We have seen in Chapter 2, Note 1 how the place occupied in nature by sodium and potassium can explain their peculiar distribution in the body. Proper to the earth crust, one of the environments through which the complex individual has passed during its phylogenetic evolution, potassium appears as an element of the secondary part of the cellular compartment in the hierarchic organization. As a monovalent heterotropic element, potassium represents the principal organizational cation of this compartment. Its influence exerted in normal and abnormal physiology can be understood through its specific intervention at the cellular level, the changes in potassium content of the other compartments of the hierarchic organization being secondary to those occurring at the cellular level.

Potassium, absent at the nuclear compartment, is thus found in the nuclear or chromosomal sap, only in minimal amounts. We have no direct information about a passage of potassium from cytoplasm into the nuclear compartment under abnormal conditions. Judging by analogy, it appears probable that such a passage would occur and result in the appearance of nuclear vacuoles.

Ample data are available concerning the relationship between potassium of the cellular and of the metazoic compartments. This information receives a special interpretation when related to the above mentioned hierarchic distribution of the elements.

The cells maintain a proper amount of potassium in the cytoplasm which corresponds to a cellular primary constant. This constant insures a normal cellular metabolism and is controlled in part by the selective intervention of the cellular membrane. Under normal conditions, only a slow passage of potassium through this membrane takes place as compared to other constituents, such as of water, for example. On using radioactive potassium, Moore has shown that it takes about fifteen hours to bring it into balance with the intracellular potassium, while for heavy water, such an equilibrium was reached in less than two hours. (254) Due to the intervention of the membrane, only minimal changes result in the cellular potassium even though rapid potassium variations take place in the extracellular compartment. Under normal circumstances, the body is insured through a regulatory mechanism against too strong or too rapid systemic changes. Normally, no potassium is stored in the body beyond that which is contained in the cell and metazoic compartment. Following a high intake, potassium is rapidly excreted. A very small amount is lost through perspiration, an additional amount, of around 10% is lost in the stool (252), and the remainder is lost through the kidney. (253) For insufficient intake, or an abnormal loss through excessive diuresis, prolonged diarrhea or vomiting, the organism tries to reduce this loss of potassium to a minimum. A prolonged systemic potassium deficiency brings about an increase in the weight of the kidney with tubular hyperplasia, which can be interpreted as a compensatory hyperthrophy, in order to insure the reabsorption of very small amounts of potassium from the glomerular filtrate, and thus save this important element for the organism. Consequently, a quantitative abnormal intake or loss of potassium will result in an abnormal amount, either too high or too low in the metazoic fluids, only in case of a concomitant deficiency of the regulatory system. Prolonged quantitative changes in the amount of potassium available to the total body, influence only up to a certain point, the potassium content of the cells. Thus when the total body potassium remains low over a period of time, the cells too lose potassium. (250) On the other hand, the potassium in the cells increases after an abundant, prolonged administration of the cation. (251)

Besides these quantitative changes we have to consider abnormal conditions as affecting the specific intervention of this element. The proper level to which potassium belongs and the characteristic changes which take place at the cellular level, could be translated in too high or too low values. We tried to further interpret its intervention through the heterotropic character of this element.

The changes seen to occur in muscles have permitted us to relate this dual occurrence observed for the potassium content of the cells to the two abnormal metabolic conditions which take place in the cells. A muscle in anabolic metabolism and characterized by a process of glycogenogenesis, shows an increase of its potassium content. On the contrary, catabolic processes such as those occurring during muscular exercise (255) or in tissues in agonic states, are related to a loss of potassium from the cells. This metabolic loss of potassium is different from that seen to result from the death of the cells.

The destruction of cells in general, results in a liberation of their potassium into the interstitial fluids. However, such a destruction explains only in part the progressive loss of potassium encountered in abnormal conditions. The erythrocytes of stored blood lose their potassium to plasma through another process than their destruction. The same is true for patients undergoing surgery. They experience a constant loss of cellular potassium into the metazoic fluids, for which the process of destruction is only partially responsible. The breakdown of cells as it occurs in starvation or dehydration for instance, releases a proportion of 2.4 gm. of potassium for every gram of nitrogen which is liberated under these conditions. (256) However, in surgical patients, the potassium loss was found to be two or three times higher than expected, considering the nitrogen loss. (257) This indicates a passage of potassium out of the cells without cellular destruction.

The study of the red cell potassium changes in stored blood and in the diphasic biological phenomenon such as in hemo shock, has increased our knowledge of the conditions which correspond to these changes. We found thus that in the first phase of hemo shock there are lower amounts of potassium in the red cells, followed by a second phase where this cellular potassium content increases. These two changes were thus connected with the characteristic offbalances occurring in hemo shock: type D in the first phase, and type A in the second. Further studies of tissues in offbalance A or D in pathological conditions have confirmed this correlation between the two fundamental offbalances and the two opposite variations in cellular potassium.

The heterotropic character of potassium as seen through the test of the second day wound crust pH, (See Note 1, Chapter 5), has correlated the changes in potassium distribution to the heterotropic or homotropic character of the occurring processes. A low cellular content in potassium would correspond thus to the homotropic character of the processes characterizing the offbalance D. Those corresponding to a high cellular content concord with the group of heterotropic processes. Increased intracellular potassium results in a heterotropic anabolic effect, while loss of cellular potassium corresponds to catabolic metabolism.

The relationship between the hierarchic compartments explains the changes under abnormal conditions in the amount of potassium present at the different compartments. The study of the diphasic phenomenon of hemo shock has permitted us to follow this relationship between cellular and plasmatic potassium. In the first phase of a hemo shock, to the low potassium of the cells corresponds a hyperkalemia, while in the second phase, to a higher cellular potassium corresponds a hypokalemia.

With potassium, a cellular element, the changes seen in the metazoic compartment can thus be considered to be secondary to those occurring at the cellular level. An abnormal cellular condition, with an increase in the cellular potassium content, would thus have an opposite effect upon the amount of potassium present in the metazoic fluids. The fact that plasma potassium values are kept below normal, has to be interpreted as a means of compensating the high values present in the cells. These low values in plasma would result in a reduction of the cellular potassium and favor its return to normal values when possible. It is especially through changes in the urinary excretion that the respective hypokalemia are induced and maintained. On the other hand, an abnormal change in the cellular condition resulting in a low amount of potassium in the cells is seen to induce a prolonged compensatory increase in the potassium content of the metazoic fluids. Oliguria with reduced loss of urinary potassium, permits the creation and maintenance of this secondary hyperkalemia.