Hypocapnia

HYPOCAPNIA (from Greek hypo - below, under, and kapnos - smoke), a term proposed by Henderson to designate a reduced CO₂ content in the blood (instead of acapnia, see), caused by enhanced pulmonary ventilation under the influence of increased activity of the respiratory center. The latter reacts in this way: 1) to an increase in the content of hydrogen ions (see) or in general to a change in the ratio in the blood (see Active reaction) and 2) to a change in the reaction in the direction of increased acidity in the respiratory center itself under the influence of metabolic processes occurring within it with an insufficient supply of O₂. Thus, in the first case, the increase in the activity of the respiratory center is of hematogenic origin (blood acidosis), and in the second, of central origin. In accordance with this, two forms of hypocapnia are also distinguished: hematogenic and centrogenic. The first is characterized by an increased hydrogen number of the blood, acidosis caused by the formation of non-volatile acids in the body (e.g., sulfuric, phosphoric, and uric—upon abundant protein food; lactic—upon increased muscular work; acetone bodies—under pathological conditions, and the like); the second is caused by a primary increase in respiratory activity, during which the hydrogen number drops, compensatory excretion of alkalis by the urine increases, and ammonia formation decreases. Under conditions inverse to those just stated, an increased CO₂ content in the blood is observed—hypercapnia, and moreover in exactly two forms: hematogenic—upon blood alkalosis (from diet or medications), with a lowered hydrogen number of the blood, and centrogenic—upon decreased activity of the respiratory center (e.g., from narcotics), with an increase in the hydrogen number of the blood. In both cases of hypocapnia, pulmonary ventilation is weakened. The normal state of the blood in relation to its CO₂ content is often designated by the term eucapnia.

M. Shaternikov. HYPOXANTHINE: C₅H₄N₄O, or 6-oxypurine. Colorless, very fine crystals, sparingly soluble in cold water (1:40,000), more easily in hot (one part of hypoxanthine dissolves in 70 parts of boiling water). Insoluble in alcohol. Easily soluble in acids and alkalis. Unlike xanthine, it does not give the murexide reaction. With silver, it gives insoluble compounds, which can serve for the quantitative determination of hypoxanthine. It is also precipitated from solutions by picric acid. Hypoxanthine is found in animal and plant cells, where it is an intermediate product of nucleic metabolism. The primary source of its formation is the nuclear substance of cells. In meat extracts, it is formed during the breakdown of inosinic acid (a nucleotide containing hypoxanthine, pentose, and phosphoric acid). In the process of normal purine metabolism, hypoxanthine is formed mainly from adenine and passes through xanthine into uric acid. This process is conditioned by the so-called xanthine oxidase—an enzyme widely distributed in animal tissue and representing an oxido-reductase. The transition of hypoxanthine into uric acid occurs both aerobically and anaerobically. In normal human urine and blood, the content of hypoxanthine is very insignificant, but it increases greatly in leukemia. Being administered per os, hypoxanthine is absorbed by the intestine and excreted in the urine in the form of uric acid.