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)

The effects of thyrotropin-releasing hormone (TRH) on brain temperature in response to pentobarbital were examined in male rats. After intraperitoneal injection of pentobarbital sodium (55 mg/kg body wt), the rats were fixed stereotaxically and received intraventricular (ivt) injection of varying doses (0.03-30 nmol) of TRH and 17 nmol atropine. Following the injection of 3 nmol TRH, 100 nmol of carbocholine was administered in the same manner. A thermocouple microprobe was unilaterally placed in the midbrain reticular formation so that brain temperature was continuously monitored at room temperature. Brain temperature after pentobarbital injection progressively decreased. While ivt injection of saline did not affect this change in temperature, ivt administration of TRH produced a dose-dependent antagonism of the brain hypothermia induced by pentobarbital. Atropine injection also reversed the pentobarbital-induced decrease in brain temperature. Carbocholine injection led to a significant decrease in brain temperature in response to TRH administration. The present study indicates that brain TRH may play a pivotal role in brain thermoregulation and its mechanism may involve at least in part the central cholinergic pathway in the rat.
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PMID:Antagonism by thyrotropin-releasing hormone of brain temperature in response to pentobarbital in the rat: possible involvement of cholinergic mechanism. 309 3

In addition to short-acting analgesic actions by itself and modulation of analgesic responses induced by endogenous opioids and neurotensin, central administration of thyrotropin-releasing hormone (TRH) potentiates footshock analgesia. The present study evaluated the effects of TRH upon the neurohormonally-mediated though nonopioid analgesia induced by swims in rats. Intracerebroventricular TRH (10 and 50 micrograms) dose-dependently potentiated swim (21, 15, 2 degrees C baths) analgesia on the tail-flick test, an effect which was not due to the hypothermic or basal pain threshold changes. Intravenous (8 mg/kg) TRH potentiated swim (21 degrees C) analgesia; the 600:1 difference in potency between routes strongly suggests central sites of neuromodulatory action. Intracerebroventricular diketopiperazine (50 micrograms), a TRH metabolite, and RX77368 (50 micrograms), a TRH analogue, also potentiated swim (21 degrees C) analgesia, effects also independent of hypothermia and basal reactivity to pain. Finally, given the excitatory interaction between TRH and acetylcholine as well as the cholinergic involvement in swim analgesia, intracerebroventricular TRH potentiated pilocarpine (10 mg/kg, IP) analgesia.
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PMID:Neuromodulatory effects of TRH upon swim and cholinergic analgesia. 310 67

The fetal respiratory and electrocortical effects of thyrotropin-releasing hormone (TRH) administered into the lateral cerebral ventricles, have been investigated in chronically catheterized unanesthetized fetal sheep at 125-140 days of gestation. Stimulatory effects on fetal breathing movements were seen at doses as low as a lug bolus. TRH given as a 5-micrograms bolus followed by a 10 micrograms/h infusion for 2 h induced a rapid switch to significantly faster, deeper, and continuous fetal breathing movements, while the electrocorticogram remained episodic. Fetal breathing movements did not stop during hypoxia. TRH given as a 2-micrograms bolus followed by a 4 micrograms/h infusion or as a 5-micrograms bolus followed by a 5 micrograms/h infusion induced the same stimulation of FBMs, but breathing essentially remained episodic, state related and inhibited by hypoxia. As hypothermia presumably induces a surge in TRH secretion at birth it is possible that TRH has some role in the switch from fetal to postnatal breathing patterns.
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PMID:The central effects of thyrotropin-releasing hormone on the breathing movements and electrocortical activity of the fetal sheep. 312 70

The thyrotropin-releasing hormone (TRH) content in the brain was determined in normothermic and hypothermic rats subjected to immobilization stress. TRH contents in the hypothalamus, midbrain and cerebral cortex significantly decreased during mild hypothermia (body temperature about 34 degrees C), but not during profound hypothermia (about 24 degrees C). The decreases in the TRH content during mild hypothermia were readily reversed by rewarming the animal. These results indicate that cerebral TRH is involved in the response to a mild body temperature drop when the animal is exposed to a cold environment.
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PMID:Effects of hypothermia on thyrotropin-releasing hormone content in the rat brain. 314 62

Two hours after i.p. administration of 2-cyclooctyl-2-hydroxyethylamine (CONH), 1-aminomethylcycloundecanol (CUNH), 2,3-dichloro-alpha-methylbenzylamine (DCMB), or 7,8-dichloro-1,2,3,4-tetrahydroisoquinoline (SKF64139), the hypothalamic and brain stem epinephrine (EPI) contents of rat brain were decreased. Depletions of brain EPI with these phenylethanolamine N-methyltransferase (PNMT) inhibitors reduced the rectal temperatures of rats at ambient temperatures of 8 and 22 degrees C. The hypothermia in response to these PNMT inhibitors was due to decreased metabolism and cutaneous vasodilatation. The locomotor stimulant responses induced by thyrotropin-releasing hormone were also reduced by administration of any one of these PNMT inhibitors. On the other hand, acute administration of any of these PNMT inhibitors enhanced the reflex bradycardia induced by i.v. infusion of EPI. The data suggest that brain (particularly the hypothalamus and brain stem) EPI-containing neurons are involved in the regulation of body temperature, reflex bradycardia, and motor performance in the rat.
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PMID:Effects of brain epinephrine depletion on thermoregulation, reflex bradycardia, and motor activity in rats. 397 46

Possible neuroanatomical substrates mediating some of the effects seen with thyrotropin-releasing hormone (TRH) in the pentobarbital (PB) narcotized rat were examined. This was accomplished by microinjecting picomole concentrations of TRH into 20 different brain sites. The behavioural effects examined were the capacity of TRH to antagonize PB-induced narcosis and hypothermia as well as TRH-induced shaking behavior. Microinjection of TRH into the septum was found to be significantly more effective in the reversal of PB narcosis than any other site examined. In contrast, the temperature and shaking response were evoked with approximately equal efficacy by TRH microinjection into a number of brain sites; including the preoptic/anterior hypothalamus, medial thalamus, thalamic, periventricular gray, interpeduncular nucleus and locus ceruleus. These results demonstrate the septal region to be the site of action for TRH reversal of PB narcosis and suggest the involvement of the septohippocampal system. In addition, they indicate that the neurogenesis of the shaking response is similar to that of the temperature response and that this differs from the neurogenesis of the analeptic response.
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PMID:Thyrotropin-releasing hormone: neurogenesis of actions in the pentobarbital narcotized rat. 610 46

The effects of administration of thyroid-stimulating hormone (TSH), thyrotropin-releasing hormone (TRH), luteinizing hormone (LH) or luteinizing hormone-releasing hormone (LHRH) into the lateral cerebral ventricle on thermoregulation and food and water intake were assessed in rats. Intracerebroventricular, but not intraperitoneal, injection of TSH, LH or LHRH produced hypothermia in rats at ambient temperatures of both 8 and 22 degrees C. The hypothermia in response to TSH injection was due to both decreased metabolic heat production and increased heat loss (cutaneous vasodilatation). The hypothermia in response to either LH or LHRH was due solely to decreased metabolic heat production. There was no change in respiratory evaporative heat loss in response to TSH, LH or LHRH injection. Furthermore, food but not water intake was greatly reduced following an intracerebroventricular injection of TSH or TRH in rats. On the other hand, intracerebroventricular administration of LH, but not LHRH, caused an increase in relative water intake (or water/food) in rats. However, intracerebroventricular administration of LH or LHRH had an insignificant effect on food intake. The data indicate that, in addition to their hormone actions, TSH, LH and their releasing hormones act through a central mechanism to influence some of the physiological or behavioral functions.
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PMID:Effects of TSH, TRH, LH and LHRH on thermoregulation and food and water intake in the rat. 641 77

Intracisternal (IC) administration of neurotensin (NT) in a dose of 10 micrograms produced a significant hypothermia and antinociception in the hot-plate test in mice. Both of these effects of IC NT were completely antagonized by concomitant administration of equimolar doses of thyrotropin-releasing hormone (TRH) and several TRH congeners including 3-methyl-His-TRH (pGlu-3-methyl-His-Pro-NH2), MK-771 (pyro-2-aminoadipyl-histidyl-thiazolidine-4-carboxamide), beta-ala-TRH (pGlu-His-Pro-beta-ala-NH2), and RX-77368 (pGlu-His-dimethyl-Pro-NH2). The antagonism by TRH and TRH analogs on NT-induced hypothermia and antinociception was dose-dependent. Of particular interest was the finding that RX-77368 not only blocked the effects of NT but also produced hyperalgesia. It appears that TRH analogs that are more resistant to biologic degradation are, like TRH, capable of blocking NT-induced behaviors.
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PMID:Neurotensin-induced antinociception and hypothermia in mice: antagonism by TRH and structural analogs of TRH. 642 94

Neurotensin (NT), an endogenous tridecapeptide, produces significant hypothermia after intracisternal (i.c.) or intracerebroventricular (i.c.v.) administration in microgram quantities in a variety of laboratory animals. The present study sought to clarify the mechanism of the hypothermic action by utilizing pharmacological treatments which alter the function of brain neurotransmitter systems. Pretreatment of rats with anti-muscarinic (atropine), anti-noradrenergic (propranolol, a beta-blocker; phenoxybenzamine, an alpha-blocker) or anti-opiate (naloxone) agents did not significantly alter NT-induced hypothermia. Similarly depletion of brain serotonin (5-HT) with parachlorophenylalanine did not affect NT-induced hypothermia. However, depletion of brain catecholamine content with 6-hydroxydopamine resulted in a significant potentiation of NT-induced hypothermia as did pretreatment with haloperidol, a dopamine (DA) receptor antagonist. Furthermore, in rats with selective depletions of brain DA, but not norepinephrine (NE), NT-induced hypothermia was significantly augmented. Thus an interaction between brain DA systems and NT appears likely. These data indicate that NT-induced hypothermia is not dependent on intact functional activity of NE, 5-HT, muscarinic ACh or endogenous opiate systems but suggests interactions between brain DA circuits and NT. In other experiments, NT-induced hypothermia was found to be antagonized significantly by i.c. injection of thyrotropin-releasing hormone (TRH), but not by pretreatment with L-triiodothyronine. Another endogenous tripeptide (Pro--Leu--Gly--NH2, MIF-I) had no effect. Thyroidectomy (THX) significantly potentiated NT-induced hypothermia; NT administered i.c. significantly reduced the high serum TSH levels of THX rats. Thus, NT and TRH, two endogenous peptides, appear to be antagonists in certain systems.
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PMID:Neurotensin-induced hypothermia: evidence for an interaction with dopaminergic systems and the hypothalamic--pituitary--thyroid axis. 644 51

Administration of anti-serum to thyrotropin-releasing hormone (TRH) into the lateral cerebral ventricle of rats produces a dose-dependent hypothermia. Neutralization of anti-TRH serum with excess TRH abolishes this hypothermic effect. These results suggest a thermoregulatory role for endogenous TRH in the rat central nervous system.
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PMID:Immunological blockade of endogenous thyrotropin-releasing hormone produces hypothermia in rats. 677 Sep 63


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