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)

Phenylethylamine (PEA, 50 and 100 microgram ivc) and octopamine (OCT, 50 and 250 microgram ivc) potentiated the tremorine (10 mg/kg ip) induced hypothermia in the rat. This effect was partially antagonized by atropine (10 mg/kg ip). PEA and OCT significantly prolonged the duration of pilocarpine (100 mg/kg iv) induced catalepsy in rats. PEA (100 microgram ivc) and OCT (250 microgram ivc) depressed the acetylcholine (ACh) level in the cerebral cortex and striatum but did not affect it in the hippocampus. In addition, these amines enhanced the synthesis of ACh in the cerebral cortex, and PEA also in the rat striatum.
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PMID:The effect of intraventricular phenylethylamine and octopamine on the central effects of tremorine and pilocarpine and the acetylcholine level in the rat brain. 679 57

The neuropharmacological profile of the total fungal extract of F. moniliforme (FM) has been investigated. FM produced dose related decrease in spontaneous motor activity (SMA) and exploratory activity, potentiated pentobarbitone hypnosis and the anticonvulsant actions of phenobarbitone and phenytoin against MES seizures, potentiated PTZ and tryptamine seizures, antagonised reserpine induced syndrome, attenuated tetrabenazine and morphine induced catalepsy and potentiated haloperidol catalepsy. FM showed per se antinociceptive activity and potentiated morphine analgesia. It increased rectal temperature, antagonised reserpine and apomorphine hypothermia and potentiated the hyperthermic response of haloperidol and 5-hydroxytryptophan (5-HTP) and hypothermic response of betaphenylethylamine (PEA) and L-dopa. FM had no per se effect on amphetamine lethality, but enhanced the lethality induced by morphine in aggregated animals. Stereotypy by amphetamine was potentiated while that of apomorphine was not affected. The behavioural response of 5-HTP and L-dopa was potentiated. FM had no effect on swim induced behavioural despair. The effect on aggressive behavior was complex, and while the cumulative aggressive score was reduced, the onset of fighting behaviour and contact period was increased. It also inhibited clonidine induced auto mutilation. Since earlier investigation had shown that FM, like nialamide, induced non-selective inhibition of monoamine oxidase (MAO), the results were compared with those induced by nialamide. A comparative profile of action reveals that the neuropharmacological action of FM are qualitatively similar to those induced by nialamide, and likely to be due to inhibition of MAO. The investigation has practical implications because F. moniliforme is a common contaminant of cereals and fruits.
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PMID:Neuropharmacological studies on Fusarium toxins--I: Total toxin extract from Fusarium moniliforme. 906 73

A 20-year-old woman presented with dyspnoea in the Emergency department and subsequently suffered a cardiac arrest. The initial rhythm was PEA (pulseless electrical activity). She had intermittent return of spontaneous circulation. Transthoracic echocardiography showed a dilated hypokinetic right ventricle and a collapsed left ventricle. The tentative diagnosis was pulmonary embolism, but she remained hemodynamically unstable despite thrombolysis. 90 min after the collapse she was put on cardiopulmonary bypass and surgical embolectomy was performed. Large masses of thrombotic material were collected from central parts of the right and left pulmonary artery. Therapeutic hypothermia was applied for 24 hours postoperatively. The remaining hospital stay was uneventful and ten days after the presentation she was transferred to her local hospital. At this point she was without neurological sequelae. The patient had used oral contraceptives (ethinyl estradiol/ drospirenone).
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PMID:[A young woman with cardiac arrest]. 2009 25

The ring of the red notification phone breaks the relative calm of an otherwise typical Monday morning and heralds the arrival of a critically ill patient. The dispatcher announces that EMS is on the way with a 57-year-old man in cardiac arrest, with an ETA of 3 minutes. Shortly after preparations for their arrival are complete, EMS personnel enter with CPR in progress and the patient already intubated. As monitor/defibrillator attachment, ETT placement confirmation, additional IV access, and complete exposure of the patient occur, you hear more about the clinical scenario from EMS. Mr. I.C. is a 57-year-old male who was moving furniture when, as described by witnesses, he complained of difficulty catching his breath and a slight tightness in his chest. He began coughing violently, vomited once, gasped, and collapsed. Emergency medical services personnel state that they arrived approximately 20 minutes after the patient had collapsed, with CPR in progress. The patient was intubated in the field, and EMS reports that the initial rhythm was PEA. Upon the patient's arrival in the ED, the rhythm is noted to be ventricular fibrillation. Defibrillation is attempted twice over the next 4 minutes, with concomitant administration of medications. During the next rhythm check, QRS complexes are noted on the monitor and a pulse is palpated. The patient has had a return of spontaneous circulation, apparently 50 minutes from onset of the arrest. As you initiate postresuscitation care, you consider the patient's prognosis and wonder if he qualifies for therapeutic hypothermia; ie, will therapeutic hypothermia make a difference in his outcome?
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PMID:Current evidence in therapeutic hypothermia for postcardiac arrest care. 2216