Cooling

COOLING, the action of cold on the organism. A. The influence of cold on lower organisms. In the literature, there is a range of data regarding the extreme endurance of many lower organisms (worms, arthropods, mollusks) to cold. Bacterial spores and encysted forms of protozoa are particularly resistant (e.g., anthrax spores germinate after cooling to -100°C). Data on the possibility of reviving both invertebrates and lower vertebrates after freezing are very contradictory. This is apparently explained by the incomplete freezing of many animals even under the action of very low temperatures (-10°C, -11°C). According to Bachmetiev, supercooling of tissues occurs in insects without their freezing; the same has been proven for lower vertebrates. According to Kochs, death under the action of cold is caused not so much by the action of low temperature, respectively the cooling of the organism, as by the formation of ice crystals in the tissues, which mechanically destroy them; furthermore, there is a withdrawal of water that turns into ice, resulting in the precipitation of proteins and salts in concentrated form and the release of gases. The cellular protoplasm forms a network-like structure in this process, in the loops of which ice crystals lie (Molisch). The formation of ice crystals in tissues can be avoided by freezing them slowly, and then, after very gradual thawing, it is possible to revive some animals even after freezing for several days at temperatures around -8°C to -15°C (experiments by Pictet, Müller-Erzbach, and others on fish and frogs). B. Local influence of cold. Erythrocytes are deformed during freezing and hemolyze upon subsequent thawing (Bunge); leukocytes die off. When cold acts on the external integuments, vasoconstriction and ischemia occur—partly due to the direct influence of cold on the neuromuscular apparatus of the vessel walls, and partly reflexively. The degree of ischemia varies greatly depending not only on the degree of temperature decrease but also on the properties of the acting cold medium: thus, the decrease in tissue temperature under the action of dry cold air occurs through heat radiation; under the action of moist air, it also occurs through conduction; the latter is especially strong with cold damp clothing or the application of snow. Intense cooling is obtained through evaporation under the action of cold wind and especially during the evaporation of ether, liquid carbonic acid, or liquid air. The individually varying sensitivity of the vascular system to cold is also of great importance: in particularly sensitive (often anemic) people, even with slight cooling (immersion of hands in cold water), sharp ischemia occurs, e.g., of the fingers (doigt mort), accompanied by a decrease in sensitivity. With more severe and prolonged cooling, painful sensations and stiffness of movement in the cooled parts occur. Following the vascular spasm, a more or less sharp dilation occurs; the skin turns red and acquires a bluish cyanotic tint (especially on the nose and ears). With prolonged and especially repeated even slight cooling, predominantly in predisposed anemic individuals and children, persistent redness and edematous swelling of tissues are observed, e.g., on the fingers and toes, with mild inflammatory phenomena (chilblain, pernio). Under the same conditions, thickening and roughness of the skin and the formation of cracks are often observed. The disruption of blood flow due to arterial spasm can be so sharp under the influence of even slight cooling that it sometimes leads to gangrene of peripheral parts (e.g., fingers); predisposing factors include increased excitability of the vasomotor system, general anemia, a state of alcohol intoxication, etc. The possibility of cold acting on even deep-seated tissues through local application to the skin has been proven, especially by B. Zondek. Thus, the temperature of the peritoneum, when an ice bag is held on the skin of the abdomen, decreases by 2.7°C after 1 hour, and by almost 4.5°C after 2 hours. In the same experiments, the subcutaneous tissue of the ulnar part of the arm cooled by 3.2°C under the action of cold air. From this, it is evident that when cold acts on the skin, superficially located nerve trunks (e.g., branches of the facial or trigeminal nerve), superficial parts of joints, and muscles can be affected, especially if there is simultaneous moistening of the skin (Lange). All these data have pathogenetic significance in terms of clarifying the influence of cold in the occurrence of such diseases as neuritis, myositis, and articular rheumatism (see Common Cold). With more severe local action of cold (around -16°C), its direct action on the tissues comes to the fore, expressed by degenerative and necrotic changes, sometimes with the formation of blisters on the skin, as in a burn. Acute inflammatory changes soon follow, sometimes also the formation of thrombi in the vessels, and the dead parts are gradually sloughed off. Tissue damage during freezing is explained by the formation of ice in the tissues associated with the withdrawal of water (Molisch, Rischpler). According to Schade, cooling causes a change in tissue colloids with a decrease in their dispersity and an approach to the state of gels, which makes cooled tissues doughy and less elastic. With repeated cooling of tissues, proliferation and hardening of connective tissue and thickening of the epidermis with the formation of giant epithelial cells may occur; therefore, repeated actions of cold were even proposed to accelerate the epithelialization of granulating surfaces. The remote, mostly reflexive action of cold during its local application has very important pathogenetic significance. Thus, the action of cold (especially moist) air on the respiratory tract, particularly when breathing through the mouth, can lead to contraction of the bronchial musculature and even trigger an attack of bronchial asthma; the cooling of the external integuments sometimes has the same effect through a reflex path. The latter often leads to reflexive dilation of the vessels of internal organs, especially in the mucosa of the upper respiratory tract, with the release of abundant liquid secretion (e.g., when cooling the feet). Experimentally, it has also been possible to induce hyperemia of the upper respiratory tract mucosa, abundant mucus secretion in them, as well as hyperemia and hemorrhages in the lungs and sometimes the formation of pneumonic foci by cooling animals. In the latter, however, bacteria were found, so there was a combined action of cooling and infection. Cooling by itself does not cause inflammatory changes in the lungs of animals. When cold acts on the skin, diarrheal phenomena are often observed on the part of the intestines, which is explained both by the dilation of the intestinal vessels and increased intestinal secretion, and by the reflexive intensification of peristalsis. Among other reflexive influences of cooling the integuments on smooth musculature, one can mention urinary disorders in the form of bladder spasms and phenomena of ischuria. It is probably due to the increase in muscle tone under the influence of cold that the symptoms of Thomsen's disease and idiopathic tetany sometimes manifest with particular force in cold and damp weather or during winter. The influence of cooling on kidney function is observed especially often, mainly in the form of so-called physiological albuminuria, which has also been established experimentally. Along with protein, hyaline casts sometimes appeared in the urine. However, the aforementioned changes were observed predominantly with very sharp cooling, especially after preliminary warming of the animals. Morphological changes in the kidneys were also by no means always found. Therefore, the pathogenetic significance of cooling as such, without simultaneous infection, in the origin of nephritis is disputed by some (see Common Cold). Some explain the remote action of cold on internal organs by reflexive contraction of capillaries followed by venous congestion. C. General influence of cooling. The organism of humans and many warm-blooded animals can adapt to severe cold (down to -40°C, -45°C) without a decrease in body temperature occurring. Along with a sharp decrease in heat loss, an increase in heat production occurs, especially if muscular activity is intensified, as often happens in the cold, and much food is consumed (the feeling of hunger is usually significantly increased at cold temperatures). With long-term exposure to cold, due to habituation, even temperatures of -40°C to -45°C are tolerated (in the absence of wind) without unpleasant sensations (Nansen). If heat production does not compensate for increased heat loss (e.g., with insufficiently warm clothing, especially in dampness or in snow), then at a certain, in different cases very different, decrease in the ambient temperature ("critical" temperature), a rapidly progressing drop in body temperature begins, continuing until death. Only hibernating animals tolerate cooling of the body to a temperature only a few degrees above zero. In small animals, even the mere deprivation of movement by tying them to a stand for a long time at room temperature leads to a sharp drop in body temperature and even to death, which is facilitated by shaving the fur, as well as tracheotomy. The latter causes sharp heat loss due to the penetration of cold air directly into the lower respiratory tract.

Furthermore, in small animals, placement in a box lined with ice causes the rectal temperature to fall to 18–25°C within as little as 1.5–2 hours, especially with simultaneous wetting of the skin; when returned to room temperature, such animals no longer warm up and perish; they can only be saved by careful artificial warming and drying; frequently, a febrile rise in temperature develops afterward, and inflammatory catarrhal phenomena are observed in the upper respiratory tract and lungs (Magendie, Claude Bernard, Walther). In the first period of the action of cold, animals exhibit muscular excitation, increased frequency and depth of respiration, acceleration of cardiac activity, and sometimes a slight rise in temperature. Then, phenomena of depression of the heart, respiration, and nervous system ensue. Cardiac activity slows down (even with the vagus nerves severed in the neck, which is explained by the direct action of cold on the heart due to the cooling of the blood). In general, the heart is quite resilient to the action of cold: it ceases to contract only when cooled to 17–18°C, and after freezing and thawing, it can be revived again. Blood pressure, after some initial rise, gradually falls during a further decrease in temperature until death. The excitability of the vasomotor center decreases but is nevertheless maintained almost until death; the excitability of peripheral nerves disappears earlier—when the body is cooled to approximately 25°C. Respiration in the later stage of cooling slows down, at first gradually, parallel to the slowing of the heart, then more sharply, and finally occurs very rarely, interrupted by pauses lasting up to several minutes. The depth of respiration first increases, then decreases; sometimes Cheyne-Stokes respiration is observed. The slowing of respiration is caused by a decrease in the excitability of the respiratory center due to the action of cooled blood upon it. The amount of CO₂ in the blood, according to some data, increases, while according to others, it even decreases; the blood often acquires a lighter, more scarlet color than usual. The number of erythrocytes in the peripheral blood decreases; sometimes hemolysis, hemoglobinemia, and hemoglobinuria are observed; the osmotic stability of erythrocytes decreases. The number of leukocytes in the peripheral blood also decreases; a large number of them accumulate in the capillaries of the internal organs, especially the lungs and kidneys. In connection with the decrease in the amount of proteins in the plasma, the erythrocyte sedimentation rate increases. The amount of sugar in the blood increases during the stage of falling body temperature; even glycosuria is observed. However, with slow cooling, hyperglycemia is not observed. Hyperglycemia during cooling is explained by some authors as an influence through the sympathetic nervous system on the adrenal glands (increased secretion of adrenaline). The amount of chromaffin substance in the adrenal medulla decreases sharply; after transection of the splanchnic nerves, hyperglycemia does not occur during cooling. The amount of lactic acid in the blood increases, and the reserve alkalinity of the blood decreases. Gas exchange during cooling increases (by 20% or more) and only decreases in the late stages. The amount of glycogen in the organs decreases to a sharp degree, especially during prolonged cooling. The humoral influences of cooling put forward recently are very interesting from a pathogenetic standpoint. Their existence is confirmed by the phenomena of hemolysis and hemoglobinuria during cooling. In some so-called common cold diseases (articular rheumatism), eosinophilia is often observed, which indicates an allergic state (Hoffmann). Remote reactions caused by cooling are in many ways similar to allergic reactions (spasms of smooth muscles, increased secretion). According to Widal and Staehelin, there is even a direct link between cooling and the onset of hemoclastic phenomena. Finally, some local changes during cooling have recently been attempted to be explained from the point of view of local allergic reactions, especially in articular rheumatism. In humans, death from cooling apparently occurs, as in warm-blooded animals, when the body temperature falls to approximately 20°C. After the body temperature falls to 24°C under the influence of cold, revival is still possible. In children, the ability to maintain a normal body temperature under the action of cold is much less developed than in adults: sometimes a cold bath leads to a fall in body temperature in a short time. The same is observed in adults during general exhaustion, anemia, and in certain endocrine disorders, especially hypothyroidism. During freezing in humans, general weakness and lethargy, sharp drowsiness, stiffness of movements, dizziness, and lividity of the integuments occur; cardiac activity weakens, respiration becomes rare and superficial; reactions to external stimuli gradually disappear, reflexes vanish, the pupils dilate and cease to react. Some consider the cause of death from cooling to be the cessation of cardiac activity and the resulting cerebral anemia; others consider it paralysis of the respiratory center. On the corpses of persons who died from freezing, sharp congestion of the internal organs is observed, especially the heart cavities. After thawing, hemolysis rapidly sets in; the blood has a light cherry color and is liquid. Hemorrhages are often observed under the pleura and in the lung tissue; on the gastric mucosa, there are hemorrhagic erosions, and sometimes ulcers in the duodenum. However, all these phenomena are inconsistent and not entirely characteristic of death from freezing. The action of cold, even to a slight degree, on the organism is of great importance in the pathogenesis of so-called common cold diseases. In most cases, however, the influence of cooling occurs in combination with infection (see Common Cold).