from 6 to 9 cubic cm of blood flows through the adrenal glands of a cat per minute. The absolute amount of adrenaline, all other conditions being equal, also changes depending on the size of the animal. Popielski determines that per kilogram of weight of a dog, about 5.76 mg of adrenaline is formed per day. Already in the blood of the inferior vena cava, the amount of adrenaline per unit volume sharply decreases not only due to the dilution of adrenal venous blood, but also because adrenaline is very rapidly destroyed in the blood. In the blood of the left heart, neither chemical nor biological methods can detect the presence of adrenaline. The discovery of adrenaline was met with enthusiasm, and it quickly took the position of 'king of hormones.' This was all the easier since among the substances claiming this name, it alone and to this day remains a substance with a firmly established chemical characterization. However, doubts and uncertainties accompany it throughout its path. Already Battelli expressed the assumption that adrenaline is not produced by the adrenal glands, but only accumulates in them. Biedl states that 'for adrenaline there is habituation of the body to the poison' - a circumstance that must serve as a serious obstacle to its hormonal action. Very recently, Gley, on the basis of numerous experiments that caused a lively polemic between him and Tournade and Chabrol, definitely asserts that adrenaline, the presence of which cannot be detected even in the blood of the right heart under normal conditions, is secreted into the blood of the adrenal veins in quantities incapable of causing a physiological effect, and considers it not a hormone but a product of cellular metabolism subject to destruction. In addition, three more series of facts - the maintenance of normal blood pressure after bilateral adrenalectomy, the preservation of the function of the splanchnic nerves and cardiac nerves, and the constancy of the action of asphyxial blood under the same conditions - destroy, in Gley's opinion, the concept of the physiological role of adrenaline. It should be noted that in a number of experiments Tournade and Chabrol could only confirm the previously known fact of increased secretion of adrenaline by the adrenal glands under the influence of irritation of the splanchnic nerve. These experiments, therefore, essentially do not contradict Gley's point of view. However, it is difficult to think that adrenaline, possessing such strong and specific action on the sympathetic nervous system, produced not only in the medulla of the adrenal glands but also in other chromaffin paraganglia closely connected with sympathetic nodes, represents merely a random by-product of cellular metabolism. In view of this, it is natural to assume that the adrenaline produced by the chromaffin system in loco nascendi, in places of its formation, exerts a tonic and possibly trophic influence on the sympathetic nervous system, while part of it, secreted into the blood, is indeed a by-product, an excess, subject to destruction. This hypothesis received confirmation in the experiments of Aver'yanov and Medvedeva in Bogomolec's laboratory. The introduction of adrenaline directly into the medulla of the adrenal glands in their experiments caused a typical increase in blood pressure and hyperglycemia. At the same time, the action of adrenaline injected into the adrenal gland, the vessels of which were ligated and whose anatomical connection with the organism was maintained only through the nerve (the second adrenal gland was previously removed), lasted considerably longer than when adrenaline was injected into the blood. The question of pathological hypo- and hyperadrenalinemia is even less definite. Addison's disease (see) is usually cited as an example of hypoadrenalinemia. In hyperadrenalinemia, various diseases were seen as causes: adrenaline sclerosis of the vessels, hypertension, adrenaline diabetes, spontaneous gangrene, epilepsy, etc. However, since neither chemically nor biologically can changes in the content of adrenaline in the blood be proven in all these diseases, one must recognize the significance of hypo- and hyperadrenalinemia in the pathogenesis of these diseases as hypothetical, based on deduction from the pharmacodynamics of adrenaline. This, of course, does not deny the possibility of clinical forms of medullary hypo- and hyperadrenocorticism (see Adrenal glands).