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)

Changes in the concentration of amino acids and other metabolites were determined in the perfusate during 24 hr of ex vivo hypothermic perfusion of dog kidneys. There was an increase in concentration of most of the amino acids. Two patterns were identified. One showed an increase in concentrations up to 12 hr, and then a leveling off as exemplified by alanine, serine, and glutamate. The other pattern was one of persistent elevation as exemplified by phenylalanine, threonine, and methionine. Glucose, lactate, pyruvate, sodium, potassium, pH, and pO2 were also measured in the perfusate. The results suggest that a degradation of kidney protein may occur during the first 24 hr of perfusion. The levels of other metabolites measured support the fact that glycolysis is responsible for a considerable portion of the total energy production in the kidney under hypothermia.
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PMID:Changes in concentration of amino acids and other metabolites during hypothermic perfusion of the canine kidney. 374 9

(D-ala2)-methionine-enkephalinamide (DAME) was injected into the third cerebral ventricle of unrestrained cats. At ambient temperature (Ta) = 22 degrees C, 3.1-50 micrograms caused dose-related hyperthermias. As dosage was increased, the hyperthermias diminished and in some cats hypothermia developed. Hyperthermia was not due to pyrogenic contamination or prostaglandin synthesis since it was not altered by pretreatment with a large IV dose of indomethacin. However, pretreatment with naloxone did cause a dose-related reduction in the hyperthermia. A low dose of DAME (12.5 micrograms) also caused hyperthermia at Ta = 4 and 32 degrees C, indicative of an increase in the level about which body temperature was regulated. On the other hand, a dose of 200 micrograms, which caused hyperthermia Ta = 22 and 32 degrees C, usually caused hypothermia at Ta = 4 degrees C, perhaps due to impairment of thermoregulatory control mechanisms. The response to DAME in the cold was reduced by naloxone pretreatment or reversed by subsequent injection of naloxone. Differences in hyperthermic patterns over a range of TaS and the lack of hypothermogenic action of morphine indicate that DAME alters thermoregulation in the cat by acting on morphine-insensitive, but naloxone-sensitive receptors. Central injection of beta-endorphin (5-50 micrograms) caused a dose-related hyperthermia. (Des-tyr1)-leucine-enkephalin (10-250 micrograms) was weakly hyperthermogenic, and kyotorphin (500 micrograms) did not consistently alter body temperature.
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PMID:Thermoregulatory effects of (D-ala2)-methionine-enkephalinamide in the cat. Evidence for multiple naloxone-sensitive opioid receptors. 625 Jun 78

Intracerebroventricular (ICV) administration of kyotorphin (L-Tyr-L-Arg) and cyclo (N-methyl-L-Tyr-L-Arg), its analog, produced significant dose-dependent hypothermic responses in mice at an ambient temperature of 24 degrees C. The hypothermic action of kyotorphin was much greater than that of Met-enkephalin (Met-ENK) but less than that of cyclo NMTA. This action was slightly but not significantly reversed by intraperitoneally administered naloxone (8 mg/kg), an opioid receptor antagonist. Met-ENK utilized as a control peptide in this study also produced a dose-dependent hypothermia which was slightly antagonized by naloxone (8 mg/kg, IP). Thyrotropin releasing hormone (TRH) injected ICV produced hyperthermia dose-dependently. The hypothermia induced by kyotorphin, its cyclic analog and Met-ENK was prevented by a small dose of TRH (0.18 microgram = 0.5 nmol/animal) which by itself had little effect on body temperature. A TRH neuronal system in the brain may explain the mechanism of kyotorphin-induced hypothermia. However, there was little evidence of involvement of opioid receptors. The present study demonstrates a potent action of kyotorphin and its analog on thermoregulation.
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PMID:Actions of intracerebroventricular administration of kyotorphin and an analog on thermoregulation in the mouse. 642 2

Nicotine produced a distinct reproducible syndrome in the conscious dog when injected intravenously or intracerebroventricularly. Intravenously administered nicotine (40 micrograms/kg/min for 20 minutes) increased cardiac and respiratory rates and produced analgesia, miosis, hypothermia, behavioral restlessness and emesis. When microinjected into the third cerebral ventricle, nicotine (100-200 micrograms) similarly increased cardiac and respiratory rates and pupillary diameter; and produced behavioral restlessness, emesis, erratic analgesia and maintained wakefulness and a desynchronized EEG. Microinjection of nicotine (5-25 micrograms) into the periaqueductal gray failed to alter any of the parameters studied. Intravenous pretreatment with the opioid antagonist naltrexone (2 mg/kg) influenced the action of intravenous nicotine on certain physiological systems. While naltrexone alone produced a significant degree of tachycardia, miosis, and analgesia, it potentiated the tachypnea and antagonized the miotic response evoked by nicotine. Methionine-enkephalin was detected in perfusates obtained from the lateral cerebral ventricles of conscious dogs. Nicotine produced a non-significant decrease in enkephalin levels. These observations suggest that there are interactions between endogenous opioid and nicotinic processes. However, they are complex and may differ from one functional system to another.
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PMID:Interaction between nicotine and endogenous opioid mechanisms in the unanesthetized dog. 717 83

The effects of intracerebroventricular (ICV) administration of two synthetic enkephalinamides, D-Ala2-Met5-enkephalinamide and D-Met2-Pro5-enkephalinamide, were compared with those of morphine on abstinence responses in morphine dependent mice. Mice were rendered dependent by morphine pellet implantation for three days. When administered six hours after pellet removal, both enkephalinamides and morphine reversed the naloxone-induced abstinence jumping response. On a molar basis, D-Met2-Pro5-enkephalinamide was the most potent compound and morphine was the least potent. Thus, substitution of D-Methionine in the two-position and prolineamide in five-position of the naturally occurring enkephalins, methionine- and leucine-enkephalin resulted in potent compound. The enkephalinamides and morphine also prevented hypothermia when injected immediately after or six hours after morphine withdrawal (pellet removal).
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PMID:Comparative effects of synthetic enkephalinamides and morphine on abstinence responses in morphine-dependent mice. 719 Mar

Bombesin (BO, 100 ng), bradykinin (BR, 10 microgram), or methionine-enkephalin (EN, 10 microgram) was administered intracerebroventricularly to adult male rats at an environmental temperature of 4 degrees C, 22 degrees C, or 35 degrees C, and rectal (Tre) and tail-skin (Tsk) temperatures were monitored for 5 hours. At 4 degrees C and 22 degrees C BO-treated animals developed acute hypothermia (max delta Tre=-3.25 degrees C and -2.71 degrees C, respectively) which persisted for 2 hours (p less than 0.05). At 22 degrees C and at 300 min post-injection, BO-treated animals became significantly (p less than 0.05) hyperthermic (deltaTre = +1.28 degrees C) when compared to controls. While BR had no effects at 22 degrees C, en-injected rats demonstrated significant (p less than 0.05) hyperthermia from 180 min through 300 min (delta Tre=+1.40 degrees C). At 22 degrees C both BO and, surprisingly, EN increased Tsk (e.g. delta Tsk =+ 3.49 degrees C and + 2.01 degrees C at 60 min). At 35 degrees C EN elicited hyperthermia which was significantly (p less than 0.05) increased from time 0 at all sampling time (mean delta Tre =+ 1.85 degrees C) and from control levels at 300 min (delta Tre =+1.07 degrees C, p less than 0.05). BO again caused a significant (p less than 0.05, BO vs control, 30 min) decrement (delta Tre =-1.22 degrees C) followed by increments (p less than 0.05) from 12-0-300 min. We conclude that the hypothermic effect of BO is dependent upon environmental temperature, partially caused by vasodilation, and possible biphasic in nature; EN treatment generally elicits hyperthermia under these conditions while BR produced no effects on thermoregulation.
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PMID:Thermoregulatory effects of centrally administered bombesin, bradykinin, and methionine-enkephalin. 727 89

L-Methionine-D,L-sulfoximine (MSO) (25 micrograms) infused locally into the dorsal raphe nucleus (DRN) induced a progressive decrease in body temperature in conscious restrained rats kept at an ambient temperature of 23 degrees C. Pretreatment with (+/-)-pindolol (3 mg/kg s.c.) significantly attenuated MSO-induced hypothermia, but pretreatment with ketanserin (0.5 mg/kg i.p.) did not alter either the magnitude or the time course of the decrease in body temperature after intra-DRN infusion of MSO. Local accumulation of gamma-aminobutyric acid (GABA) after infusion of gamma-vinylGABA (10 micrograms) and (+/-)-nipecotic acid (6 micrograms) inhibited MSO-induced hypothermia. Blockade of GABAA receptors by infusion of (-)-bicuculline (25 ng) had no effect on the decrease in body temperature elicited by MSO, but blockade of GABAB receptors by infusion of 2-OH-saclofen (13.3 ng) significantly attenuated MSO-induced hypothermia. In conclusion, local infusion of MSO into the DRN must have slowed down the rate of 5-HT turnover in serotonergic neurons and decreased the release and synthesis of GABA. 5-HT1A somato-dendritic autoreceptors and GABAB postsynaptic receptors both appear to be involved in these neurocytochemical processes leading to hypothermia.
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PMID:Hypothermia induced by infusion of methionine sulfoximine into the dorsal raphe nucleus of the rat: involvement of 5-HT1A and GABAB receptors. 838 14

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is considered to be one of the most toxic environmental contaminants, named dioxin. Exposure to TCDD induces a plethora of intoxication symptoms, including anorexia and hypothermia, in several mammals and human. Enkephalin, an endogenous pentapeptide, is an important neuroregulator of autonomic functions, such as food intake and body temperature. In this study, we investigated the effects of TCDD gastric administration on methionine-enkephalin (MEK) immunoreactivity in the brain of the Long-Evans rat, the species strain considered to be the most TCDD-susceptible, using immunohistochemical staining. A single dose of TCDD (dissolved in olive oil, 50 microg/kg) or olive oil alone was administrated to the rats by gavage. Compared with the vehicle-treated rat, a marked increase in the density of MEK immunoreactive cell bodies, fibers and terminals was found 2 weeks after TCDD treatment in the forebrain of the TCDD-treated rat, i.e. the central amygdaloid nucleus, field CA3 of the hippocampus, paraventricular hypothalamic nucleus, medial preoptic nucleus, interstitial nucleus of the posterior limb of the anterior commissure, lateral globus pallidus, ventral pallidum and lateral division of the bed nucleus of the stria terminalis. These results demonstrated for the first time a site-specific increased enkephalinergic activity in certain brain regions of the Long-Evans rat. It is suggested that the increased MEK immunoreactivity may act as a compensatory adaptation for the pathophysiological alterations caused by TCDD exposure.
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PMID:Up-regulation of methionine-enkephalin-like immunoreactivity by 2,3,7,8-tetrachlorodibenzo-p-dioxin treatment in the forebrain of the Long-Evans rat. 1266 56

While alterations in dopamine (DA) uptake appear to be a critical mechanism underlying locomotor and reinforcing effects of cocaine (COC), many centrally mediated physiological and affective effects of this drug are resistant to DA receptor blockade and are expressed more quickly following an intravenous (i.v.) injection than expected based on the dynamics of drug concentration in the brain. Because COC is also a potent local anesthetic, its rapid action on Na+ channels may be responsible for triggering these effects. We monitored temperatures in the nucleus accumbens, temporal muscle and skin together with conventional locomotion during a single i.v. injection of COC (1 mg/kg), procaine (PRO, 5 mg/kg; equipotential anesthetic dose), a short-acting local anesthetic drug that, like COC, interacts with Na+ channels, and cocaine methiodide (COC-MET, 1.31 mg/kg, equimolar dose), a quaternary COC derivative that is unable to cross the blood-brain barrier. In this way, we explored not only the importance of Na+ channels in general, but also the importance of central vs. peripheral Na+ channels specifically. COC induced locomotor activation, temperature increase in the brain and muscle, and a biphasic temperature fluctuation in skin. Though PRO did not induce locomotor activation, it mimicked, to a greater degree, the temperature effects of COC. Therefore, Na+ channels appear to be a key substrate for COC-induced temperature fluctuations in the brain and periphery. Similar to PRO, COC-MET had minimal effects on locomotion, but mimicked COC in its ability to increase brain and muscle temperature, and induce transient skin hypothermia. It appears therefore that COC's interaction with peripherally located Na+ channels triggers its central excitatory effects manifested by brain temperature increase, thereby playing a major role in drug sensing and possibly contributing to COC reinforcement.
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PMID:The role of peripheral Na(+) channels in triggering the central excitatory effects of intravenous cocaine. 1693 Apr 44

Liver grafts are frequently discarded due to steatosis. Steatotic livers can be classified as suboptimal and deteriorate rapidly during hypothermic static preservation, often resulting in graft nonfunction. Hypothermic machine perfusion (MP) has been introduced for preservation of donor livers instead of cold storage (CS), resulting in superior preservation outcomes. The aim of this study was to compare CS and MP for preservation of the steatotic donor rat liver. Liver steatosis was induced in male Wistar rats by a choline-methionine-deficient diet. After 24 hours hypothermic CS using the University of Wisconsin solution (UW) or MP using UW-Gluconate (UW-G), liver damage (liver enzymes, perfusate flow, and hyaluronic acid clearance) and liver function (bile production, ammonia clearance, urea production, oxygen consumption, adenosine triphosphate [ATP] levels) were assessed in an isolated perfused rat liver model. Furthermore, liver biopsies were visualized by hematoxylin and eosin staining. Animals developed 30 to 60% steatosis. Livers preserved by CS sustained significantly more damage as compared to MP. Bile production, ammonia clearance, urea production, oxygen consumption, and ATP levels were significantly higher after MP as compared to CS. These results were confirmed by histology. In conclusion, MP improves preservation results of the steatotic rat liver, as compared to CS.
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PMID:Preservation of steatotic livers: a comparison between cold storage and machine perfusion preservation. 1739 43


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