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The body responds to thermal perturbations (body temperatures differing from the appropriate threshold) by activating effector mechanisms that increase metabolic heat production or alter environmental heat loss. Each thermoregulatory effector has its own threshold and gain, so there is an orderly progression of responses and response intensities in proportion to need. In general, energy-efficient effectors such as vasoconstriction are maximized before metabolically costly responses such as shivering are initiated. The interaction between thermal input, central control, and effector responses is shown in Figure 40-2 ; this figure also shows normal values for the major autonomic response thresholds.
Effectors determine the ambient temperature range that the body will tolerate while maintaining a normal core temperature. When specific effector mechanisms are inhibited (e.g., shivering prevented by the administration of muscle relaxants), the tolerable range is decreased. Still, temperature will remain normal unless other effectors cannot compensate for the imposed stress. Quantitatively, behavioral regulation (e.g., dressing appropriately, modifying the environmental temperature, assuming positions that oppose skin surfaces, and voluntary movement) is the most important effector mechanism.
Infants regulate their temperatures remarkably well. In contrast, advanced age, infirmity, or medications can diminish the efficacy of thermoregulatory responses and increase the risk of hypothermia. For example, decreased
Figure 40-2
Schematic illustrating thermoregulatory control mechanisms.
Mean body temperature is the integrated thermal input from a variety of tissues,
including the brain, skin surface, spinal cord, and deep core structures. This input
is shown entering the hypothalamus from the left.
However, thresholds are usually expressed in terms of core temperature. A core
temperature below the thresholds for response to cold provokes vasoconstriction,
nonshivering thermogenesis, and shivering. Core temperature exceeding the hyperthermic
thresholds produces active vasodilation and sweating. No thermoregulatory responses
are initiated when the core temperature is between these thresholds; these temperatures
identify the interthreshold range, which in humans is usually only about 0.2°C.
(Threshold data from Lopez M, Sessler DI, Walter K, et al: Rate and gender
dependence of the sweating, vasoconstriction, and shivering thresholds in humans.
Anesthesiology 80:780–788, 1994. Figure redrawn from Sessler DI: Perioperative
hypothermia. N Engl J Med 336:1730–1737, 1997.)
Cutaneous vasoconstriction is the most consistently used autonomic effector mechanism. Metabolic heat is lost primarily through convection and radiation from the skin surface, and vasoconstriction reduces this loss. Total digital skin blood flow is divided into nutritional (mostly capillary) and thermoregulatory (mostly arteriovenous shunt) components.[12] The arteriovenous shunts are anatomically and functionally distinct from the capillaries supplying nutritional blood to the skin (thus vasoconstriction does not compromise the needs of peripheral tissues). Shunts are typically 100 µm in diameter, which means that one shunt can convey 10,000-fold as much blood as a comparable length of capillary 10 µm in diameter.
Control of blood flow through arteriovenous shunts tends to be "on" or "off." In other words, the gain of this response is high. Local α-adrenergic sympathetic nerves mediate constriction in the thermoregulatory arteriovenous shunts, and flow is minimally affected by circulating catecholamines. Roughly 10% of cardiac output traverses arteriovenous shunts; consequently, shunt vasoconstriction increases mean arterial pressure approximately 15 mm Hg.
Nonshivering thermogenesis increases metabolic heat production (measured as whole-body oxygen consumption) without producing mechanical work. It doubles heat production in infants[13] but increases it only slightly in adults.[14] The intensity of nonshivering thermogenesis increases in linear proportion to the difference between mean body temperature and its threshold. Skeletal muscle and brown fat tissue are the major sources of nonshivering heat in adults. The metabolic rate in both tissues is controlled primarily by norepinephrine release from adrenergic nerve terminals and is further mediated locally by an uncoupling protein.[15]
Sustained shivering augments metabolic heat production 50% to 100% in adults. This increase is small in comparison to that produced by exercise (which can, at least briefly, increase metabolism 500%) and is thus surprisingly ineffective. Shivering does not occur in newborn infants and is probably not fully effective until children are several years old. The rapid tremor (up to 250 Hz) and unsynchronized muscular activity of thermogenic shivering suggest no central oscillator. However, superimposed on the fast activity is usually a slow (4 to 8 cycle/min), synchronous "waxing-and-waning" pattern that presumably is centrally mediated.[16]
Sweating is mediated by postganglionic cholinergic nerves.[17] It is thus an active process that is prevented by nerve block or atropine administration. [18] Even untrained individuals can sweat up to 1 L/hr, and athletes can sweat at twice that rate. Sweating is the only mechanism by which the body can dissipate heat in an environment exceeding core temperature. Fortunately, the process is remarkably effective, with 0.58 kcal of heat dissipated per gram of evaporated sweat.
Active vasodilation is mediated by a yet-to-be-identified factor released from sweat glands; the mediator may be a protein because it is not blocked by any standard drugs.[19]
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