Heat-induced acute hyperthermia results in a reversible depression of cold defence in the rat (Rattus norvegicus)

Szelényi, Zoltán; Palkó, Ágnes; Székely, Miklós

doi:10.1016/0306-4565(95)00041-0

Cited by 3 publications

(4 citation statements)

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“…Thus, anapyrexia is certainly one of the strategies of animals to depress metabolism for saving oxygen and energy under life-threatening conditions. In a notable case, anapyrexia is shown to be induced after severe heat exposure or heat stroke in various species of animals [36][37][38][39], being named hyperthermia-induced hypothermia. Unfortunately, the merit of this phenomenon has not been clarified [40].…”

Section: Merit Of Anapyrexia and Application Of Cryogens In Human Actmentioning

confidence: 98%

Possible Human Endogenous Cryogens

Shido¹,

Sugimoto²

2011

CPPS

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Anapyrexia, which is a regulated fall in core temperature, is beneficial for animals and humans when the oxygen supply is limited, e.g., hypoxic, ischemic, or histotoxic hypoxia, since at low body temperature the tissues require less oxygen due to Q(10). Besides hypoxia, anapyrexia can be induced various exogenous and endogenous substances, named cryogens. However, there are only a few reports investigating endogenous cryogens in mammals. We have experienced one patient who suffered from severe hypothermia. The patient seemed to be excessively producing endogenous peptidergic cryogenic substances the molecular weight of which may be greater than 30 kDa. In animal studies, the patient's cryogen appeared to affect metabolic functions, including thermogenic threshold temperatures, and then to produce hypothermia. Since endogenous cryogenic substances may be regarded as useful tool in human activities, e.g., during brain hypothermia therapy or staying in a space station or spaceship, further studies may be needed to identify human endogenous cryogens.

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Section: Merit Of Anapyrexia and Application Of Cryogens In Human Actmentioning

confidence: 98%

Possible Human Endogenous Cryogens

Shido¹,

Sugimoto²

2011

CPPS

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“…In several animal species, both whole-body heat exposure (Adolph 1947;Lord et al 1984;Szelényi et al 1996;Wilkinson et al 1988;Wright 1976) and IPH Blatteis 1994, 1996;Shido et al 1991) have been shown to result in hypothermia that develops after the heating ceases. A priori, the thermoregulatory mechanism of this phenomenon could involve either the inhibition of metabolism or the enhancement of heat loss (e.g., generalized peripheral vasodilation).…”

Section: Discussionmentioning

confidence: 99%

“…1996) and present experiments was accompanied by marked skin vasoconstriction. Moreover, Szelényi et al (1996) have demonstrated that hyperthermia-induced hypothermia involves the transient depression of cold defenses, i.e., a pronounced but reversible decrease in the threshold T b-thresh for activation of metabolic heat production. After the T b-thresh for heat production is decreased, the body is passively cooled by the environment along an exponential curve, and no cold-defense responses are triggered until the T b curve crosses the T b-thresh curve, thus reaching a new, lower T b-thresh .…”

Section: Discussionmentioning

confidence: 99%

“…In fact, if the heat exposure is followed by an exposure to a near-thermoneutral environment, hypothermia rather than hyperthermia is likely to occur. In animal experiments, whole-body heat exposure in guinea pigs (Adolph 1947), rats (Lord et al 1984;Szelényi et al 1996), mice (Wilkinson et al 1988;Wright 1976) and cats (Adolph 1947), as well as intraperitoneal heating (IPH) in rats (Shido et al 1991) and guinea pigs Blatteis 1994, 1996), all result in a paradoxical fall in T b occurring after heating ceases ("hyperthermia-induced hypothermia"). Moreover, the longer and more intensive the initial heat exposure is, the deeper and longer is the consequent hypothermia (Romanovsky and Blatteis 1994;Wilkinson et al 1988).…”

Section: Introductionmentioning

confidence: 99%

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Heat defense control in an experimental heat disorder

Romanovsky¹,

Blatteis

2000

International Journal of Biometeorology

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Both whole-body heat exposure and intraperitoneal heating (IPH) result in a body temperature (T(b)) fall that occurs once heating is abated ("hyperthermia-induced hypothermia"). This phenomenon involves a decrease in the threshold T(b) (T(b-thresh)) for activation of metabolic heat production (cold defense). Whether the T(b-thresh) for ear skin vasodilation (heat defense) also changes during hyperthermia-induced hypothermia remains unknown. In experiment 1, we applied IPH to guinea pigs by perfusing water through a preimplanted intraperitoneal thermode and delivered the total heat load of either approximately 1.5 kJ ("short" IPH; perfusion duration: 14 min) or approximately 3.0 kJ ("long" IPH; 40 min). Short IPH caused skin vasodilation and a 1.1 degrees C rise in T(b); no hypothermia occurred when IPH ceased. Long IPH caused vasodilation and hyperthermia of a comparable magnitude (1.4 degrees C) that were followed by a T(b) fall to 1.9 degrees C below the preheating value. In experiment 2, the Tb-thresh for skin vasodilation was measured twice: at the beginning of long IPH and at the nadir of the post-IPH hypothermia. The two T(b-thresh) values were 39.0 (SEM 0.1)degrees C and 39.2 (SEM 0.2)degrees C respectively. In the controls, the T(b-thresh) was measured at the beginning and after short IPH; both control values were 39.0 (SEM 0.2)degrees C. We conclude that the hyperthermia-induced hypothermia, although previously shown to be coupled with a decrease in the T(b-thresh) for cold defense, occurs without any substantial change in the T(b-thresh) for heat defense. We speculate that postheating thermoregulatory disorders are associated with threshold dissociation, thus representing the poikilothermic (wide dead-band) type of T(b) control.

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