Sweat Glands

SWEAT GLANDS, the secretion of sweat by the tubular glands of the skin. It has excretory, water-exchange, and thermoregulatory values. The excretory role of sweat glands is evident from the composition of sweat (see). The value of sweat glands for water exchange is seen in Metabolism, Water Exchange, and Skin, Physiology. After sweating, the blood thickens: its specific gravity, number of erythrocytes, concentration of hemoglobin, and pH increase (Talbert et al.; 1930). The thermoregulatory role of sweat glands is seen in Thermoregulation. Regarding the mechanism of sweating, one should distinguish between local, reflex, and centrally conditioned sweating. Local sweating apparently does not occur under physiological conditions; experimentally it is caused by pilocarpine at the site of injection (Cloetta; 1877). Strong heating (up to 46°) of small areas of skin (20 cm²) also gives local sweating, whereas heating of large areas leads to reflex sweating (Saito, 1930). The latter is more sensitive than local sweating, since it occurs at a lower degree of heating. The possibility of axon-reflex sweating is not excluded (Frohlich, Zak; 1930). Reflex sweating is excited, as already stated, by heating of the skin, as well as by various sensory irritations (irritation of the central end of the femoral or peroneal nerves), and can be regional (e.g., sweating of the skin covering working muscles) or, more often, general; in this case, the reflex excitability of the sweat glands in different parts of the body depends on their state at the moment of irritation; thus, cooling of the extremities can cause the cessation of reflexively induced sweating in them (Langley); feeding with liver increases the reflex excitability of the sweat glands (Frohlich, Zak; 1930). The pathway of the sweat reflex is as follows: thermal irritation of the skin is transmitted by centripetal pathways and dorsal roots to the cells of the sweat center in the lateral horn of the same side; from there goes the effector neuron. The preganglionic fibers of these nerves emerge from the spinal cord together with its anterior roots [according to data by Andre Thomas and Bowing (1922) from C₃ to D₅ for the head, neck, and upper part of the chest, from D₆ to D₁₂ for the upper extremities and chest, from D₁₂ to D₉ for the lower parts of the trunk, from the lower thoracic and first lumbar vertebrae for the lower extremities, from the sacral part for the perineum] and terminate in the cells of the ganglia of the sympathetic trunk (for the lower extremities-in the lower ganglia, for the upper-in the stellate ganglion). The postganglionic fibers enter the corresponding peripheral nerves through gray rami communicantes [for the lower extremities-the sciatic nerve, for the upper extremities-the ulnar and median nerves (Langley, 1895), for the head-through the cervical sympathetic nerves and some branches of the trigeminal nerve] and together with these nerves go to the sweat glands. Thus, the only, so far anatomically established innervation of the sweat glands is sympathetic, which, however, does not exclude the possibility of humoral parasympathetic influences on sweating. Thus, Platz (O. Platz) distinguishes sticky, not abundant sympathetic sweat and liquid, abundant, parasympathetic sweat. The sweat-secreting nerves pass everywhere together with the fibers innervating the smooth muscles of the sweat glands and with the vasomotor nerves; sweating increases and decreases in parallel with the dilation and constriction of the skin vessels; nevertheless, the sweat nerves are true secretory nerves, and their action is not reducible to the dilation of blood vessels, since their irritation causes sweating even on an amputated limb, i.e., after the complete cessation of circulation, and the engorgement of the skin vessels caused by compression of the veins does not lead to sweating. Therefore, sweating is possible even with strongly constricted skin vessels ("cold sweat"). It is possible that the sympathetic nervous system possesses not only an excitatory but also, under certain conditions, an inhibitory action on sweating: thus, Burns (1922) obtained increased secretion of sweat from pilocarpine after removal of the stellate ganglion. The centers of sweating are located in the spinal cord, corresponding to the place of origin of the preganglionic fibers of the sweat nerves (subordinate centers), and in the medulla oblongata (a general center according to Adamkiewicz). The existence of a general sweat center in the diencephalon is assumed. Sweating is also influenced by the cerebral cortex: sweating during mental strain (Kyo, 1930), during an affect, and upon irritation of the anterior sigmoid gyri (Danilevsky). Spinal centers of sweating are directly excited by ordinary spinal cord poisons—strychnine, picrotoxin, camphor—but they are little sensitive to the direct action of heat: with an increase in body temperature they are excited either reflexively by afferent impulses from the skin or through the action of the diencephalic sweat centers, which are very sensitive to the direct action of venosity and the temperature of the blood surrounding them (experiments by Kahn, 1904 with isolated warming of the blood of the head). Thus, sweating of the whole body during strong muscular work and upon the intake of a large amount of hot fluid depends not only on the action of the thermoregulatory centers on the sweat center but also on the direct action on them of the blood, warmed due to increased heat production. Hasama (1930) described a sweat center in the dorsal nucleus of the vagus nerve, consisting, in his opinion, of a vagal (inhibited by atropine) and a sympathetic (inhibited by ergotamine) half; reflex sweating caused by body heating is intensified by moistening this center with a Ringer's acidic solution and weakened by moistening it with an alkaline solution. The pharmacology of sweating is in contradiction with morphological data: as already stated, only sympathetic innervation of the sweat glands is anatomically established; meanwhile, sweating is excited only by parasympathetic poisons (pilocarpine, muscarine, physostigmine), acting both peripherally and on the centers, and is suppressed by atropine, while adrenaline, according to most authors, does not act, and according to Billigheimer (1920), inhibits both spontaneous and pilocarpine-induced sweating, which, however, Langley and Uyeno consider to be the consequence of the vasoconstrictor action of adrenaline. Nicotine, due to its action on the ganglia of the sympathetic chain, first excites and then paralyzes the conduction of sweat impulses through them, but in addition stimulates the spinal centers of sweating.

a. Zubkov. At present, diaphoretic agents are rarely used (see Diaphoretic agents). As agents that limit sweating (antidiaphoretics), the following are applied: 1) Atropinum sulfuricum (0.5 mg in a 0.1% solution under the skin), Extractum Belladonnae (0.01–0.015 per dose in the form of pills, powders, or suppositories). 2) Eumidrin, methylatropine nitrate (1 mg twice a day or at night). It acts similarly to atropine but is significantly less toxic than the latter. With repeated administration, tolerance develops. 3) Acidum agaricinicum, agaricin (0.01–0.02 per dose in powders or pills 5 hours before the expected sweat). It acts paralytically on the endings of the sweat nerves; in contrast to atropine, it does not reduce salivation and therefore does not cause dryness in the mouth and throat. The action is quite reliable, but patients quickly become accustomed to agaricin. The side effect (irritation of the intestine, diarrhea) is eliminated by opium. Large doses produce a narcotic effect. The single maximum dose is 0.1. It is not applied subcutaneously due to its strongly irritating local action. 4) Acidum camphoricum, camphoric acid (1.0–2.0 in amylic capsules 2–3 hours before the expected sweat) — a product of the oxidation of camphor; poorly soluble in water. No side effect has been noted. Reduction of sweating is achieved far from always. 5) Much less frequently and with much less certainty acts the acidic camphoric salt of pyramidone, alkaline salts of tellurium and selenium, etc. In limiting sweating, the main significance here apparently lies in the reduction of the blood filling of the sweat glands due to a change in the redistribution of blood (Zuntz). To eliminate local hyperhidrosis (namely, sweat of the feet), the following are applied: 1) astringent agents containing tannin; among the latter, especially an infusion of sage leaves (Folium Salviae), 2) antiseptic agents acting simultaneously and astringently — formalin, salicylic acid, chromic acid, picric acid, alum, etc. Limitation of sweating and reduction of the foul odor are due to the astringent action of the above-mentioned agents, which prevents the functions of the sweat glands for a longer or shorter period of time, as well as limiting putrefactive processes.