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

We reported an 11-year-old boy who suffered from transient hypernatremia, hypothermia, and circadian rhythm disturbances of sleep-wakefulness and body temperature from the age of 4 years, as sequelae of acute subdural hematoma. T1-weighted magnetic resonance imaging (MRI) of the brain revealed low intensity consistent with necrotic change in the whole left cerebral hemisphere, hypothalamic region, and the right-sided brain stem including tegmentum, while the pituitary structure was well preserved. Anterior pituitary function was almost normal. ADH (antidiuretic hormone) was neither stimulated by hyperosmolality nor suppressed by hyposmolality but continued to be secreted at almost constant level approximating the normal basal state. This pattern seemed to be due to complete destruction of the osmoreceptor located in the anterior hypothalamus. He exhibited a dispersed-type sleep with differentiated stages of NREM (non-rapid eye movement), although the percentage of sleep was higher at night than in the daytime. It is suggested that circadian rhythm of sleep-wakefulness and differentiation of NREM sleep stages are regulated by different neuromechanisms. Brain stem lesion on MRI may be connected with the pathogenesis of the dispersed-type sleep with special respect to amplitude reduction of sleep-waking circadian rhythm. Circadian rhythm of body temperature (BT) was irregular in amplitude, phase, and period without synchronization with sleep-wakefulness rhythm. Hypothermia was also demonstrated at the basal state, while BT increased when he suffered from respiratory infection. It is likely that hypothermia in our case is caused by the BT shift to the lower side due to malfunction of BT integrating system including preoptic area and anterior hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Sodium regulation disorder, hypothermia, and circadian rhythm disturbances of the body temperature and sleep-wakefulness as sequelae of acute subdural hematoma]. 205 28

We examined the effects of two degrees of hypothermia on hepatic oxygen delivery and uptake, hepatic lactate uptake as a marker of hepatic function, and the effect of hypothermia on ischemia-reperfusion injury in the liver in miniature pigs (n = 18, 21-30 kg body wt). Hepatic arterial and portal venous blood flows were measured while hepatic oxygen delivery was progressively decreased without venous congestion in the preportal area. With decreases in hepatic blood and oxygen supply, oxygen extraction gradually increased from 50 to 90% in the normothermic group and from 25 to 70 and 84% in the hypothermic (30. and 34 degrees C, respectively) groups. The values of critical hepatic oxygen delivery were between 7.3 and 11.9 ml O2.min-1.100 g-1 without significant differences among the groups. During reperfusion after ischemic insult, hepatic oxygen uptake returned to base-line values in both hypothermic groups but remained substantially below base-line values in normothermic groups of animals. Hepatic enzyme concentrations (lactate dehydrogenase, alanine aminotransferase, aspartate aminotransferase, and alcohol dehydrogenase) were substantially increased (up to 30-fold) in normothermic animals, but the concentrations did not increase in either of the hypothermic groups. These results demonstrated that hypothermia per se does not affect hepatic oxygen delivery but decreases hepatic oxygen demand and uptake, provides an effective protection from hepatic oxygen deprivation, and lessens reperfusion injury.
 ...
PMID:Hypothermia, hepatic oxygen supply-demand, and ischemia-reperfusion injury in pigs. 236 Jun 37

The responses of fed, fasted, and hyperthyroid (T4) Sprague-Dawley male rats to 50 mg 1,1-dichloroethylene (1,1-DCE)/kg were compared. Hyperthyroid rats received three sc injections of thyroxine (100 micrograms/100 g) at 48-hr intervals; all other rats were sham-injected. 1,1-DCE was given po in mineral oil 24 hr after the last T4 dose; controls received only mineral oil. Animals were killed at 2, 4, and 8 hr. Liver GSH contents were lowered about 55% by both fasting and T4 while GSH transferase activities were lowered about 20% by fasting and 35% by T4. Only T4 pretreatment lowered alcohol dehydrogenase activities. Liver injury (i.e., serum glutamate pyruvate transaminase, histology) after 1,1-DCE was minimal in fed rats, moderate in fasted rats, and intermediate in T4 rats. Fasted rats showed a more pronounced depletion of liver GSH after 1,1-DCE than T4 rats and only in fasted rats did the toxicant decrease activities of the detoxification enzymes. Hypoglycemia after 1,1-DCE occurred in fed rats, but more rapidly in T4 rats. In contrast, fasted rats unexpectedly became hyperglycemic after the toxicant. Patterns of body temperature change after the toxicant, which might be due to its metabolites, were dissimilar. Hypothermia was not observed in fed rats, was only transiently evident in T4 rats, but occurred rapidly within 1 hr in fasted rats and steadily became more severe. The dissimilar patterns of liver enzyme and body temperature and serum glucose change after the toxicant in the three groups are indicative of different pathways of injury potentiation by fasting and hyperthyroidism.
 ...
PMID:Potentiation of 1,1-dichloroethylene hepatotoxicity: comparative effects of hyperthyroidism and fasting. 341 96

The effect of short-term administration of chlorpromazine and phenobarbital on cytoplasmic alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) was studied in distinct brain regions of the male rat. The effect of exposure to cold environment on the same enzymes was also evaluated. Chlorpromazine treatment resulted in inhibition of ADH and ALDH in the striatum and in the cerebellum, respectively. This inhibition was determined only when the animals were sacrificed 30 min but not 18 hr post terminal drug treatment. The pons-medulla content of ALDH was reduced by chlorpromazine treatment from controls 18 hr of terminal treatment. Hypothermic animals showed an inhibition of ADH in the diencephalon from corresponding controls. The phenobarbital treatment was devoid of action on hepatic ADH and ALDH. Concomitantly, an induction of both ADH and ALDH by pentobarbital was observed in the cerebellum and in the diencephalon, respectively. The effect of the drugs studied may contribute to their adverse interaction with ethanol on the central nervous system.
 ...
PMID:Effect of centrally acting drugs on ethanol detoxification enzymes in distinct rat brain regions. 388 86

We examined the renal function in 18 brain dead patients 2-0 h before removing the kidneys and 72 h after their transplantation to the recipient. The kidneys were preserved by simple hypothermia. In brain dead patients we found no demonstrable relationships between PCr and CCr or between Purea and CCr. At this time the Purea and PCr values are not a sufficiently accurate indicator of renal function. We also examined the plasma and urinary concentrations of Na, K, urea and osmotically active substances and calculated their excretion fractions. We found that, prior to removal, the kidneys were in a state of combined osmotic and water diuresis. The osmotic diuresis was chiefly of a non-sodium type and was produced by a mannitol load. Water diuresis was evidently caused by inhibition of ADH output consequent to brain hypoxia. We also investigated the relationship between the CCr values before nephrectomy and in the early posttransplantation phase. We found that there was a relationship between the recipient's CCr values in the early posttransplantation period and donor's CCr/total ischaemic time index. Calculation of this index can be valuable, especially in high risk transplantations.
 ...
PMID:Renal function in brain dead patients with respect to transplantation. 621 7

As follows from the experiments on the genotypic related populations of Drosophila melanogaster with different frequency of ADH allozymes selection for postponement of ageing and resistance to hypothermia lead to saturation of population with S-allozyme ADH, and genotypic adaptation to ethanol-to increasing of frequency of F-allozyme. It is supposed that genotypic adaptation is realized by selection of specimens with the most favourable alleles of genes. At the same time ontogenetic adaptation is accompanied by biochemical modification of existing allozymes.
 ...
PMID:[Gene-enzyme alcohol dehydrogenase system and adaptability in Drosophila melanogaster]. 927 30

Patients with multiple sclerosis sometimes show subthalamic lesions presenting syndrome of inappropriate secretion of ADH (SIADH), hypothermia, hyperprolactinemia, weight loss, and cachexia. Hyperprolactinemia also has been found in the patients with active systemic lupus erythematosus, because prolactin can be produced from human activated lymphocytes. We described a case of multiple sclerosis showing galactorrhea-amenorrhea syndrome with hyperprolactinemia. A 31-year-old woman showed a high level of prolactin in the serum (79.6 ng/ml) during remission stage 5 months after the onset of multiple sclerosis. She showed galactorrhea-amenorrhea syndrome 3 years later. She showed dysesthesia in her limbs, relapsing monoparesis, visual disturbance and Gd-enhanced plaques in Brain MRI for 6 years. She was admitted to our hospital on November 24, 1995. A neurological examination showed hyporeflexia of the upper extremities, hyperreflexia of the lower extremities, bilateral ankle clonus, truncal ataxia, and neurogenic bladder. Laboratory tests revealed increased level of serum prolactin, exaggerated secretion of serum prolactin after intravenous injection of 500 micrograms TRH, and marked suppression after oral administration of 2.5 mg bromocriptine. Brain MRI showed demyelinating lesions near the lateral ventricle, and cervical MRI (T2 image) showed high signal intensity lesions in the spinal cord from C2 to C5. In the previous case, galactorrhea-amenorrhea syndrome was found during the exacerbation stage of multiple sclerosis. Hyperprolactinemia may be caused from subthalamic lesions or by activated lymphocytes in multiple sclerosis. We considered that hyperprolactinemia and galactorrhea-amenorrhea syndrome in our patient might be caused from subthalamic lesions because lymphocytes were not activated during the remission stage of multiple sclerosis.
 ...
PMID:[A case of multiple sclerosis with galactorrhea-amenorrhea syndrome]. 936 74

1,4-Butanediol (1,4-BD) is the dihydroxy precursor of gamma-hydroxybutyrate (GHB), a popular recreational drug that has been banned by the United States Food and Drug Administration (FDA) and controlled as a federal schedule I drug. 1,4-BD is enzymatically converted in vivo to GHB by alcohol dehydrogenase (ADH), and overdoses can result in coma, severe respiratory depression, bradycardia, hypothermia, seizures, and death. Presently, there is no antidote. We pretreated CD-1 mice with the ADH antagonist, 4-methylpyrazole (4-MP), to determine if blocking ADH can prevent or decrease toxicity from 1,4-BD overdose. Pretreatment with 4-MP increased the Toxic Dose-50 (TD(50)) of 1,4-BD for the righting reflex from 585 mg/kg (95% CI, 484-707 mg/kg) in control mice to 5,550 mg/kg (95% CI, 5,353-5,756 mg/kg) in pretreated mice. Pretreatment with 4-MP also increased the TD(50) of 1,4-BD for the rotarod test from 163 mg/kg (95% CI, 136-196 mg/kg) in control mice to 4,900 mg/kg (95% CI, 4,812-4,989 mg/kg) in pretreated mice. Pretreatment with 4-MP significantly decreased the toxicity of 1,4-BD in CD-1 mice, presumably by inhibiting its ADH biotransformation to GHB. 4-MP warrants further investigation as a potential antidote for this increasingly abused drug.
 ...
PMID:Pretreatment of CD-1 mice with 4-methylpyrazole blocks toxicity from the gamma-hydroxybutyrate precursor, 1,4-butanediol. 1207 36

Ethyl alcohol (ethanol) is readily absorbed from all parts of the gastrointestinal tract due to its hydrophilic potential. The biological effects in humans refer to practically every organ and system. The basic enzyme involved in its oxidation is alcohol dehydrogenase. Another important metabolic pathway is the Microsomal Ethanol-Oxidizing System (MEOS). Toxic effect on basic cell functions is produced both by ethanol and acetic aldehyde, its oxidation product which accounts for most of the acute and delayed effects of ethanol toxicity. In acute ethanol intoxication's the CNS symptoms are the first to manifest. Ethanol affects the CNS functions mainly through stimulating opiate and benzodiazepine receptors and a number of neurotransmitters. However, the attempts to diminish the toxic effects of ethanol on CNS by blocking the affected receptors have proved to be ineffective. In acute poisoning a basic essential is to sustain vital functions by following the principles of intensive care. Each case of acute ethanol intoxication must be subject to neurological examination for possible cerebro-cranial traumas. The diagnostics and treatment procedures should take account of the possible symptoms: convulsions, respiratory and cardiac failure, hypoglycemia, hypothermia, and severe gastric dysfunction. Vital signs monitoring and control of acid-base and water-electrolyte balance are a must. The toxic properties of ethanol metabolites can be particularly hazardous to patients treated with disulfiram. The patients who develop "antabuse response" should be given immediately iron and vitamin C intravenously.
 ...
PMID:[Biological and toxic effects of ethanol: diagnostics and treatment of acute poisonings]. 1456 85

Propylene glycol is a diluent found in many intravenous and oral drugs, including phenytoin, diazepam, and lorazepam. Propylene glycol is eliminated from the body by oxidation through alcohol dehydrogenase to form lactic acid. Under normal conditions, the body converts lactate to pyruvate and metabolizes pyruvate through the Krebs cycle. Lactic acidosis has occurred in patients, often those with renal dysfunction, who were receiving prolonged infusions of drugs that contain propylene glycol as a diluent. We describe a 50-year-old man who experienced severe lactic acidosis after receiving an accidental overdose of lorazepam, which contains propylene glycol. The patient was acutely intoxicated, with a serum ethanol concentration of 406 mg/dl. He had choked on a large piece of meat and subsequently experienced pulseless electrical activity with ventricular fibrillation cardiac arrest. He was brought to the emergency department; within 2 hours, he was admitted to the intensive care unit for initiation of the hypothermia protocol. The patient began to experience generalized tonic-clonic seizures 12 hours later, which resolved after several boluses of lorazepam. A lorazepam infusion was started; however, it was inadvertently administered at a rate of 2 mg/minute instead of the standard rate of 2 mg/hour. Ten hours later, the administration error was recognized and the infusion stopped. The patient's peak propylene glycol level was 659 mg/dl, pH 6.9, serum bicarbonate level 5 mEq/L, and lactate level 18.6 mmol/L. Fomepizole was started the next day and was continued until hospital day 3. Continuous renal replacement therapy was started and then replaced with continuous venovenous hemofiltration (CVVH) for the remainder of the hospital stay. The patient's acidosis resolved by day 3, when his propylene glycol level had decreased to 45 mg/dl. Fomepizole was discontinued, but the patient's prognosis was poor (anoxic brain injury); thus care was withdrawn and the patient died. Although the patient's outcome was death, his lactic acidosis was treated successfully with fomepizole and CVVH. Clinicians should be aware that an iatrogenic overdose of lorazepam may result in severe propylene glycol toxicity, which may be treated with fomepizole and CVVH.
 ...
PMID:Severe lactic acidosis after an iatrogenic propylene glycol overdose. 2009 97


1 2 Next >>