This section is from the book "Research In Physiopathology As Basis Of Guided Chemotherapy With Special Application To Cancer", by Emanuel Revici. Also available from amazon: Research In Physiopathology
The changes in the amount of potassium could be connected to its relationship to sodium, and further interpreted in the frame of the hierarchic organization. Both are members of the same series in the periodic chart, but they correspond to different compartments of the organization. Sodium is the cation of the metazoic compartment, and potassium that of the cellular. They would consequently act differently towards cells, for instance. Under abnormal conditions, sodium is able to enter the cells. For example, following an injury, the cellular membrane which is almost impermeable to sodium, lets it pass through. A penetration of sodium into cells occurs, as demonstrated by the use of radioactive sodium. (42) As a consequence, potassium is released from the cells in order to maintain the necessary osmotic pressure constant. Many abnormal processes occur following the penetration of the sodium in the cells and others occur due to the release of potassium. The sodium which entered in the cells is partly isolated together with water, to form cellular vacuoles. The response of the metazoic compartment to those changes are interesting. Hyperkalemia, with a simultaneous hyponatremia occurs in the first phase of the diphasic phenomenon. The opposite happens in the second phase, when hypokalemia coincides with a hypernatruria.
This antagonism between sodium and potassium is seen further in the pharmacologic activity of these elements. The administration of potassium salts induces a greater elimination of sodium and water, which explains its diuretic action with dehydration of tissues and progressive alkalinization of the urine. The effect upon the different organs is also antagonistic. For instance, in their effect upon the heart, as Merrill and co workers have shown, the characteristic electrocardiographic effects of hyperkalemia appear only when the sodium level of blood is lowered. (259) A high sodium content prevents the cardiac effects of hyperkalemia.
In opposition to the atrophy of the adrenal glomerulosa induced by an excess of sodium administration, a potassium overdose can cause an enlargement of these zones in rat adrenals.
The hyperkalemia due to external intake such as in potassium poisoning, or due to systemic response to low cellular potassium, specifically influences certain functions. The peripheral vascular collapse with lowered blood pressure, cold clammy skin, pallor, listlessness and mental confusion, are symptoms related to the offbalance D, and encountered in high plasma potassium. They appear in conditions such as shock and burns which correspond to a prolonged first phase of the diphasic phenomenon. Pares thesis and flaccid paralysis (260) (261) are also important results of hyperkalemia. The most important changes appear in cardiac physiology and can be interpreted to correspond to low cellular automatism. Hyperkalemia will thus induce dromotropic positive changes, such as the increase of the duration of the Q R S complex, or that of the P R interval, with a delay in the ventricular contraction, or a block which can lead to the arrest of the heart in diastole. (262), (263) Characteristically appears the changes in wave T, which increased became even angular. The change seen in offbalance D, are similar to those induced by a prolonged administration of potassium. In a study of the pharmacological activity of various agents upon the heart, made in collaboration with I. Eroglu, we used these changes as an indication of the type of offbalance they induce.
Fig. 216B shows some examples of this effect on rabbits. One group comprises agents considered as able to induce an offbalance D. They induce changes in the T wave which high amplitude is characteristic for a hyperkalemia. An opposite effect is seen in the other group, formed by agents able to induce an offbalance A, and where the T waves are remarkedly depressed. (See page 574).
All these considerations have led to a more precise use in therapy of the information furnished by the study of potassium distribution. The quantitative deficiency—recognized by low potassium in total blood and serum—is controlled by oral and parenteral administration of potassium. A quantitative excess—with high values in serum and total blood—is treated with the administration of ionic exchange compounds, diet, laxatives and more sodium intake. For the offbalances, the treatment is especially directed to those agents which seem to influence more strongly the cellular potassium metabolism. Selenium lipoids and sulfurized tetra hydronaph thalene are used for offbalance A, and heptanol for offbalance D.
The fact that the cellular membrane plays an important role in the metabolism through which the abnormal changes in potassium occur, has led us to use agents acting upon these membranes. Adrenaline has been seen to favor the discharge of potassium from the liver cells, simultaneously with glycogen. We thus used adrenaline for cases of offbalance A in which an especially high cellular potassium was present. On the opposite side, the administration of insulin together with an increased intake of glucose was seen to increase the cellular potassium. (258) A similar effect was seen for cortisone, and ACTH, for heptanol, cholesterol and also for the un saponifiable fractions of organs. These agents have been used in the treatment of offbalance D at the cellular level, where abnormal high values of serum potassium are present.