Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present study, the thermal responses induced by intraventicular administration of pyrogen prostaglandin E1, the brain monoamines norepinephrine and serotonin, and the antipyretic sodium acetylsalicylate (aspirin) were measured in conscious rabbits to assess the possible involvement of these substances in fever production. The body temperatures, metabolic rate, respiratory evaporative heat loss and vasomotor activity in response to the administration of these drugs were measured. The results showed that sodium acetylsalicylate, an inhibitor of prostaglandin synthetase, antagonizes the norepinephrine induced fever but not the prostaglandin fever. The data also showed that the serotonin induced hypothermia was reversed by prostaglandin administration. Thus, the fact strongly suggest that the prostaglandin E1 serves as a fever-prducing mediator in the central nervous system. Also, the norepinephrine fever and serotonin hpyothermia, respectively, may be associated with an increase and a decrease in prostaglandin synthesis in the brain.
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PMID:Brain monoamines act through the prostaglandin release to influence the body temperature. 1 25

1. The role of 5-hydroxytryptamine (5-HT) in temperature regulation and in fever in the rabbit has been investigated. 2. Intrahypothalamic microinjections of 5-HT in the conscious rabbit alters body temperature in a dose-dependent manner. 3. Low doses (5-5nmol) of 5-Ht and control saline injections produced a small, non-significant increase in temperature, with a long latency. 4. Doses of 14 nmol 5-HT produce a hyperthermia with a 45 min delay; while microinjections of 28 nmol result in a biphasic response; an initial short hypothermia is followed later by a hyperthermia. 5. Depleting the rabbit's brain of 5-HT by pretreatment with p-chlorophenylalanine (PCPA) fails to affect its body temperature at thermoneutral temperatures but significantly impairs the ability to thermoregulate against a cold stress. 6. PCPA pretreatment did not, however, impair the febrile response to bacterial pyrogen and prostaglandin E1. 7. These results reveal a dissociation between the effects of 5-HT depletion on temperature regulation, and on fever. The site of action of 5-HT in temperature regulation must be proximal to the fever input, but distal to the convengence of peripheral and hypothalamic temperature inputs.
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PMID:A dissociation between temperature regulation and fever in the rabbit. 14 Feb 37

In 5--10 day-old kittens at thermoneutral environmental temperature cerebroventricular injections of 10 microgram serotonin or noradrenaline caused hyperthermia and hypothermia, respectively. Central injections of 20 and 200 ng prostaglandin E1 induced hyperthermia. Monophasic fever followed the cerebroventricular injections of 0.2 or 0.002 microgram E. coli endotoxin, both in thermoneutral and moderately cool environments. In kittens pretreated with para-chlorophenylalanine (PCPA) the endotoxin induced rise in body temperature was attenuated within 60 to 90 min after the endotoxin. Indomethacin pretreatment prevented the first part of the febrile response and only a slight temperature rise occurred after a long latency. Central injections of phentolamine did not modify the fever response, while centrally applied propranolol modified the fever course so that it resembled that seen in PCPA treated kittens. The central mediation of endotoxin fever in the kitten is complex, despite that the pattern of the temperature change is simple (monophasic). Arachidonic acid metabolites and serotonin of the central nervous system may be involved in the reaction, while the activation of central noradrenergic mechanisms does not seem to be indispensable for the response. The changes in mediators are similar to those in newborn guinea pigs, although the fever course is different in the two species.
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PMID:Endotoxin fever in the newborn kitten. The role of prostaglandins and monoamines. 16 15

A short review of the role of cyclic nucleotides and prostaglandins (PGs) in normal and pathological functions of the heart is given. Possible interrelationships of these two regulatory systems have been studied by using spontaneously beating rat atria preparations. Addition of noradrenaline (NA) to the incubate (1 . 10(-6) M) caused an increase in amplitude and frequency which was preceded and parallelled by an elevation of the tissue cAMP level. A transient increase in cGMP and PGE values was also seen. Propranolol (5 . 10(-6) M) abolished the increase in amplitude and frequency as well as in cAMP and PGE concentrations. Indomethacin (1 . 10(-5) M) inhibited the formation of PGE. The increase in cGMP was blocked by phenoxybenzamine. Interchange between beta- and alpha-receptors according as the temperature is lowered has been described earlier. Hypothermia (20 degrees C) had a positive inotropic effect on the atria and increased the tissue cAMP concentration. Loading of the atria caused an increase in cAMP without any effects on cGMP or PGs. Slight hypoxia did not change the cAMP or PG levels, but elevated the cGMP values. Arrhythmias induced by hypo- or hyperpotassemia did not modify the biochemical parameters measured. PGF2alpha (1. 10(-5) M) normalized the atrial rhythm and increased the amplitude without changing cyclic nucleotide or PG levels. PGE1 (1 . 10(-4) M) increased the amplitude of normorhythmic atria and the tissue concentration of cAMP. PGE2 was the only PG tested which stimulated the heart adenylate cyclase in vitro. There seems to be close but complicated relationships between cyclic nucleotides and PGs in the heart.
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PMID:The role of cyclic nucleotides and prostaglandins in heart function. 21 11

1 The antipyretic activity of tilorone hydrochloride was studied in conscious, unrestrained cats provided with implanted jugular venous catheters, third cerebral ventricular (i.c.v.) cannulae and retroperitoneal thermocouples. 2 In afebrile animals, 10 mg/kg i.v. or 1 mg i.c.v. tilorone hydrochloride did not alter body temperature, but 20 mg/kg i.v. or 2 to 5 mg i.c.v. caused hypothermia and various behavioural responses. 3 Non-hypothermogenic doses of tilorone (i.v. or i.c.v.) antagonized hyperthermic responses to leucocytic pyrogen (i.v. or i.c.v.), bacterial pyrogen (i.c.v.) and sodium arachidonate (i.c.v.) but did not antagonize prostaglandin E1 (i.c.v.). 4 These results indicate that tilorone has an antipyretic action within the central nervous system that is distinct from its hypothermogenic action. Although there is no published evidence to indicate that tilorone can inhibit prostaglandin synthesis peripherally, its ability to reduce hyperthermic responses to arachidonate suggests that it can inhibit prostaglandin synthesis within the brain.
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PMID:The antipyretic effect of tilorone hydrochloride in the cat. 30 49

The effects of intraperitoneal administration of prostaglandin E1 (PGE1) on thermoregulatory responses were assessed in unanesthetized rats at ambient temperatures (Ta) of 8, 22 and 29 degrees C. The body temperatures, metabolic rate, respiratory evaporative heat loss and vasomotor activity in response to PGE1 were observed. Intraperitoneal administration of PGE1 produced dose-dependent hypothermia at Ta's of both 8 and 22 degrees C. The PGE1 hypothermia was due to both the decreased metabolic rate and the cutaneous vasodilation. However, at a Ta of 29 degrees C, intraperitoneal administration of PGE1 produced no changes in rectal temperature, since the thermoregulatory responses were not affected by PGE1 application at this Ta. The data indicate that peripheral administration of PGE1 decreases metabolic heat production and increases heat loss, which leads to hypothermia in rats, in contrast to hyperthermia seen after central administration.
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PMID:Systemic administration of prostaglandin E1 produces hypothermic effects in unanesthetized rats. 43 11

While some salicylates (salicyclic acid and salicylaldehyde, especially) are as potent as aspirin as acute, orally-active anti-flammatory drugs in the rat, they are either inactive or far less potent as PG synthesis inhibitors when added directly to isolated platelets or when given orally. Although PGE1 and PGE2 produce anti-ulcerogenic effects when given to rats in the presence of selected non-steroidal anti-flammatory drugs, they fail to inhibit the acute anti-flammatory and anti-nociceptive effects of these drugs. They are anti-flammatory and anti-nociceptive under certain experimental conditions. PGE1 and PGE2 can also behave as hypothermic agents when given subcutaneously. Related studies, using PG synthesis stimulators in vivo and in vitro (substituted phenylureas), also cause anti-nociception and hypothermia. All of these indirect studies, when taken together, infer that PG synthesis inhibition per se fails to explain, entirely, the pharmacologic effects of non-steroidal anti-inflammatory drugs. They also suggest that the precise role of certain PGs in toxicopharmacology is far from simple and straightforward.
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PMID:Anomalous biological effects of salicylates and prostaglandins. 49 43

The thermal responses produced by both systemic and central administration of prostaglandin E1 (PGE1) at the three different ambient temperatures (Ta) of 2, 22 and 32 degrees C were measured to assess the possible involvement of PGE1 in temperature regulation. The body temperatures, metabolic rate, respiratory evaporative heat loss and vasomotor activity in response to PGE1 were measured. Intravenous administration of PGE1 produced dose-dependent hypothermia at Ta's of both 2 and 22 degrees C. The PGE1 hypothermia was due to cutaneous vasodilation. However, at a Ta of 32 degrees C, intravenous PGE1 produced no changes in rectal temperature and ear blood flow. On the other hand, the direct injection of PGE1 into the third ventricle produced dose-dependent hyperthermia. At a Ta of 22 degrees C, PGE1 fever was due to decreased heat loss along with a small increase in heat production. In the cold, PGE1 fever was due to increased heat production while in the heat heat losses were decreased. The data suggest that elevating PGE1 levels in the periphery causes a hypothermia, while elevating PGE1 levels in the central nervous system causes a hyperthermia at Ta's of both 2 and 22 degrees C.
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PMID:Effects of intravenous and intraventricular prostaglandin E1 on thermoregulatory responses in rabbits. 61 34

It is known that central administration of prostaglandins of the E series has marked effects on body temperature. The purpose in the present experiments was to learn whether stable analogs of the cyclic endoperoxide precursors of PGE2, PGF2alpha and PGD2, injected into the primary temperature control in the preoptic/anterior (PO/AH) hypothalamic region and into a presumed secondary control in the medulla oblongata, can produce rises in body temperature similar to those caused by PGE2. Injection of the analogs U-44069 and U-46619 (1.0 and 2.0 microng) into the PO/AH region of the rat, where both PGE2 and PGE1 caused hyperthermia, had no effect on Tre. Likewise, injections into the medulla oblongata, in the region where PGE2 and PGE1 caused hypothermia, were ineffective in altering body temperature. That neurons important to the control of body temperature are selectively sensitive to PGE2 and not to analogs of prostaglandin precursors suggests that local cyclic endoperoxides can influence body temperature only through bioconversion to prostaglandin.
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PMID:Analogs of endoperoxide precursors of prostaglandins: failure to affect body temperature when injected into primary and secondary central temperature controls. 84 28

1. Intracerebroventricular (I.C.V.) injections of taurine into rabbits resting at an ambient temperature (Ta) of 10 degrees or 23 degrees C caused hypothermia but at 30 degrees C ambient temperature, rectal temperature was unchanged. 2. An I.C.V. bolus of 0=5 mg taurine immediately followed by a slow infusion of taurine (0-01--0-2 mg/min) into rabbits at 23 degrees C ambient temperature caused sedation and peripheral vasodilation and blocked the febrile response to Salmonella typhosa endotoxin (1 microng/kg i.v.). Sustained fevers, characteristic of fevers caused by central administration of pyrogens, developed after taurine infusions were stopped. Control infusions of taurine at the same rates in the same rabbits when they were afebrile had little effect on rectal temperature. 3. An I.C.V. injection of 0-5 mg taurine reduced the hyperthermia caused by prostaglandin E1 (PGE1; 2 microng) given I.C.V. A dose of 5-0 mg not only blocked PGE1 hyperthermia but also caused marked hypothermia. 4. Bilateral injections of taurine into the preoptic/anterior hypothalamic region, at sites where injections of Salmonella typhosa endotoxin caused long-lasting fevers, had no effect on rectal temperature. Similar injections into the reticular substance of the medulla oblongata, in the region believed to be concerned with a secondary temperature control function, were also without effect on body temperature. 5. Taurine (0-5 and 5-0 mg, I.C.V.) had no consistent effect on hyperthermia induced by amphetamine (2 mg/kg, I.V.) 6. We conclude that the hypothermic effect of taurine is not due to an action on the central neurone pool or pools concerned with the integrative control of thermoregulatory effectors. This amino acid appears to inhibit neuronal activity in efferent pathways which control peripheral vasomotor tone and heat production and to depress the level of arousal. Taurine delays the onset and extends the duration of endotoxin-induced fever, perhaps by two separate action: by inhibiting activity in central thermoregulatory pathways and by promoting accumulation of endogenous pyrogen in the brain.
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PMID:Intracerebroventricular taurine in rabbits: effects of normal body temperature, endotoxin fever and hyperthermia produced by PGE1 and amphetamine. 85 4


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