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  • 1
    Electronic Resource
    Electronic Resource
    Involvement of adrenergic receptor mechanisms within hypothalamus in the fever induced by amphetamine and thyrotropin-releasing hormone in the rat (1983)
    Springer
    Journal of neural transmission 58 (1983), S. 213-222 
    Details
    ISSN: 1435-1463
    Keywords: Amphetamine ; thyrotropin-releasing hormone ; fever ; aspirin ; adrenergic blockade ; thermoregulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The mechanisms underlying the thermal effects induced by intrahypothalamic administration of either d-amphetamine or thyrotropin-releasing hormone (TRH) has been investigated in conscious rats. Direct administration of d-amphetamine (1–10μg in 1μl) or TRH (1–4μg in 1μl) into the preoptic anterior hypothalamus caused hyperthermia or fever at the ambient temperature (Ta∶ 8, 22 and 30 °C) studied. The fever induced by d-amphetamine or TRH was due to increased metabolic heat production at Ta 8 °C, while at Ta 30 °C the fever was due to cutaneous vasoconstriction in the rat. At Ta 22 °C, the fever was due to both increased metabolism and cutaneous vasoconstriction. Furthermore, the fever induced by intrahypothalamic administration of TRH was greatly reduced by pretreatment with intrahypothalamic administration of either yohimbine (a blocking agent of alpha-adrenergic receptors), phentolamine (a blocking agent of alpha-adrenergic receptors) or DL-propranolol (a blocking agent of beta-adrenergic receptors) in the rat. However, the fever induced by d-amphetamine was antagonized by pretreatment with yohimbine or phentolamine, but not with DL-propranolol in the rat. These observations indicate that the adrenergic receptor mechanisms within the hypothalamus are involved in the fever induced by both d-amphetamine and TRH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01252807
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  • 2
    Electronic Resource
    Electronic Resource
    Endogenous pyrogen formation by human blood monocytes stimulated by polyriboinosinic acid:Polyribocytidylic acid (1993)
    Springer
    Cellular and molecular life sciences 49 (1993), S. 157-159 
    Details
    ISSN: 1420-9071
    Keywords: Monocytes ; fever ; endogenous pyrogen ; polyriboinosinic acid:polyribocytidylic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The pyrogenic response to supernatants from human blood monocytes stimulated with polyriboinosinic acid:polyribocytidylic acid (poly I:C) was characteristic of a response to endogenous pyrogen in that it was brief and monophasic, and was destroyed by heating the supernatants at 70°C for 30 min. Pyrogen production was unimpaired when the incubations were carried out in the presence of cycloheximide (50 μg/ml; an inhibitor of protein synthesis) or indomethacin (50 μg/ml; an inhibitor of prostaglandin synthesis). Also, neither interferon, interleukins, tumor necrosis factor nor prostaglandin E2 were detectable in the supernatants from the poly I:C-stimulated human monocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01989421
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  • 3
    Electronic Resource
    Electronic Resource
    Cerebral ischemia is the main cause for the onset of heat stroke syndrome in rabbits (1992)
    Springer
    Cellular and molecular life sciences 48 (1992), S. 225-227 
    Details
    ISSN: 1420-9071
    Keywords: Heat stroke ; fever ; cerebral blood flow ; cerebral perfusion pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract During the onset of heat stroke, rabbits displayed hyperthermia (42.8°C), and decreased cerebral perfusion pressure and decreased cerebral blood flow (as reflected by a prolonged cerebral circulation time) compared to those of normothermic rabbits. On the other hand febrile rabbits, during the fever plateau did not show the above responses, although they had a similar level of hyperthermia (42.4°C). The data support the concept that cerebral ischemia is the main cause for the onset of the heat stroke syndrome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01930459
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  • 4
    Electronic Resource
    Electronic Resource
    The hypothalamic somatostatinergic pathways mediate feeding behavior in the rat (1989)
    Springer
    Cellular and molecular life sciences 45 (1989), S. 161-162 
    Details
    ISSN: 1420-9071
    Keywords: Hypothalamus ; somatostatin ; anorexia ; food intake ; starvation ; cysteamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The level of somatostatin in the hypothalamus was higher in satiated rats than in hungry rats. Elevating hypothalamic somatostatin levels by administering somatostatin into the hypothalamus produced a decrease in food intake, whereas lowering hypothalamic somatostatin levels by administering cysteamine into the peritoneal cavity produced an increase in food intake in rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01954859
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  • 5
    Electronic Resource
    Electronic Resource
    Hypothalamic somatostatin may mediate endotoxin-induced fever in the rat (1989)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 339 (1989), S. 608-612 
    Details
    ISSN: 1432-1912
    Keywords: Somatostatin ; Endotoxin ; Fever ; Hypothalamus ; Cysteamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary (1) The changes in rectal temperature produced by an injection of a bacterial endotoxin piromen (10–40 ng in 1.0 μl) or somatostatin-14 (SS-14; 0.1–0.3 pg in 1.0 μl) into the preoptic anterior hypothalamic area were assessed and compared in control rats, in rats with hypothalamic SS depletion, and in rats with hypothalamic SS receptor blockade. (2) Intrahypothalamic injection of either piromen or SS-14 produced a dose-related rise in rectal temperature in intact, control rats. The fever induced by intrahypothalamic injection of piromen or SS-14, as well as that induced by intraperitoneal injection of piromen, was antagonized by pretreatment of the hypothalamus with a SS-14 receptor antagonist (0.1 ng in 1.0 μl) in rats. (3) On the other hand, intraperitoneal administration of cysteamine (30–100 mg/kg), in addition to producing a dose-related fall in rectal temperature, also caused a dose-related fall in hypothalamic SS-levels in rats. Furthermore, the fever induced by intrahypothalamic injection of piromen, but not SS-14, was antagonized by depletion of hypothalamic SS levels with an intraperitoneal dose of cysteamine (30 mg/kg). (4) The results indicate that a somatostatinergic pathway in the hypothalamus may mediate endotoxin-induced fever in the rat.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168651
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  • 6
    Electronic Resource
    Electronic Resource
    Pyrogenicity of polyadenylic · polyuridylic acid in rabbits (1991)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 343 (1991), S. 551-557 
    Details
    ISSN: 1432-1912
    Keywords: Polynucleotides ; Pyrogen ; Interferon ; Prostaglandins ; Hypothalamus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Polyadenylic polyuridylic acid injected intraveneously into rabbits produced a rapid-onset, monophasic fever. Pyrogenic tolerance occurred in rabbits following daily injections of polyadenylic polyuridylic acid. However, direct injection of the agent into the preoptic anterior hypothalamic region of rabbit's brain produced a markedly different fever. After an intrahypothalamic injection of polyadenylic - polyuridylic acid, fever was delayed in onset and persisted for a longer period. At room temperature, the fever was due to both increased metabolism and cutaneous vasoconstriction. In a colder atmosphere the fever was due solely to increased metabolism, whereas in the heat the fever was due to reduction in cutaneous blood flow and respiratory evaporative heat loss. In addition, the fever induced by intravenous polyadenylic · polyuridylic acid injection was reversed by a cyclooxygenase inhibitor, but not by a protein synthesis inhibitor. Polyadenylic - polyuridylic acid was shown to stimulate PGE2 production from rabbit's hypothalamus in vitro. The results reveal that this agent is a prostaglandin-dependent pyrogen.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169561
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  • 7
    Electronic Resource
    Electronic Resource
    Depletion of hypothalamic norepinephrine reduces the fever induced by polyriboinosinic acid: polyribocytidylic acid (Poly I:Poly C) in rats (1989)
    Springer
    Cellular and molecular life sciences 45 (1989), S. 720-722 
    Details
    ISSN: 1420-9071
    Keywords: Hypothalamus ; norepinephrine ; fever ; pyrogen ; polyriboinosinic acid ; polyribocytidylic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Administration of either Poly I:Poly C (0.05–0.50 μg) or norepinephrine (2–8 μg) into the anterior hypothalamic area produced a dose-related fever in rats. The fever induced by Poly I:Poly C was attenuated after selective depletion of norepinephrine in the hypothalamus. However, selective depletion of hypothalamic norepinephrine did not affect the fever induced by intrahypothalamic norepinephrine. The data indicate that Poly I:Poly C may act to induce fever through the endogenous release of norepinephrine from the rat's hypothalamus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01974567
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  • 8
    Electronic Resource
    Electronic Resource
    Insulin acts on the hypothalamic glucose-facilitated neurons to induce hyperglycemia and hyperinsulinemia in the rat (1991)
    Springer
    Cellular and molecular life sciences 47 (1991), S. 942-944 
    Details
    ISSN: 1420-9071
    Keywords: Hypothalamus ; insulin ; hyperglycemia ; hyperinsulinemia ; neuronal activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Microinjection of insulin (0.04–0.12 IU/μl) into the anterior hypothalamus or the lateral hypothalamus, but not the vertromedial hypothalamus of the rat brain, caused a dose-dependent rise in blood glucose and in serum insulin. The majority (71.5%) of the glucose-facilitated neurons recorded in the lateral hypothalamic area were excited by intracerebral injection of insulin. The data indicate that insulni acts on the hypothalamic glucose-facilitated neurons to induce hyperglycemia and hyperinsulinemia. It is unknown whether insulin normally reaches the hypothalamic area, or how it might do so.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01929887
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  • 9
    Electronic Resource
    Electronic Resource
    Clonidine-induced hypothermia: Possible involvement of cholinergic and serotonergic mechanisms (1984)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 326 (1984), S. 124-128 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00517308
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  • 10
    Electronic Resource
    Electronic Resource
    Effects of cholecystokinin octapeptide on thermoregulatory responses and hypothalamic neuronal activity in the rat (1985)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 328 (1985), S. 363-367 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00692901
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