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  • Articles: DFG German National Licenses  (13)
  • Thermoregulation  (9)
  • Hypothermia  (7)
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  • Articles: DFG German National Licenses  (13)
Material
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 51 (1981), S. 257-269 
    ISSN: 1435-1463
    Keywords: Thermoregulation ; db cyclic AMP ; hypothermia ; hyperthermia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of intraventricular administration of dibutyryl adenosine 3′, 5′-cyclic monophosphate (db cyclic AMP) on the thermoregulatory responses of unanesthetized rats and rabbits to different ambient temperatures (Ta) were assessed. Administration of db cyclic AMP (10–60 mM) produced dose-dependent hypothermia in both rats and rabbits at Ta 2–22 °C. The hypothermia in response to db cyclic AMP was due to decreased metabolic heat production and cutaneous vasodilatation. There was no change in respiratory evaporative heat loss. In contrast, in the heat (30–32 °C), db cyclic AMP administration produced dose-dependent hyperthermia in these animals. The hyperthermia was due to increased metabolism (due to muscular shivering) and decreased heat losses. The reduction in heat losses was shown by a decrease in both cutaneous circulation and respiratory evaporative heat loss. The data demonstrate that the thermoregulatory responses induced by central administration of db cyclic AMP are Ta-dependent.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 326 (1984), S. 124-128 
    ISSN: 1432-1912
    Keywords: Clonidine ; Hypothalamus ; 5-Hydroxytryptamine ; Acetylcholine ; Thermoregulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The thermoregulatory effects (including metabolic, vasomotor and respiratory activities) produced by an injection of clonidine (1–3 μg in 0.5 μl) into the preoptic anterior hypothalamus were assessed in conscious rats at ambient temperatures (T a) of 8, 22 and 30°C. 2. Intrahypothalamic administration of clonidine caused a dose-dependent fall in rectal temperature at T a 8°C and 22°C. The hypothermia in response to clonidine was due to decreased metabolic heat production and/or cutaneous vasodilation. There was no change in respiratory evaporative heat loss. 3. The clonidine-induced hypothermic response was attenuated by pretreatment of the rats with either 5,7-dihydroxytryptamine (10 μg, administered intrahypothalamicly, 14 days before clonidine injection), yohimbine (0.2 μg, administered intrahypothalamicly, 10 min before clonidine injection), cyproheptadine (1 μg, administered intrahypothalamicly, 10 min before clonidine injection), or atropine (0.1 μg, administered intrahypothalamicly, 10 min before clonidine injection). 4. The data indicate that clonidine may act on α-adrenoceptors located on a serotonin-acetylcholine pathway within the preoptic anterior hypothalamus to induce hypothermia by promoting a reduction in metabolic heat production and/or an enhancement in dry heat loss in rats.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 328 (1985), S. 363-367 
    ISSN: 1432-1912
    Keywords: Cholecystokinin ; Thermoregulation ; Hypothalamus ; Neuronal activity ; Metabolism ; Vasodilation ; Hypothermia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Rats were chronically implanted with a hypothalamic cannula to allow chemical stimulation of the hypothalamus on the conscious animals in repeated experiments. Direct administration of cholecystokinin octapeptide (CCK-8) (20–60 ng) into the preoptic anterior hypothalamic area caused a dose-related fall in rectal temperature at ambient temperatures of 8° C and 22° C. 2. The hypothermia induced by CCK-8 was produced by a decrease in metabolism at an ambient temperature of 8° C, whereas at 22° C, it was caused by both a decrease in metabolism and an increase in cutaneous temperature. 3. However, at an ambient temperature of 30° C, intrahypothalamic administration of CCK-8 caused an insignificant change in thermoregulatory responses. Furthermore, neither intrahypothalamic injection of 0.9% saline nor intraperitoneal injection of CCK-8 (60 ng) had any effect on thermoregulatory responses at the ambient temperatures of 8°–30° C studied. 4. Under urethane anaesthesia, 59 single neurons in the preoptic anterior hypothalamic area were examined in 29 rats. Each animal was subjected to scrotal warming or cooling and to the administration of CCK-8. Microiontophoretic application of CCK-8 resulted in inhibition of the majority (75%) of cold-responsive neurons as well as excitation of the majority (77.8%) of warm-responsive neurons recorded in the preoptic anterior hypothalamic area. However, the majority (69%) of thermally unresponsive cells were not affected by CCK-8 application. 5. The data indicate that CCK-8, when administered intrahypothalamically, excites warm-responsive neurons and inhibits cold-responsive neurons within the preoptic anterior hypothalamic area to induce hypothermia by promoting an increase in heat loss and a decrease in heat production.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 382 (1979), S. 87-90 
    ISSN: 1432-2013
    Keywords: Temperature regulation ; Beta-endorphin ; Hypothermia ; Serotonin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of intraventricular administration of beta-endorphin on thermoregulatory responses of unanesthetized rats to different ambient temperatures (T a ) of 8, 22 and 30°C were assessed. Administration of beta-endorphin produced a fall in rectal temperature at bothT a 8 and 22°C. The hypothermia in response to beta-endorphin was brought about by both cutaneous vasodilation (as indicated by an increase in both the tail and the foot skin temperatures) and decreases in metabolic heat production. However, atT a 30°C, administration of beta-endorphin produced no change in rectal temperature or other thermoregulatory responses. Furthermore, the hypothermic effect induced by beta-endorphin was greatly attenuated by either the depletion of brain serotonin levels (with 5,6-dihydroxytryptamine andp-chlorophenylanine) or the blockade of opiate receptors (with naloxone). The data indicate that beta-endorphin leads to hypothermia in rats by increasing sensible heat loss and decreasing metabolic heat production, probably via the release of endogenous serotonin within brain.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 378 (1978), S. 181-184 
    ISSN: 1432-2013
    Keywords: Temperature regulation ; Antipyretics ; Hypothermia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of intraperitoneal administration of sodium acetylsalicylate (aspirin) on thermoregulatory responses (Ta) of 15, 22 and 29°C were assessed. Intraperitoneal administration of aspirin produced dose-dependent hypothermia at both 15 and 22°C. The hypothermia was brought about by cutaneous vasodilation (as indicated by an increase of the tail and foot skin temperatures). However, in the heat (29°C), i. p. administration of the same amount of aspirin produced no change in rectal temperature, since the thermoregulatory responses were unaffected by aspirin application at this Ta. Thus it appears that aspirin increases heat loss and leads to hypothermia in rats.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1459
    Keywords: Pain ; Morphine ; Hypothermia ; Hyperglycemia ; Prolactin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of analgesic, thermoregulatory and endocrine functions of administering morphine sulphate (0.3mg) into the lateral cerebral ventricle via an Ommaya catheter were assessed in eight patients with cancer pain. Satisfactory control of intractable pain was obtained in these patients, without any change in other sensory modalities. The delay in the onset of pain relief and the duration of analgesia ranged, respectively, from 20 to 40 min and from 12 to 16 h after drug injection. In addition, intraventricular administration of morphine caused a reduction in rectal temperature in these patients at an ambient temperature of 24°C. The hypothermia in response to the injection of morphine was due to cutaneous vasodilation and sweating. There was no change in metabolism or in respiratory evaporative heat loss after morphine injection. Further, 10 to 20 min after intraventricular administration of morphine, the blood levels of prolactin, growth hormone and glucose were elevated in these patients. The changes in temperature and endocrine levels lasted for 1–3 h. In addition to the pain relief, these side-effects of morphine treatment were short-lasting and disappeared as the morphine treatment continued. The results indicate that activation of opiate receptors in the brain produced pain relief, hypothermia (due to cutaneous vasodilation and sweating), and increased blood levels of prolactin, growth hormone and glucose in patients with cancer pain.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 417 (1990), S. 418-424 
    ISSN: 1432-2013
    Keywords: Paramedian reticular nucleus ; Medulla oblongata ; Thermoregulation ; Thermolysis ; Hypothermia ; Chlorpromazine ; Pyrogen ; Fever
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of stimulation or ablation of the paramedian reticular nucleus (PRN) of the rat medulla oblongata on the thermal responses induced by ambient temperature changes, a pyrogen, or a hypothermic substance were assessed. Electrical stimulation of the PRN elicited thermolytic reactions (including decreased metabolism, cutaneous vasodilation and hypothermia) which could be mimicked by micro-injection of kainic acid (an excitotoxic amino acid) into the same region. Bilateral electrolytic lesions in the PRN prevented the animals from responding to heat stress (35° C for 30 min) to some extent, but did not prevent responses to cold stress (4° C for 60 min). In addition, the thermogenic reactions induced by intrahypothalamic injection of polyriboinosinic acid: polyribocytidylic acid (a pyrogenic substance), or the thermolytic reactions induced by intraperitoneal administration of chlorpromazine (a tranquilizer), were antagonized respectively by activation or ablation of the PRN. This suggests that the PRN of the caudal medulla may function as a thermolytic area.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 413 (1989), S. 528-532 
    ISSN: 1432-2013
    Keywords: Thermoregulation ; Hypothalamus ; Somatostatin ; Metabolism ; Vasoconstriction ; Vasodilation ; Cysteamine ; Brain ; Ambient temperature
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The changes in both the thermoregulatory responses and brain somatostatin (SS) levels produced by ambient temperature (T a) changes were assessed in rats after they had been equilibrated to each of theT a for a period of about 90 min. Cold exposure, in addition to elevating hypothalamic SS-levels, led to increased metabolism and cutaneous vasoconstriction atT a=8° C. In contrast, heat exposure, in addition to lowering hypothalamic SS-levels, resulted in decreased metabolism and cutaneous vasodilation atT a=30° C. Rats were chronically implanted with a hypothalamic cannula to allow intrahypothalamic injection of SS on the conscious rats. Direct administration of SS (0.1–0.3 μg) into the preoptic anterior hypothalamic area caused a dose-related rise in colon temperature at threeT a tested. The SS-induced hyperthermia was produced by increased metabolism atT a=8° C, whereas atT a=30° C, it was caused by cutaneous vasoconstriction. AtT a=22° C, the hyperthermia was caused by increased metabolism and cutaneous vasoconstriction. Systemic administration of cysteamine, in addition to lowering hypothalamic SS-levels, produced a dose-related fall in colon temperature atT a of 8°C and 22°C. The hypothermia induced by cysteamine was produced by decreased metabolism atT a=8° C, whereas atT a=22° C, it was caused by both decreased metabolism and cutaneous vasodilation. The data indicate that the hypothalamic SS-levels mediate normal body temperature responses in rats.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 315 (1981), S. 195-201 
    ISSN: 1432-1912
    Keywords: Clonidine ; 5-Hydroxytryptamine ; Hypothermia ; Metabolic rate ; Cutaneous vasodilatation ; Respiration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The thermoregulatory outputs (including metabolic, respiratory and vasomotor activities) produced by an injection of clonidine or 5-hydroxytryptamine (5-HT) into the third cerebral ventricle of conscious rabbits were assessed at three different ambient temperatures (T a) of 2, 22 and 32°C. 2. When injected into the third cerebral ventricle, both clonidine and 5-HT produced a dose-dependent hypothermia in rabbits at both 2 and 22°C T a. The hypothermia was due to a decrease in metabolic heat production (M) at 2°C T a, while at 22°C T a the hypothermia was due to cutaneous vasodilatation. There were no changes in respiratory evaporative heat loss. 3. Furthermore, the clonidine-induced hypothermia was greatly reduced by pretreatment of the animals with either 5,6-dihydroxytryptamine (impairment of central 5-HT pathways) or yohimbine (alpha-adrenergic blocking agent), but not by 6-hydroxydopamine (impairment of central catecholamine pathways). 4. The results indicate that clonidine may act on the α-adrenergic receptors located on central 5-HT pathways to produce a hypothermic action by promoting a decrease in heat production or an increase in heat loss in the rabbit.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 322 (1983), S. 271-278 
    ISSN: 1432-1912
    Keywords: 5-Hydroxytryptamine ; Hypothalamus ; Thermoregulation ; Raphe nucleus ; Hypothermia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Either electrical stimulation of midbrain raphe nuclei or administration of 5-hydroxytryptamine (5-HT; serotonin) into the preoptic anterior hypothalamus caused hypothermia in conscious rats at ambient temperatures (T a) of both 8° C and 22°C. The hypothermia was due to decreased metabolic heat production at T a=8°C, while at T a=22°C the hypothermia was due to both decreased metabolism and increased heat loss (cutaneous vasodilatation). However, at T a=30°C, electrical stimulation of midbrain raphe or intrahypothalamic injection of 5-HT caused an insignificant change in the thermoregulatory responses. There was no changes in respiratory evaporative heat loss in response to these treatments at various T a's. 2. Direct administration of the serotonergic receptor antagonists such as cyproheptadine and methysergide into the preoptic anterior hypothalamus caused hyperthermia in conscious rats at T a's of 8°C, 22°C and 30°C. The hyperthermia was due to increased metabolism and cutaneous vasoconstriction. 3. The hypothermia induced by intrahypothalamic administration of 5-HT was antagonized by pretreatment with an intrahypothalamic dose of either cyproheptadine or methysergide in rats at T a=22°C. 4. Inhibition of 5-HT neuronal activity with administration of 5-HT into the midbrain raphe regions also caused hyperthermia, increased metabolism and cutaneous vasoconstriction in rats at T a's of 8°C, 22°C and 30°C. 5. These observations tend to suggest that the functional activity of serotonergic receptors in the preoptic anterior hypothalamus mediates thermoregulatory responses in the rat. Activation of serotonergic receptors in the hypothalamus decreases heat production and/or increases heat loss, while inhibition of serotonergic receptors in the hypothalamus increases heat production and/or decreases heat loss in the rat.
    Type of Medium: Electronic Resource
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