Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085631 (agitation)
 12,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1 A series of peptides derived from porcine lipotropin was examined for analgesic and other morphine-like properties on infusion into the cannulated third ventricle of cats.2 Lipotropin (LPH 1-91) itself produced no analgesia or other morphine-like effects when infused in a dose of 150 mug.3 C-fragment (LPH 61-91) produced strong long-lasting analgesia when infused in a dose of 10 or 20 mug; on a molar basis the potency was between 90 and 180 times that of morphine. The following morphine-like effects were also produced: shivering leading to fever, vasodilatation of the pinnae, mydriasis, opening of the palpebral fissures, tachypnoea with bouts of panting, vocalization, hyperexcitability, restlessness and catalepsy. All the effects, including analgesia, were abolished by an intraperitoneal injection of naloxone (1 mg/kg).4 Hyperglycaemia, another central effect produced by morphine, was obtained with C-fragment infused in a dose of 60 mug.5 On intravenous injection, C-fragment produced analgesia with a dose of about 200 mug/kg. Administered by this route, C-fragment was again more potent than morphine.6 C'-fragment (LPH 61-87), LPH 61-78 and LPH 61-69, either had no analgesic effect or produced weak short-lasting analgesia when infused in doses up to 100 mug.7 Methionine enkephalin (LPH 61-65) either produced very weak short-lasting analgesia or had no analgesic effect when infused in doses of between 30 and 400 mug.8N-methyl methionine enkephalin amide in which both termini of methionine enkephalin were protected against degradation by exopeptidases produced long-lasting analgesia when infused in doses of 150 to 180 mug; its analgesic potency was approximately 100 times less than that of C-fragment. Blocking only one terminus of methionine enkephalin did not appear to endow the peptide with analgesic properties. The N-methyl pentapeptide amide produced other morphine-like effects of which the most striking was catalepsy. All the effects were abolished by intraperitoneal naloxone (1 mg/kg).
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PMID:C-fragment of lipotropin--an endogenous potent analgesic peptide. 56 Aug 94

A case of intentional intoxication with pentachlorophenol has been described. Salient features observed included pyrexia, diaphoresis, hyperkinesis, muscle twitching, tremors, epigastric tenderness, leg pain, tachypnea, and tachycardia. The patient's restlessness and agitation were controlled with phenytoin and phenobarbital. Forced diuresis with furosemide and mannitol resulted in a large increase in urinary excretion of pentachlorophenol. It is suggested that such therapy may be life saving in such intoxications.
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PMID:Human poisoning with pentachlorophenol and its treatment. 61 97

In unasthetized dogs naloxone induced effects opposed to those of morphine (tachycardia, agitation, hyperthermia, tachypnea) and mydriasis. These effects were moderate and transient; some of them were elicited with low doses being border-line after 0.03 mg.kg-1 s.c., statistically significant after 0.1 mg.kg-1 s.c.; they increased slightly with the dose. After repeated administrations, acute tolerance developed and some moderate morphine-like effects (miosis, sedation) were observed. The stimulatory effects described here may result from antagonism of a morphinomimetic natural ligand,and represent thus indirect arguments in favour of normal functions of this ligand; these functions would be to temper not only algesic but also other stimulant reactions. The limitation of the effects might result from the limited release of this ligand in normal dogs and (or) from interfering morphinomimetic properties of naloxone, which are apparently unmasked when administrations are repeated. Both, stimulatory and inhibitory effects of naloxone are not liable to represent noticeable side-effects of this drug, but they both might play some role in the mechanisms of precipitated abstinence.
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PMID:[Reversal by naloxone of the effects of morphine on the unanesthetized dog]. 98 83

The case is reported of a non-diabetic young woman who attempted suicide by ingesting 2,500 mg of phenformin. The most marked clinical and laboratory findings during the first 24 hrs included nausea, vomiting, anxiety, agitation, polydipsia, polyuria, increased appetite, tachycardia, tachypnea, persistent lactic acidosis, hypoglycemia and hypokalemia. Treatment at the ICU 10 hrs after ingestion of the overdose was essentially symptomatic and included measures to correct acidosis and hypoglycemia. The patient recovered completely.
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PMID:Acute self-poisoning with phenformin. 102 Jun 9

The fat embolism syndrome is a well-defined clinical entity that can usually be recognized in patients who have long-bone fractures. Cerebral symptoms of restlessness, confusion, stupor, and coma correlate with the autopsy findings of fat in the brain, but the amount of fat or amount of petechial hemorrhage cannot be quantitated with the severity of the cerebral symptoms. There is a correlation between the clinical manifestations of dyspnea and tachypnea and the autopsy findings in the lungs, which are heavy from edema and alveolar hemorrhage; however, we cannot correlate the degree of pathologic change in the lung, including lung weights, with the severity of findings clinically.
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PMID:The clinical and pathologic correlation of fat embolism syndrome. 115 33

Amphetamine poisoning is rare in children. Here we report two male infants with acute poisoning due to accidental amphetamine ingestion. One infant had a family history of drug abuse and the other was due to poor supervision of the parents. Although typical clinical symptoms and signs (including restlessness, hyperactivity, hypertension, tachycardia and tachypnea....etc.) were found, both were completely recovered after treatment. The principle of management of amphetamine poisoning are presented.
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PMID:Amphetamine poisoning in infant: report of two cases. 165 42

Endogenous opioid peptides have been implicated in the regulation of pain perception, behaviour, gastrointestinal activity and other physiological responses. However, the functional role of these peptides in the horse has yet to be elucidated. The opioid antagonist, naloxone, is often administered to infer endogenous opioid effects. In the present study, naloxone (0.75 mg/kg bodyweight) was administered to eight Thoroughbred racehorses and a number of behavioural and autonomic responses were measured. Naloxone produced rapid onset diarrhoea, restlessness, abdominal checking, tachycardia, tachypnoea, paradoxical yawning and diaphoresis. These responses described an acute abdominal distress syndrome similar to spasmodic colic. Results from this study suggest that, in the horse, endogenous opioids: 1) influence behaviour, 2) modify intestinal activity and sensation, and 3) if perturbed, may be involved in pathophysiology of colic.
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PMID:Naloxone-induced abdominal distress in the horse. 220 19

The effects of eight neuroleptic drugs injected into the cerebral ventricles on behavior, autonomic and motor activity of unanesthetized cats have been studied. Chlorpromazine, trifluorpromazine, droperidol, haloperidol, domperidone and spiperone induced emotional behavior (restlessness, miaowing, rage, attack, defense, fighting with paws, biting), autonomic (mydriasis, tachypnoea, dyspnoea, panting, salivation, defecation, urination, licking, vomiting) and motor (ataxia, muscular weakness, adynamia) phenomena. The main and the most consistent effect was the motor impairment, while the aggression was inconsistent and of moderate intensity. Of the neuroleptic drugs injected, only spiperone, domperidone and trifluorpromazine produced a dose-dependent motor impairment. The autonomic effects were also inconsistent and of low intensity. Metoclopramide induced inconsistent autonomic and motor effects, while sulpiride was devoid of any visible behavioral, autonomic and motor activity. It appears, therefore, that the motor impairment as well as the aggression caused by the neuroleptic drugs is perhaps related to central D-1 rather than to central D-2 dopamine receptors, but an effect on central norepinephrine and on central serotonin receptors cannot be excluded.
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PMID:Behavioral, autonomic and motor effects of neuroleptic drugs in cats: motor impairment and aggression. 286 89

The effect on behavior of eight anticholinergic agents: atropine, scopolamine, trihexyphenidyl, biperiden, homatropine, eucatropine, hexocyclium and propantheline, injected into the cerebral ventricle (ICV) of the cat was investigated and compared. The anticholinergic agents evoked: (1) psychomotor stimulation such as miaowing, loud calling, restlessness, impelling locomotion, jumping, vacant staring, apprehension and loss of interest of the surroundings; (2) aggression, hissing, threat, attack, defense, fighting with paws and flight; (3) autonomic responses including mydriasis, tachypnea, dyspnea, licking, vomiting, salivation, micturition and defection; and (4) motor phenomena comprising scratching, ataxia, rigidity, tremor, weakness with adynamia or myoclonic jerks. Convulsions appeared only after ICV injections of atropine and homatropine. The most characteristic behavioral effect of anticholinergic agents was psychomotor stimulation accompanied by mild aggressive responses. The only exception was propantheline which caused a muscular weakness and adynamia. Atropine and scopolamine alone induced a dose-dependent impelling locomotion as well as fighting behavior. Carbachol and eserine injected intracerebroventricularly reversed the locomotion autonomic and motor phenomena produced by anticholinergic agents administered similarly. It is suggested that anticholinergic agents acting as partial agonists, can produce their behavioral effects through central cholinoceptive sites.
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PMID:Comparative behavioral effects of anticholinergic agents in cats: psychomotor stimulation and aggression. 370 93

Two cases of atropine toxicity in monozygotic twins presented with the usual systemic manifestations: hyperpyrexia, agitation, mydriasis, tachypnea, tachycardia, decreased gastrointestinal motility, anhydrosis, and skin flush. Intravenous physostigmine, the treatment of choice, was used to resolve the toxic crisis. Physostigmine counteracts atropine's anticholinergic effects at the postganglionic nerve synapses of the autonomic nervous system. The chance of atropine toxicity occurring with ophthalmic usage may be lessened by careful parental instruction about dosages and about the warning signs of its systemic toxicity.
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PMID:Atropine toxicity in identical twins. 668 22


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