BIOCHEMICAL AND HEMODYNAMIC CHANGES FOLLOWING THE SUBCUTANEOUS INJECTION OF GLUCOSE SOLUTION

It is well known that the loss of extracellular electrolyte may contribute to or even produce cardiovascular collapse. This is manifest in its most striking form in the crisis of Addison's disease (1), in diabetic acidosis and coma (2, 3) and in patients losing large amounts of fluid from the gastrointestinal tract (4, 5). In these conditions the losses of the sodium ion, the chloride ion, and water are often the primary and sole cause of circulatory collapse. The chain of events which ends in clinical shock following salt depletion has been experimentally studied (6, 7). Abstraction of salt from a healthy animal via the peritoneal route according to the Darrow-Yannet technique (8) produces hypotonicity of the extracellular fluid. Water then moves into the cells in response to osmotic forces. The consequent decrease in extracellular fluid volume occurs in both the interstitial fluid and the plasma. Diminution in the latter. is readily detected by the rise in the hematocrit and in the concentration of the total serum protein. It is of particular significance that some of the circulating plasma protein is lost and that in terms of proportionate change, the plasma volume diminishes much more than does the extracellular fluid as a whole (7). These alterations in the composition of the fluid in the extracellular and intracellular compartments are an invariable accompaniment of salt depletion. If acutely induced, and of sufficient magnitude, the loss of salt results in a shock state akin to that seen following burns, trauma, or hemorrhage (9). The circulation slows and the venous pressure falls. These changes are associated with a diminished cardiac output (7). If untreated, death ensues. It seems highly probable that during absorption of a glucose hypodermoclysis salt is removed from the circulation in a manner identical with that ob-