Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For evaluation of the state of excitability of motoneurons in the dorsal flexor of the foot in patients with drug-induced muscle rigidity curves of excitability of motoneurons in the anterior tibial muscle were plotted in 10 patients not receiving psychotropic agents (controls) and 10 patients treated with chlorpromazine. Two variants of experiment wase used: in the 1st variant stimulation of the peroneal nerve behind the fibular capitulum served as the conditioning and testing stimulus, in the 2nd variant stimulation of the tibial nerve in the popliteal fossa was the conditioning stimulus and stimulation of the peroneal nerve in the above way was the testing stimulus. The investigations were carried out before and 30-50 min after intramuscular injection of ethylbenzatropine 5 mg. In the 1st variant the curve of excitability of the motoneurons of the anterior tibial muscle showed the same configuration as the curve of excitability of motoneurons of the soleus muscle in the control group as well as in the treated group. Similarly as in the excitability curve of the soleus muscle five phases could be differentiated in it. Phase III of depression was, however, deeper and phase IV of returning excitability was more evident. In variant II in phase III depression was observed lasting only 40 msec., then in place of return of excitability its decrease was observed. These results were similar to these obtained in the case of conditioning stimulation of afferent fibres of the anterior tibialis muscle, and testing stimulation of the afferent fibres of the soleus muscle. After ethylbenzatropine injection no changes were found in variant I, on the other hand, in variant II a rise of excitability was present in phase III in the control group and in phases III and IV in treated patients. Ethylbenzatropine seemed, thus, to have no effect on the excitability of motoneurons in the dorsal flexor of the foot in the case of conditioning afferent stimulation of the dorsae flexor of the foot.
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PMID:[Excitability curve of alpha motor neurons of the foot dorsal flexor in chemically induced parkinsonian rigidity prior to and following ethylbenzatropine administration]. 112 51

Intracellular free Mg2+ concentration ([Mg2+]i) was measured in isolated single fibres of Xenopus muscle using the fluorescent Mg2+ indicator furaptra. In resting muscle the [Mg2+]i was 1.7 mM in a Mg(2+)-free Ringer solution. There was no significant change in [Mg2+]i over 2 h in Mg(2+)-free Ringer solution. Elevating extracellular [Mg2+] to 40 mM for 5 min caused a small rise (0.13 mM) in [Mg2+]i. There was no detectable rise in [Mg2+]i after 5 min in Na(+)-free Ringer solution. These results suggest that the membrane is relatively impermeable to Mg2+ and that there was no detectable Na(+)-Mg2+ exchange over 5 min. When muscle fibres were fatigued by repeated tetani continued until force declined to about 40% of control, [Mg2+]i showed characteristic changes. During the early period of fatigue when force first showed a small decline and then became almost stable, [Mg2+]i was unchanged; during the final period of fatigue when force declined more rapidly, [Mg2+]i increased by 0.8 mM. Recovery of [Mg2+]i took about 30 min. Recovery of force was complex: tetanic force first declined (post-contractile depression) and then slowly recovered to control. Since the minimum force occurred at about the time when [Mg2+]i had recovered, it seems unlikely that post-contractile depression is caused by elevated [Mg2+]i. Rigor, produced by inhibiting oxidative phosphorylation and glycolysis, was associated with a larger increase (1.6 mM) in [Mg2+]i than fatigue. The rise in [Mg2+]i during fatigue and metabolic blockade could be explained as release of Mg2+ normally bound to ATP. A model of the metabolic changes and the resulting increase in [Mg2+]i explains our results reasonably well.
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PMID:Myoplasmic Mg2+ concentration in Xenopus muscle fibres at rest, during fatigue and during metabolic blockade. 141 55

In the last two decades, opioid analgesics have assumed an important place in general anesthetic practice in the United States. Part of the reason for this has been the introduction of the potent new agonists fentanyl, sufentanil, and alfentanil. Because of problems with morphine-oxygen anesthesia (incomplete amnesia, occasional histamine-related reaction, marked increases in intra- and postoperative respiratory depression), a suitable alternative was sought but not found among existing opioids. A breakthrough came in 1960, when fentanyl was synthesized, laying the foundation for a better understanding of the structure-activity relationships of narcotic analgesics and stimulating interest in developing compounds with even greater potency and safety margins. Investigators interested in opioid anesthesia began to study fentanyl in animals and then in humans. Fentanyl (50-100 micrograms/kg) with oxygen (100%) was evaluated as an anesthetic in patients undergoing mitral valve and coronary artery surgery. Changes in cardiovascular dynamics with induction doses ranging from 8 to 30 micrograms/kg consisted of small decreases in heart rate and arterial blood pressure. All other cardiovascular variables studied, including cardiac output, remained unchanged, even with additional doses up to 100 micrograms/kg. It was determined that fentanyl had use as a narcotic anesthetic, despite its potential for cardiovascular depression and stimulation, respiratory depression, muscle rigidity, and, occasionally, incomplete anesthesia. Since the introduction of fentanyl, two other potent synthetic opioids have been introduced into clinical practice--sufentanil and alfentanil.
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PMID:The history and development of the fentanyl series. 151 29

In addition to producing antinociception and mild sedation, opiates diminish spontaneous movement and produce muscle rigidity. Examination of the relationship between different opiate effects may lead to a better understanding of the mechanism and sites of action of opiate anesthesia. Previous studies have compared the dose-effect relationships for morphine and fentanyl between antinociception and loss of righting reflex. However, neither muscle rigidity nor lack of spontaneous movement (as measured by catalepsy) has been fully examined or directly compared with either antinociception or loss of righting reflex. This study, therefore, compared five clinically relevant opiate endpoints (antinociception, muscle rigidity, catalepsy, loss of righting reflex, and respiratory depression) using the mu-selective agonist alfentanil in the spontaneously ventilating rat. Rats were randomized to receive alfentanil (0-500 micrograms/kg) subcutaneously. For muscle rigidity, 59 rats had electromyographic activity measured with percutaneous hindlimb electrodes. After alfentanil injection, electromyographic data were recorded for 60 min. For antinociception and catalepsy, 49 rats were studied for 120 min after alfentanil. Catalepsy was measured from the time the rat's forelimbs were placed on a 10-cm-high bar until either limb was removed. Antinociception was studied by measuring tail-flick response to hot (55 degrees C) water. For righting reflex, 40 rats were studied for 120 min. Alfentanil-induced respiratory depression was assessed in 40 rats with indwelling tail arterial catheters. Alfentanil was administered after baseline arterial blood gas measurements, and then additional samples were obtained for 45 min. For each effect, data were converted into quantal responses and were then transformed to probit-log dose-response curves for analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elucidation of dose-effect relationships for different opiate effects using alfentanil in the spontaneously ventilating rat. 160 89

27 gifted students in junior high and high school from north central Kansas school districts were administered the Children's Depression Inventory, the Beck Depression Scale, Test Anxiety Scale, General Anxiety Scale, and Breskin's Rigidity Scale. Sex, age, and grade were not considered, as the sample was small. The gifted students' mean scores for depression were below the cut-off score while their test anxiety, general anxiety, and rigidity scores were at moderate levels. Pearson correlations were significant for Beck Depression with the Children's Depression (r = .82) and General Anxiety Scales (r = .60). Scores on the General Anxiety Scale correlated significantly with those on the Children's Depression Inventory (r = .69) and the Test Anxiety Scale (r = .55). Rigidity scores were not correlated significantly with any other measure and scores on the depression scales did not correlate significantly with those on the Test Anxiety Scale.
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PMID:Depression, general anxiety, test anxiety, and rigidity of gifted junior high and high school children. 179 79

Piglets less than 8 wk of age that are known by genotype to be malignant hyperthermia-susceptible (MHS) do not usually develop characteristic hyperthermia and limb muscle rigidity in response to a brief halothane exposure (5 min of 3%). To determine whether a malignant hyperthermia (MH) episode could nevertheless be provoked by a more rigorous challenge, both genetically MHS (Pietrain) and normal (Yorkshire) 5-wk-old piglets were exposed to a combined halothane-succinylcholine challenge. Only two of eight MHS piglets developed limb rigidity; however, all MHS piglets (and no normal piglets) developed clinical signs of MH episode initiation during the 30-min challenge. Temperatures rose from 37.4 to 38.6 degrees C in MHS piglets while falling slightly in normal piglets. In MHS piglets, venous pH fell from 7.46 +/- 0.02 to 6.88 +/- 0.07, PVCO2 rose from 36 +/- 2 to 126 +/- 17 mmHg, and plasma concentration of K+ rose from 4.0 +/- 0.1 to 7.1 +/- 0.6 mM, whereas all values remained stable in normal piglets. Muscles removed from the same piglets before the halothane-succinylcholine challenge were exposed to halothane in vitro. The muscles from genetically MHS piglets responded to halothane with characteristic depression of tetanic tension and prolonged tetanus relaxation time but did not develop halothane-induced contractures. We conclude that, in the absence of either halothane-induced limb rigidity or in vitro contractures, these young animals were still susceptible to potentially fatal MH episodes on exposure to appropriate triggering agents. The MH defect is apparently partially masked in piglets and expressed fully only in older pigs.
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PMID:Halothane sensitivity of young pigs in vivo and in vitro. 237 22

Alfentanil mask anaesthesia was performed in 63 patients undergoing termination of pregnancy or curettage. Three different types of premedication were used: a) pethidine, promethazine, and atropine; b) diazepam and atropine; c) atropine. The patients were ventilated either with nitrous oxide and oxygen or with halothane and oxygen. Halothane reduced the frequency of muscular rigidity (32%; N2O 75%), postoperative sickness, and vomiting (23%; N2O 50%). On the other hand, patients regained consciousness earlier if nitrous oxide was used. Premedication a) also reduced the frequency of nausea and emesis (21%; other premedications 63%).-Alfentanil intubation anaesthesia was performed in 52 patients undergoing laparoscopy. Premedication and inhalation anaesthetic varied as described above in the group with mask anaesthesia. Muscular rigidity did not occur, and nausea/emesis were rare events (8%). Halothane prolonged the recovery phase of consciousness and respiration. Premedication a) also resulted in respiratory depression.
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PMID:[Influence of various premedication agents, inhalation anesthetics and adjuvants on anesthesia with an opioid, alfentanyl]. 286 27

Systemic pretreatment with ketanserin, a relatively specific type-2 serotonin receptor antagonist, significantly attenuated the muscle rigidity produced in rats by the potent short-acting opiate agonist alfentanil. Following placement of subcutaneous electrodes in each animal's left gastrocnemius muscle, rigidity was assessed by analyzing root-mean-square electromyographic activity. Intraperitoneal ketanserin administration at doses of 0.63 and 2.5 mg/kg prevented the alfentanil-induced increase in electromyographic activity compared with animals pretreated with saline. Chlordiazepoxide at doses up to 10 mg/kg failed to significantly influence the rigidity produced by alfentanil. Despite the absence of rigidity, animals that received ketanserin (greater than 0.31 mg/kg i.p.) followed by alfentanil were motionless, flaccid, and less responsive to external stimuli than were animals receiving alfentanil alone. Rats that received ketanserin and alfentanil exhibited less rearing and exploratory behavior at the end of the 60-min recording period than did animals that received ketanserin alone. These results, in combination with previous work, suggest that muscle rigidity, a clinically relevant side-effect of parenteral narcotic administration, may be partly mediated via serotonergic pathways. Pretreatment with type-2 serotonin antagonists may be clinically useful in attenuating opiate-induced rigidity, although further studies will be necessary to assess the interaction of possibly enhanced CNS, cardiovascular, and respiratory depression.
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PMID:Ketanserin pretreatment reverses alfentanil-induced muscle rigidity. 311 50

The use of a computer-assisted infusion of alfentanil, combined with 66% nitrous oxide in oxygen, for induction and maintenance of anaesthesia was evaluated in 18 elderly patients. The target alfentanil concentration for induction was varied between 300 and 475 ng/ml, to be achieved in 2 minutes. During maintenance, the alfentanil concentration was increased or decreased according to each patient's responses. Arterial blood samples were taken for measurement of alfentanil concentration. There were high incidences of muscle rigidity, bradycardia and hypotension during induction. Hypotension was dose- and concentration-dependent. Signs of light anaesthesia during maintenance were controlled rapidly by increasing the target plasma concentration. Nine patients required naloxone at the end of surgery. Ventilatory depression recurred in three of these. The use of published alfentanil pharmacokinetic data from elderly patients to predict plasma concentrations during prolonged infusion resulted in significant prediction errors, notably in the higher concentration range.
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PMID:Alfentanil infusion in the elderly. Prolonged computer-assisted infusion of alfentanil in the elderly surgical patient. 314 92

Reduction in the anesthetic requirement of halothane by narcotics has been studied extensively in humans and animals. Problems of respiratory depression, cardiovascular depression, muscle rigidity, and abuse potential make narcotics less than ideal as supplements to general anesthesia with inhalational agents. Spiradoline, a clinical candidate, is a highly potent and selective kappa-agonist. As such it was considered important to study the effects of spiradoline on the minimum anesthetic concentration (MAC) of halothane required to block responses to noxious stimulation. The results of these experiments in rats showed a dose and plasma concentration-dependent reduction in halothane MAC over a wide range of subcutaneous doses of spiradoline (0.03 to 300 mg/kg). A maximum MAC reduction of 70% was obtained. Plasma levels of spiradoline (6 to 1800 ng/ml) were linearly related to dose. Measurement of blood pressure, heart rate, and PCO2 determined over the course of each experiment showed minor variations which would be acceptable if observed in a clinical setting. It is concluded that spiradoline has promise as an anesthetic supplement.
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PMID:Enhancement of anesthetic effect of halothane by spiradoline, a selective kappa-agonist. 341 91


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