Temperature hypothalamic

The hypothalamic temperature controller (Bl) can be inactivated by neuroleptics (p. 236), without impairment of other centers. Thus, it is possible to lower a patient s body temperature without activating counter-regulatory mechanisms (thermogenic shivering). This can be exploited in the treatment of severe febrile states (hyperpyrexia) or in open-chest surgery with cardiac by-pass, during which blood temperature is lowered to 10°C by means of a heart-lung machine. 

Pyrogens (e.g., bacterial matter) elevate—probably through mediation by prostaglandins (p. 196) and interleukin-1—the set point of the hypothalamic temperature controller (B2). The body responds by restricting heat loss (cutaneous vasoconstriction chills) and by elevating heat production (shivering), in order to adjust to the new set point (fever). Antipyretics such as acetaminophen and ASA (p. 198) return the set point to its normal level (B2) and thus bring about a defervescence. 

Alcohol produces dilation of the skin vessels, flushing, and a sensation of warmth. Alcohol also interferes with the normal cutaneous vasoconstriction in response to cold. The body heat is therefore lost very rapidly and the internal temperature consequently falls. At toxic alcohol levels, the hypothalamic temperature-regulating mechanism becomes depressed and the fall in body temperature becomes pronounced. For these reasons, consuming alcoholic beverages for the purpose of keeping warm in cold weather is obviously irrational. 

Intracerebroventricular injection of sulfolane in dosages of 300, 1000, and 3000 p.g caused the preoptic/anterior hypothalamic area temperature to rise 0.23, 0.47, and 0.56%, respectively. This hyperthermia was considered significant at the 3000-p.g dosage (30). 

Pyrogens are substances that, when they enter the blood stream, influence hypothalamic regulation of body temperature, usually resulting in fever. Medical control of pyrogen-induced fever proves very difficult, and in severe cases results in patient death. 

Thermoregulation. PG raise the set point of hypothalamic (preoptic) thermoregulatory neurons body temperature increases (fever). 

Heat stroke is the state in which heat stress induces a dangerously high core temperature that leads to tissue damage and particularly cerebral disturbance. The core temperature usually exceeds 40°C. The condition may follow heat exhaustion but the temperature rise may occur before salt or water depletion have had time to become manifest. Many organ systems may be affected by acute heat stroke including the brain, kidney, liver and muscles. Disturbance of the hypothalamic heat regulatory centre can lead to a loss of physiological responses to the... 

Injection studies have shown that nickel can decrease body temperature (Gordon 1989 Gordon et al. 1989 Hopfer and Sunderman 1988 Watanabe et al. 1990). Because nickel also disturbs the circadian rhythm of temperature regulation, this decrease is thought to result from an effect on the central nervous system. It has been speculated that nickel may mimic the effect of calcium on the hypothalamic thermoregulatory center resulting in hypothermia (Hopfer and Sunderman 1988). 

Most of the serotonin in the brain is in the brainstem, specifically in the raphe nuclei considerable amounts also are present in areas of the hypothalamus, the limbic system, and the pituitary gland. Current evidence indicates that serotonin is involved in the regulation of several aspects of behavior, including sleep, pain perception, depression, sexual activity, and aggressiveness. Some of the most important antidepressant agents are believed to prevent the reuptake of serotonin (see Chapter 33). Serotonin also may be involved in temperature regulation and in the hypothalamic control of the release of pituitary hormones. 

The salicylates are also potent antipyretic agents, with the exception of diflunisal, which is only weakly active. Aspirin acts at two distinct but related sites. It decreases prostaglandin-induced fever in response to pyrogens and induces a decrease in interleukin-1 modulation of the hypothalamic control of body temperature. Thus, the hypothalamic control of body temperature returns, vasodilation occurs, heat dissipates, and fever decreases. Other uses of aspirin include inhibition of platelet aggregation via inhibition of thromboxanes, which has been shown to decrease the incidence of blood clots, myocardial infarction, and transient ischemic attacks. 

Antipyretic action Salicylates lower the elevated body temperature. Hypothalamic thermoregulatory centre acts as a thermostat of the body which maintains the balance between heat production and heat loss. Salicylates reset the hypothalamic thermostat which is disturbed during fever. They do not affect the heat production but they increase the heat loss by causing vasodilatation and sweating. The antipyretic action of salicylates is probably due to the inhibition of PG synthesis. 

Fever. Prostaglandins appear to be pyretogenic that is, they help produce the elevated body temperature during fever.55 Although the details are somewhat unclear, prostaglandins produced in hypothalamic blood vessels may promote fever by altering the thermoregulatory set-point within the hypothalamus so... 

Aspirin does not alter the normal body temperature, which is maintained by a balance between heat production and dissipation. In a fever associated with infection, increased oxidative processes enhance heat production. Aspirin acts by causing cutaneous vasodilation, which prompts perspiration and enhances heat dissipation. This effect is mediated via the hypothalamic nuclei, as proved by the fact that a lesion in the preoptic area suppresses the mechanism through which aspirin exerts its antipyretic effects. The antipyretic effects of aspirin may be due to its inhibition of hypothalamic prostaglandin synthesis. Although aspirin-induced diaphoresis contributes to its antipyretic effects, it is not an absolutely necessary process, because antipyresis takes place in the presence of atropine. 

M., and Voigt, K. Temperature dependent burst discharges in magnocellu-lar neurons of the paraventricular and supraoptic hypothalamic nuclei recorded in brain slice preparations of the rat. In ... 

The middle cerebral artery occlusion model (MCAO) is commonly used in experimental focal cerebral ischemia. This technique causes hypothalamic injury resulting in hyperthermia, worsening outcome and possibly masking neuroprotective effects. Thus, careful temperature monitoring is needed in those preclinical studies. Recently, Gerriets et al. (10) introduced a new MCAO model that involves intraarterial embolizationusing macrospheres. Unlike the traditional MCAO suture model, this macrosphere model does not result in hyperthermia and yet provides reproducible infarcts. 

Ferguson AV, Veale WL, Cooper KE (1984) Changes in the hypothalamic mechanisms involved in the control of body temperature induced by the early thermal environment. Brain Res 290 291-306. 

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