HYDRATES

HYDRATES (from Greek hydor-water), compounds formed by the attachment of water molecules to molecules of various chemical substances. Even substances that are chemically saturated in general are capable of such attachment. For example: a) when white dehydrated copper sulfate (CuSO₄) reacts with water, five molecules of water attach to each of its molecules, forming blue crystalline hydrate (CuSO₄·5H₂O); b) calcium oxide CaO (quicklime) reacts vigorously with water, forming hydrate of calcium oxide Ca(OH)₂ (slaked lime). In the formation of hydrates, water can attach as such, or the elements of water attach, with redistribution of bonds between the atoms of both molecules. The strength of the water bond in hydrate molecules varies greatly. Thus, the hydrate formed by chlorine gas with water can exist only at temperatures below 9.6°C. Many salts lose their crystallization water (weather) already at room temperature. It is extremely difficult to extract water from Ca(OH)₂: a temperature of at least 400°C is required. Accordingly, the reaction of CaO with water (slaking of lime) is accompanied by exceptionally abundant heat release. The class of hydrates is extremely large and diverse. As the most typical examples, we cite the following: metal oxides, when combined with water, give basic hydrates, alkalis: for example, Na₂O+H₂O = Na₂O·H₂O = 2NaOH, caustic soda, an extremely stable hydrate; metalloid oxides, when combined with water, give acids, for example, SO₃ + H₂O = H₂SO₄, sulfuric acid; CO₂ + H₂O = H₂CO₃, carbonic acid (exists only in aqueous solution and here already partially decomposes into CO₂ + H₂O); most salts bind water in the form of crystallization water: CuSO₄·5H₂O, Na₂SO₄·10H₂O (Glauber's salt), Na₂CO₃·10H₂O (crystalline soda), and in this case the strength of the bond in the molecules of various salts is far from the same. In elements, the ability to form hydrates is expressed very weakly: thus, chlorine forms with water the hydrate Cl₂·8H₂O, and bromine forms Br₂·10H₂O (unstable compounds). Hydrates can also be called compounds of the sugar type (C₆H₁₂O₆-hexose; C₁₂H₂₂O₁₁-cane sugar), cellulose [nC₆H₁₀O₅·(n-1)H₂O], etc. When water is removed from these compounds (for example, by the action of concentrated sulfuric acid), charring occurs, i.e., the release of free C in the form of coal. This group of compounds represents completely definite individual substances, from which it is impossible to extract water without destroying the molecule as a whole. The complete opposite of this last type of hydrate are the hydrates contained in aqueous solutions. It turns out that molecules of the dissolved substance have the ability to form compounds with molecules of the solvent, in particular in aqueous solutions-with water molecules. The resulting hydrates in many cases cannot be isolated in the free state and represent compounds of variable composition, i.e., compounds with a different number of water molecules. For example, when anhydrous sulfuric acid is mixed with water, strong heating occurs and further hydration of the monohydrate takes place, i.e., H₂SO₄(SO₃·H₂O) combines with water molecules. The existence of hydrates in aqueous solution was first pointed out by Mendeleev. At present, the very fact of chemical interaction between solvent and solute molecules in aqueous solution is generally recognized (see also Hydration). M. Konstantinova-Shlezinger. HYDREMIA (from Greek hydor-water and haima-blood), literally-concentration, water content in the blood. However, usually instead of this grammatically precise definition, in medical literature, Hydremia refers only to hyperhydremia, i.e., increased water content in the blood, thinning of the blood. Hydremia depends on two conditions: 1) the exchange of water between blood and tissues and 2) the concentration of proteins in the blood. In some cases, both factors act simultaneously and in the same direction, for example, both retention of fluid in the blood and its depletion of proteins occur. To determine hydremia, blood is dried to constant weight in a desiccator at room temperature (drying methods at high temperatures are inaccurate) or refractometric determination of serum proteins is used. Previously, determination of the specific gravity of blood was also used. The normal water content in whole blood ranges from 75 to 85%, in serum it can be taken as 90%, erythrocytes contain water from 57 to 64%. The organism extremely strictly regulates hydremia, which is determined to a large extent by the molecular concentration and osmotic tension of the blood. Physiological hyperhydremic states, as well as hypohydremia (thickening of the blood, inspissatio sanguinis), are distinguished by extreme brevity and negligible deviation from the norm. The introduction of even very large amounts of fluid into the body causes only slight hyperhydremia (water concentration changes by 1.5-3%). After this, sometimes thickening of the blood can be observed. Some authors (Veil), obviously making determinations exactly at these moments, come to the paradoxical conclusion that the introduction of water causes hypohydremia. This circumstance clearly demonstrates the importance of tissue factors in the regulation of hydremia-it depends on the hydrophilicity of tissue colloids, the rate of water absorption into the blood, and other regulators of intermediate water exchange. Accordingly, old, purely mechanical, views on hyperhydremia, which caused justified criticism and even denial of its existence, now give way to the neuro-reflex theory, according to which the introduced water is only an irritant of fluid exchange between tissues and blood. Similarly, in this direction, some other substances act, for example, dextrose and glycocol. The fluid content in the blood also increases after the introduction of large amounts of table salt into the body, due to the transition of water from tissues to blood. The same mechanism occurs in a number of pathological conditions, when compensatory hydremia protects the body from increased concentration of substances determining osmotic tension in the blood, resp. from osmotic hypertension. Hydremia depends on age; according to refractometric observations by Reiss, children have compared to adults 'physiological hydremia', since the protein content in their serum is only 6.5%. The nature of hydremia after the introduction of fluid is subject to individual fluctuations and depends on age and type of nutrition. According to the latest data, the liver plays an exceptional role in the regulation of hydremia, apparently performing its barrier function also in relation to water. In view of the novelty of the question, the number of clinical observations (e.g., in liver diseases) in this direction is still small, but there are already convincing experimental data (Molitor, Mautner and Pick) on dogs with Eck fistula: the introduction of fluid causes them to have more significant and prolonged hyperhydremia than in normal ones. The reticulo-endothelial system participates in the regulation of hydremia: according to experiments by Saxl and Donath, blockade of the latter with collargol increases hyperhydremia in rabbits after intravenous administration of physiological solution. To a certain extent, hydremia depends on blood pressure: vasoconstriction causes thickening of the blood, vasodilation-thinning. In connection with this stands the hypohydremic effect of adrenaline (up to 15%); according to some data, however, the thickening of the blood after adrenaline injections does not depend on its vasoconstrictive effect. Some other hormones also have an effect on hydremia. It is interesting that the diuretic effect of pituitary preparations is not accompanied by constant or regular fluctuations in hydremia. Even less common are physiological shifts in the direction of hypohydremia (see Anhydremia). In kidney diseases, even accompanied by abundant loss of water with urine, thickening of the blood does not occur; on the contrary, they are characterized by sharp hyperhydremia. Only the depletion of blood proteins due to albuminuria cannot serve as an explanation for this hyperhydremia: from the modern point of view, renal hydremia is 'edema of the blood', one of the manifestations of general edema of the organism. Hyperhydremias accompanied by an increase in the total mass of blood are observed with decompensation of the heart and other circulatory disorders-this is the so-called 'plethora serosa'. Its cause is, on the one hand, 'edema of the blood', as in nephrogenic hydremia, on the other-the transition of water from tissues to blood, due to a drop in blood pressure. Hyperhydremias in cachectic conditions, during starvation, are caused by hypalbuminemia, depletion of blood proteins.

Old experiments by Grawitz, who produced hyperhydremia in rabbits after the introduction of extracts of cancerous tumors, gave rise to the assumption that, in addition to protein starvation, products affecting water exchange from the tumor play a role in cancerous cachexia. In tuberculosis and some cases of pernicious anemia, normal hydration is found, so that nutritional disturbance under certain conditions leads to true oligohemia. In posthemorrhagic anemias, in the first hours after blood loss, a marked hyperhydremia is observed, occurring due to the transition of fluid from the tissues into the blood to restore the blood volume; this hyperhydremia lasts for several days. In diabetes mellitus, hyperhydremia is almost always present. Diabetes insipidus occurs with normal hydration, and sometimes with thickening of the blood.