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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Volunteers with normal hearing were tested for vegetative balance with the aid of vegetative reflexes and with the aid of the atropine test. The effect of white noise stimulated on hearing thresholds was then investigated together with their recovery. The vegetative system was affected experimentally by intravenous administration of atropine, and the beginning and recession of hearing fatigue was observed. Atropine caused a small change only. In a similarly arranged experiment, 1% pilocarpin administered subcutaneously in a dose of 1.4 minus 1.6 ml, resulted in increased hearing fatigue and retarded recovery at higher frequencies. The effect of pilocarpin is explained by the fact that it supports the inhibitory processes checked by the parasympathetic nervous system on the periphery.
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PMID:The effect of the parasympathetic autonomic nervous system on auditory fatigue. 12 96

Maximum velocity and amplitude of repetitive ( 1-per-second) 30 degrees saccadic eye movements were quantitatively assessed for 4 minutes before and after intravenous edrophonium chloride as a diagnostic test for myasthenia gravis. Atropine was given initially to suppress muscarinic side effects. Eye movements were recorded by electrooculography and a digital computer identified saccadic eye movements and plotted amplitude-velocity relationships. When compared with control subjects, eleven of twelve patients with proven MG had a significant increase in saccade amplitude and/or maximum velocity after edrophonium chloride. Only three of twelve proven MG patients had clinically apparent extraocular muscle weakness. The initial period of fatigue improved the sensitivity of the test in those patients who began with normal saccade amplitude and maximum velocity. Two of the patients with positive saccade fatigue tests had no change in optokinetic nystagmus amplitude before and after edrophonium chloride. It is concluded that, quantitative assessment of repetitive large angle saccades before and after edrophonium chloride is a sensitive test for extraocular muscle involvement in MG.
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PMID:Saccade fatigue and response to edrophonium for the diagnosis of myasthenia gravis. 106 99

Clinical and metabolic responses to atropine plus pethidine and to scopolamine plus morphine premedication were studied in 45 ASA physical status III patients undergoing gynaecological procedures. Atropine 0.5 mg plus pethidine 50 mg intramuscularly (Group 1), scopolamine 0.24 mg plus morphine 8 mg (Group 2), or intramuscular placebo (Group 3) premedication were given in random, double-blind fashion. Scopolamine-morphine premedication caused a significant decrease in energy expenditure (EE) and oxygen consumption (VO2) (from 1229 +/- 193 to 1184 +/- 221 kcal/24 h, P = 0.004 and from 105 +/- 11 to 102 +/- 12 ml/min/m2, P = 0.006, respectively) simultaneously with a decrease in rate-pressure product (RPP) (P = 0.0001) and an increase in pressure-rate quotient (PRQ) (P = 0.034). Atropine-pethidine premedication induced a decrease in RPP but not in EE or VO2. In the placebo group both RPP and VO2 first increased and then slowly returned to the levels measured prior to premedication. The RPP was significantly lower in Group 2 than in Groups 1 and 3 at both 30 and 60 min. The degrees of subjective tiredness and anxiolysis were significantly greater in Groups 1 and 2 (showing good sedative and anxiolytic effect) than in Group 3. These results show that in ASA III patients, atropine-pethidine premedication does not decrease the sympathoadrenal reaction to the degree its anxiolytic and sedative effect would suggest. This may indicate neuroendocrine stress induced by atropine-pethidine.
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PMID:Clinical and metabolic responses to different kinds of premedication in ASA III patients. 146 14

Clinical and metabolic responses to three types of premedication were studied in ASA physical status I patients given any one of the following: (a) 0.5 mg of atropine and 50 mg of meperidine given intramuscularly plus an oral placebo tablet (n = 14), (b) 10 mg of oral diazepam and an intramuscular placebo (2 mL NaCl, concentration = 0.9) (n = 14), or (c) oral and intramuscular placebo (n = 14). Based both on subjective estimates (tiredness, fear, anxiety, dryness of mouth) and, especially, on metabolic responses (energy expenditure, oxygen consumption), oral diazepam appears to be superior to the combination of an opiate (meperidine) plus an anticholinergic (atropine). Atropine plus meperidine significantly increased energy expenditure above predicted values (2061 +/- 365 vs 1714 +/- 361 kcal/24 h, P = 0.004), calculated using the Harris-Benedict equation, based on sex, weight, height, and age, as well as increased oxygen consumption above levels seen with diazepam premedication (160 +/- 29 vs 137 +/- 17 mL.min-1. m-2). These findings indicate an iatrogenic stress factor induced by premedication with atropine plus meperidine.
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PMID:Clinical and metabolic responses to different types of premedication. 185 90

Intracellular recording from neostriatal neurons in rat brain slices revealed effects of the acetylcholine (ACh) agonist carbachol (Cch, 1-10 mumol/l), of the anticholinesterase physostigmine (10 mumol/l) and of the muscarinic antagonist atropine (10 mumol/l) on plateau potentials elicited in the presence of K-blockers. Plateau potentials elicited in the presence of K-blockers were Ca-dependent, since they persisted in Na-free solution, were resistant to tetrodotoxin (TTX, 3 mumol/l) and blocked by Cd (0.1-0.5 mmol/l). Cch reduced the duration of the plateau potentials and made them more susceptible to fatigue. These effects were antagonized by atropine (1-10 mumol/l), but not by Ba (100-200 mumol/l) or 4-aminopyridine (4-AP, 0.5 mmol/l). Physostigmine (10 mumol/l) had the same atropine-sensitive effects as Cch on the plateau potential. Atropine (10 mumol/l), by itself, prolonged the duration of the plateau potential. High concentrations (100 mumol/l) of Cch did not further reduce the duration of the plateau potential, instead, the duration re-increased with prolonged exposure. The re-increase of the plateau-spike duration was later masked by bursting activity. The opposing effects of low and high concentrations of Cch on the plateau potential duration corresponded to effects of this drug on intrastriatally evoked EPSPs in that low concentrations of Cch reduced the EPSP amplitude, but high concentrations re-increased it after a transient decrease. It is concluded that the muscarinic effect of ACh in the neostriatum is to modulate Ca-influx and that this effect is exerted in a tonic manner.
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PMID:Muscarinic modulation of calcium dependent plateau potentials in rat neostriatal neurons. 378 9

1. Our aim was to determine if sympathetic vasodilatation occurs in the human forearm, and if the vasodilating substance nitric oxide contributes to this dilatation. We also sought to determine if the nitric oxide might be released as a result of cholinergic stimulation of the vascular endothelium. 2. Blood flow was measured in the resting non-dominant forearm with venous occlusion plethysmography. To increase sympathetic traffic to the resting forearm, rhythmic handgrip exercise to fatigue followed by post-exercise ischaemia was performed by the dominant forearm. A brachial artery catheter in the non-dominant arm was used to selectively infuse drugs. 3. During control conditions, there was mild vasodilatation in the resting forearm during exercise followed by constriction during post-exercise ischaemia. When exercise was performed after brachial artery administration of bretylium (to block noradrenaline release) and phentolamine (an alpha-adrenergic antagonist), profound vasodilatation was seen in the resting forearm during both exercise and post-exercise ischaemia. 4. When the nitric oxide synthase blocker NG-monomethyl-L-arginine (L-NMMA) was administered in the presence of bretylium and phentolamine prior to another bout of handgripping, little or no vasodilatation was seen either during exercise or post-exercise ischaemia. Atropine also blunted the vasodilator responses to exercise and post-exercise ischaemia after bretylium and phentolamine. 5. These results support the existence of active sympathetic vasodilatation in the human forearm and the involvement of nitric oxide in this phenomenon. They also suggest nitric oxide might be released as a result of cholinergic stimulation of the vascular endothelium.
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PMID:Evidence for nitric oxide-mediated sympathetic forearm vasodiolatation in humans. 903

Rivastigmine is a non-competitive reversible inhibitor of acetylcholinesterase which is approved as one of the fi rst-line treatment options for Alzheimer's disease. We present the case of a 33-year-old woman with acute cholinergic syndrome secondary to deliberate rivastigmine poisoning. The patient presented at the emergency department (ED) with drowsy consciousness, dizziness, vomiting, diarrhea, sweating, and hypertension (171/103 mmHg). At the scene, an empty bottle of Rivast 120 mL/Bot, containing rivastigmine 2 mg/mL, was found beside the patient. Two hours later, we noted bronchorrhea and persistent salivation along with drowsiness, agitation, fatigue, incontinence, and limbs paralysis. A notably low serum cholinesterase level (651 U/l) was identified. Acute cholinergic syndrome secondary to rivastigmine intoxication was diagnosed. Endotracheal intubation with ventilator support was required due to respiratory failure. Atropine (0.5 mg intravenous injection) was administered. She was subsequently admitted to the intensive care unit for further care. Extubation was performed on the third day. The patient insisted on being discharged on the second day after extubation, and after administration of a total of 11 mg of atropine, no signs of either intermediate syndrome or delayed polyneuropathywere noted. rivastigmine, an acetylcholinesterase inhibitor, can precipitate an acute cholinergic crisis in cases of intoxication. Typical clinical features of cholinergic excess include increased secretions in the airway and oral cavity, miosis, diarrhea, anxiety, twitching, bronchoconstriction, convulsions, confusion, and gastrointestinal and muscular cramps. The treatment for acute cholinergic crisis is administration of atropine alone or in combination with an antidote to the cholinesterase inhibitor (such as pralidoxime). Patients often recover well with atropine supplements and optimal supportive care.
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PMID:Successful Resuscitation of a Young Girl Who Drank Rivastigmine With Respiratory Failure. 3299 49