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)

Thyrotropin releasing hormone (TRH) administered via the intracerebroventricular (icv) route in doses ranging between 0.1 and 100 mug decreased the duration of pentobarbital-induced narcosis in rabbits. Antagonism of narcosis occurred whether TRH was administered before or after the barbiturate. TRH doses above 10 mug produced, in addition, behavioral excitation and hyperthermia. The antagonism of phenobarbital-induced narcosis was not as profound; animals were aroused only for a short period of time, after which the narcotized state returned. However, TRH exerted a prolonged antagonism or reversal of the phenobarbital-induced hypothermia. The central nervous system depression and analgesia produced by morphine were unaffected by TRH, but hypothermia and respiratory depression were reversed. TRH may represent an arousal factor in mammalian brain.
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PMID:Influence of thyrotropin releasing hormone (TRH) on drug-induced narcosis and hypothermia in rabbits. 82 48

Mechanisms underlying the elimination or marked depression of renal function in hibernation and hypothermia were investigated through measurements of blood pressure, heart rate, red blood cell and plasma volumes, and relative distribution of cardiac output. Hamsters (Mesocricetus auratus) were made hypothermic (rectal temperature (Tre), 7 degrees C) by exposure to helox and cold, or permitted to hibernate with several weeks of cold exposure (Ta approximately 5 degrees C). Mean arterial pressure, 120 Torr in normothermic control animals, demonstrated a 55% and 60% decrease during hibernation and hypothermia, respectively. As the animals rewarmed from hypothermia or aroused from hibernation, blood pressure increased rapidly at 8-12 degrees C, more gradually at 12-17 degrees C, and plateaued thereafter. Blood pressure rapidly returned to near control levels whereas heart rate remained at less than one-half control value at the highest temperature examined. Red blood cell volume, 26.2 +/- 0.6 ml/kg body wt in the control animals appeared unaffected by hypothermia. Plasma volume, by contrast, decreased from control values of 33.0 +/- 0.8 to 21.3 +/- 0.6 ml/kg body wt in hypothermia, a decrease of approximately 35%. Distribution of cardiac output to various organs in hibernation and hypothermia followed a similar pattern. Relative flow to the heart, lung, diaphragm, and brown fat increased while the fraction distributed to the visceral organs appeared to decrease. The normothermic control kidney received approximately 16% of the cardiac output while the hibernating and hypothermic kidneys received approximately 10% and 6%, respectively. The data are discussed in terms of the determinants of glomarular filtration rate and explain, in part, the elimination or marked reduction in renal function observed in depressed metabolic states.
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PMID:Mechanisms responsible for decreased glomerular filtration in hibernation and hypothermia. 83 61

Extracellular potassium activity, [K+]0, was continuously measured using potassium specific microelectrodes in the cerebral cortex of cats before and after hypoxic or anoxic insults. Two patterns of [K+]0 increase were seen. A slow, linear rise occurred during hypoxia and hypothermia and was correlated with changes in mean blood pressure (B/P). A fast, complex, exponential rise resembling spreading depression occurred during anoxia and was unassociated with B/P changes. The fall of [K+]0 after reversal of the insult was described by a single exponential function with rate constants from 0.009 to 0.0194 sec-1. It is suggested that the linear rise is primarily a result of sodium pump inhibition and that the exponential rise is due to a superimposed sudden increase in cell membrane permeability perhaps secondary to transmitter release. The kinetics of the fall of [K+[0 is consistent with the normalization of the sodium and potassium gradients across the cell membranes secondary to Na+-K+ATPase activity.
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PMID:The kinetics of extracellular potassium changes during hypoxia and anoxia in the cat cerebral cortex. 84 9

delta9-Tetrahydrocannabinol (THC; 2.5, 5.0, 10.0 mg/kg, PO) impaired avoidance and rotarod performance, and caused bradycardia and hypothermia. Phencyclidine (PCP; 1.25, 2.5, 5.0 mg/kg, IP) impaired avoidance and rotarod performance and caused a marked increase in photocell activity. When combined, the depressant properties of each drug were enhanced and the stimulation of photocell activity cg/kg THC and its interactions with PCP followed subacute treatment for six days, whereas many of the effects of PCP were enhanced after subacute treatment with a dose of 2.5 mg/kg. Open-field behavior was affected by each drug alone and in combination in a similar way as photocell activity, but the depression caused by their interaction was greater; both drugs caused an increase in urination. Response rates on an FR-10 schedule of food reinforcement were decreased by 2.5 mg/kg PCP, but not by 5.0 mg/kg THC; the combination caused greater response suppression than either drug alone. The functional interactions between THC and PCP were not related to changes in the concentrations of 14C or 3H in plasma or brain derived from 14C-delta9-THC and 3H-PCP, respectively.
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PMID:Interactions between delta9-tetrahydrocannabinol and phencyclidine hydrochloride in rats. 85 Jun 86

To determine the effects of variations in temperature on the neuromuscular blockade produced by pancuronium, the drug was infused intravenously into 18 cats anesthetized with chloralose and urethane at a constant continuous rate to produce and maintain 90 per cent depression of twitch tension of the anterior tibial muscle following supramaximal stimulation of the peroneal nerve. The mean (+/-SE) infusion rates of pancuronium needed were 0.44 +/- 0.05, 0.99 +/- 0.11, and 1.05 +/- 0.09 microng/kg/min (r = 0.73) at 29, 37, and 41 C, respectively. In contrast, the doses of neostigmine necessary for 50 per cent antagonism of the pancuronium-induced depression of twitch tension were not significantly different at the three temperatures. The time required to achieve peak neostigmine effect was longer at the lowest temperature. The durations of neostigmine action were longer at 29 and 37 than at 41 C. It is concluded that hypothermia augments neuromuscular blockade produced by pancuronium and prolongs the time to peak effect, and possibly the duration of action, but not the dose of neostigmine needed to antagonize the blockade.
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PMID:Pancuronium-induced neuromuscular blockade, and its antagonism by neostigmine, at 29, 37, and 41 c. 85 Dec 42

5-hydroxydopamine, unspecific centrally acting false neurotransmitter. Acta Physiol. Pol., 1977, 28 (1): 13-22. 3,4,5-trihydroxyphenetylamine-5-hydroxydopamine (5-OHDA) injected intracerebro-ventricularly decreases the level of noradrenaline, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in different parts of the rat brain. It does not affect acetylcholine level. 5-OHDA causes dose-dependent hypothermia, transient hypertension and depression of locomotor and exploratory activity in rats. This behavioral phenomena are reversed by central chemical sympathectomy elicited by 6-hydroxydopamine. It is concluded that 5-OHDA is an unspecific centrally acting false transmitter.
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PMID:5-hydroxydopamine, unspecific centrally acting false neurotransmitter. 86 21

Urethral obstruction induced in adult male cats caused clinical signs identical with those observed in naturally occurring disease. Central nervous system depression, anorexia, dehydration, vomiting, muscle weakness, and hypothermia occurred. Weight loss (due to water loss and catabolism), metabolic acidosis, mild hyponatremia, hyperkalemia, hypermagnesemia, hypocalcemia, hyperphosphatemia, hyperglycemia, azotemia, and hyperproteinemia were also observed. Serum amylase, alkaline phosphatase, and alanine aminotransferase activities were normal. Ten of 13 cats (group 1), with 72 hours' induced obstruction but not treated with parenteral fluids, died either before the obstruction was relieved or within 8 days afterward. Eight cats (group 2) with induced obstruction for 49 to 98 hours developed severe clinical and biochemical alterations. Treatment with a multiple-electrolyte solution, in addition to relief of urethral obstruction, resulted in favorable clinical and biochemical responses. These cats survived and were clinically healthy at 9 to 10 days after relief of obstruction. It was concluded that use of a multiple-electrolyte solution to correct acidosis, restore circulatory volume, and enhance renal excretion of potassium was effective supportive therapy after urethral obstruction was removed.
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PMID:Characterization and treatment of water, electrolyte, and acid-base imbalances of induced urethral obstruction in the cat. 87 80

Reserpine, a well-known CNS depressant which depletes central monoamine stores, was found to produce in the brains of 11-day-old rats a severe depression in cell proliferation in terms of the rate of [3H]thymidine incorporation into DNA. The effect was studied in detail 12 h after ther administration of the drug (2.5 mg/kg, s.c.) when the rate of in vivo DNA synthesis in the forebrain was about one-third of control: the decrease was less marked in the cerebellum (rate about two-thirds of control). It was possible to exclude side effects of the drug, such as restricted food intake, hypothermia and an elevation of the level of blood corticosteroids being responsible for the reduction of [3H]thymidine incorporation into DNA. Kinetic studies showed that reserpine had no marked effect on the entry of [3H]thymidine from blood to brain, but it caused some retardation in the rate of [3H]thymidine conversion into [3H]thymidine nucleotides. Nevertheless, the severe depression of DNA labelling was evident even after correcting the values on the basis of [3H]thymidine nucleotide concentrations. In contrast to these effects, thymidine kinase activity was normal in the brain of reserpine-treated animals.
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PMID:Effect of reserpine on cell proliferation in the developing rat bran: a biochemical study. 88 5

The tetrahydrocannabinols are among the most potent hypothermic agents known. A comparison of the hypothermic action of delta9-tetrahydrocannabinol (delta9-THC) with chlorpromazine (CPZ) and morphine shows the following order of hypothermic potency: CPZ greater than delta9-THC greater than morphine. A marked depression of oxygen consumption is produced by delta9-THC both in vivo and in the isolated perfused liver preparation. Simultaneous measurement of core temperature and tail temperature after delta9-THC shows that tail temperature is decreased more by delta9-THC than it is in animals that attain comparable core hypothermia without drug treatment. From these results, it is concluded that delta9-THC-induced hypothermia results primarily from decreased heat production and not from increased heat loss. Therefore, the processes involved in the hypothermic response to delta9-THC appear to differ from those that mediate CPZ- or morphine-induced hypothermia. A hypothesis is discussed in which the hypothermic action of delta9-THC is related to inhibition of membrane ATPase.
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PMID:Profound hypothermia in mammals treated with tetrahydrocannabinols, morphine, or chlorpromazine. 91 17

Lisuride hydrogen maleate induced stereotyped behaviour in normal as well as in reserpinized mice. It antagonized the motor depression and hypothermia induced by reserpine. On i.p. administration the compound was about as effective as apomorphine and D-amphetamine. As with apomorphine and in contrast to D-amphetamine the effects of lisuride hydrogen maleate in reserpinized mice were not impaired by additional treatment with alpha-methyl-p-tyrosine methylester. In untreated mice, the substance was very potent in lowering body temperature with significant hypothermia measured after dosages as low as 0.10 mg/kg i.p. Occurrence of stereotyped behaviour and hypothermia could be prevented by the dopaminergic antagonist haloperidol. From these data it is concluded that lisuride hydrogen maleate in addition to its interaction with serotoninergic systems is a potent dopaminergic agonist with a probably direct action on dopaminergic receptors. Further arguments in support of such an action of lisuride hydrogen maleate are, in addition to biochemical data, its serum prolactin lowering effect in rats, its strong emetic action in dogs and its effects on rat behaviour.
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PMID:Direct dopaminergic action of lisuride hydrogen maleate, an ergot derivative, in mice. 94 66


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