Thematische Bibliographien / Neuromuscular transmission / Zeitschriftenartikel

Zeitschriftenartikel zum Thema „Neuromuscular transmission“

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Autor: Grafiati
Veröffentlicht am 4. Juni 2021
Zuletzt aktualisiert am 2. März 2023

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1

MacLean, Ian C. „Neuromuscular Transmission“. Physical Medicine and Rehabilitation Clinics of North America 1, Nr. 1 (November 1990): 43–52. http://dx.doi.org/10.1016/s1047-9651(18)30745-9.

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2

Parker, C. „Neuromuscular transmission“. Postgraduate Medical Journal 74, Nr. 870 (01.04.1998): 255. http://dx.doi.org/10.1136/pgmj.74.870.255-a.

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3

Torda, T. A. „Monitoring Neuromuscular Transmission“. Anaesthesia and Intensive Care 30, Nr. 2 (April 2002): 123–33. http://dx.doi.org/10.1177/0310057x0203000202.

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Persistent neuromuscular blockade is not uncommon in the recovery room and contributes to postoperative morbidity and possibly mortality. The use of neuromuscular monitoring and intermediate rather than long-acting neuromuscular blocking drugs have been shown to reduce its incidence. Clinically available methods of detecting and quantitating neuromuscular blockade are reviewed. The writer concludes that such monitoring should be routine when neuromuscular blocking drugs are used.
4

Beemer, G. H., und P. H. Goonetilleke. „Monitoring neuromuscular transmission“. Current Anaesthesia & Critical Care 7, Nr. 2 (April 1996): 101–6. http://dx.doi.org/10.1016/s0953-7112(96)80065-2.

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5

Pascuzzi, Robert. „Disorders of Neuromuscular Transmission“. Seminars in Neurology 24, Nr. 02 (15.07.2004): 137. http://dx.doi.org/10.1055/s-2004-830898.

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6

Weissman, J. D. „Electromyography: Neuromuscular Transmission Studies“. Neurology 39, Nr. 8 (01.08.1989): 1141. http://dx.doi.org/10.1212/wnl.39.8.1141-b.

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7

Meistelman, Claude. „Monitoring of neuromuscular transmission“. Current Opinion in Anaesthesiology 6, Nr. 4 (August 1993): 720–25. http://dx.doi.org/10.1097/00001503-199308000-00024.

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8

Wareham, Anthony C. „Neuromuscular function and transmission“. Anaesthesia & Intensive Care Medicine 6, Nr. 6 (Juni 2005): 203–5. http://dx.doi.org/10.1383/anes.6.6.203.65787.

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9

Krendel, David. „Hypermagnesemia and Neuromuscular Transmission“. Seminars in Neurology 10, Nr. 01 (März 1990): 42–45. http://dx.doi.org/10.1055/s-2008-1041252.

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10

WINDSOR, J. P. W., P. S. SEBEL und P. J. FLYNN. „The neuromuscular transmission monitor“. Anaesthesia 40, Nr. 2 (22.02.2007): 146–51. http://dx.doi.org/10.1111/j.1365-2044.1985.tb10705.x.

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11

Henning, R. H. „Purinoceptors in neuromuscular transmission“. Pharmacology & Therapeutics 74, Nr. 1 (Januar 1997): 115–28. http://dx.doi.org/10.1016/s0163-7258(97)00015-6.

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12

Fletcher, Allan. „Neuromuscular function and transmission“. Anaesthesia & Intensive Care Medicine 9, Nr. 6 (Juni 2008): 256–58. http://dx.doi.org/10.1016/j.mpaic.2008.04.005.

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13

Fletcher, Allan. „Neuromuscular function and transmission“. Anaesthesia & Intensive Care Medicine 12, Nr. 6 (Juni 2011): 245–48. http://dx.doi.org/10.1016/j.mpaic.2011.03.012.

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14

MAELICKE, ALFRED, T. COBAN, A. SCHRATTENHOLZ, B. SCHRÖDER, S. REINHARDT-MAELICKE, A. STORCH, J. GODOVAC-ZIMMERMANN, CHRISTOPH METHFESSEL, E. F. R. PEREIRA und EDSON X. ALBUQUERQUE. „Physostigmine and Neuromuscular Transmission“. Annals of the New York Academy of Sciences 681, Nr. 1 Myasthenia Gr (Juni 1993): 140–54. http://dx.doi.org/10.1111/j.1749-6632.1993.tb22880.x.

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15

Martin, A. Robert. „Principles of Neuromuscular Transmission“. Hospital Practice 27, Nr. 8 (15.08.1992): 147–58. http://dx.doi.org/10.1080/21548331.1992.11705473.

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16

Torda, T. A. „Book Review: Neuromuscular Transmission.“ Anaesthesia and Intensive Care 29, Nr. 4 (August 2001): 439. http://dx.doi.org/10.1177/0310057x0102900420.

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17

Hirst, G. D. S., S. De Gleria und D. F. van Helden. „Neuromuscular transmission in arterioles“. Experientia 41, Nr. 7 (Juli 1985): 874–79. http://dx.doi.org/10.1007/bf01970004.

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18

Sherman, Howard B. „Electromyography: Neuromuscular transmission studies“. Surgical Neurology 31, Nr. 2 (Februar 1989): 163. http://dx.doi.org/10.1016/0090-3019(89)90336-4.

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19

Schelhaas, H. Jurgen, Bart P. C. Van De Warrenburg, Hubertus P. H. Kremer und Machiel J. Zwarts. „Neuromuscular transmission in SCA6“. Annals of Neurology 55, Nr. 3 (2004): 451–52. http://dx.doi.org/10.1002/ana.20015.

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20

Pascuzzi, Robert. „Introduction to the Neuromuscular Junction and Neuromuscular Transmission“. Seminars in Neurology 10, Nr. 01 (März 1990): 1–5. http://dx.doi.org/10.1055/s-2008-1041246.

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21

UEDA, NAOYUKI. „Clinical Assessment of Neuromuscular Transmission.“ JOURNAL OF JAPAN SOCIETY FOR CLINICAL ANESTHESIA 15, Nr. 3 (1995): 197–201. http://dx.doi.org/10.2199/jjsca.15.197.

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22

Vincent, Angela. „Autoantibodies in neuromuscular transmission disorders“. Annals of Indian Academy of Neurology 11, Nr. 3 (2008): 140. http://dx.doi.org/10.4103/0972-2327.42932.

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23

Fagerlund, M. J., und L. I. Eriksson. „Current concepts in neuromuscular transmission“. British Journal of Anaesthesia 103, Nr. 1 (Juli 2009): 108–14. http://dx.doi.org/10.1093/bja/aep150.

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24

Marshall, Ian G. „Prejunctional aspects of neuromuscular transmission“. Current Opinion in Anaesthesiology 4, Nr. 4 (August 1991): 577–82. http://dx.doi.org/10.1097/00001503-199108000-00021.

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25

Martyn, J. A. J., M. Jonsson Fagerlund und L. I. Eriksson. „Basic principles of neuromuscular transmission“. Anaesthesia 64 (März 2009): 1–9. http://dx.doi.org/10.1111/j.1365-2044.2008.05865.x.

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26

Engel, Andrew. „Congenital Disorders of Neuromuscular Transmission“. Seminars in Neurology 10, Nr. 01 (März 1990): 12–26. http://dx.doi.org/10.1055/s-2008-1041248.

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27

Lange, D. J. „Electrophysiologic testing of neuromuscular transmission“. Neurology 48, Supplement 5 (01.04.1997): 18S—22S. http://dx.doi.org/10.1212/wnl.48.suppl_5.18s.

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28

Sieb, J. P. „Fluoroquinolone antibiotics block neuromuscular transmission“. Neurology 50, Nr. 3 (01.03.1998): 804–7. http://dx.doi.org/10.1212/wnl.50.3.804.

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29

JONES, R. M. „Neuromuscular transmission and its blockade.“ Anaesthesia 40, Nr. 10 (Oktober 1985): 964–76. http://dx.doi.org/10.1111/j.1365-2044.1985.tb10551.x.

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30

Schulze, J., M. Toepfer, K.-C. Schroff, S. Aschhoff, J. Remien, W. Müller-Felber und S. Endres. „Clindamycin and nicotinic neuromuscular transmission“. Lancet 354, Nr. 9192 (November 1999): 1792–93. http://dx.doi.org/10.1016/s0140-6736(99)02881-0.

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31

Enomoto, Koh-Ichi, und Charles Edwards. „Thiamine blockade of neuromuscular transmission“. Brain Research 358, Nr. 1-2 (Dezember 1985): 316–23. http://dx.doi.org/10.1016/0006-8993(85)90976-x.

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32

Kaminski, Henry J., und Robert L. Ruff. „Congenital Disorders of Neuromuscular Transmission“. Hospital Practice 27, Nr. 9 (15.09.1992): 73–85. http://dx.doi.org/10.1080/21548331.1992.11705484.

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33

Mahadeva, Branavan, Lawrence Phillips und Vern Juel. „Autoimmune Disorders of Neuromuscular Transmission“. Seminars in Neurology 28, Nr. 2 (April 2008): 212–27. http://dx.doi.org/10.1055/s-2008-1062260.

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34

Saldien, V., und K. M. Vermeyen. „Neuromuscular transmission monitoring in children“. Pediatric Anesthesia 14, Nr. 4 (April 2004): 289–92. http://dx.doi.org/10.1046/j.1460-9592.2003.01152.x.

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35

Sieb, Jo¨rn P., und Andrew G. Engel. „Ephedrine: effects on neuromuscular transmission“. Brain Research 623, Nr. 1 (September 1993): 167–71. http://dx.doi.org/10.1016/0006-8993(93)90025-i.

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36

Sanders, D. B. „WS6-1 Neuromuscular transmission — overview“. Clinical Neurophysiology 121 (Oktober 2010): S79. http://dx.doi.org/10.1016/s1388-2457(10)60335-5.

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37

Kurenkov, D. A., S. Yu Chizhevskaya und E. M. Nikolaenko. „Objective monitoring of neuromuscular transmission in laparoscopic surgery“. Kazan medical journal 94, Nr. 6 (15.12.2013): 866–69. http://dx.doi.org/10.17816/kmj1808.

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Aim. To assess the importance of quantitative neuromuscular transmission monitoring in laparoscopic surgery. Methods. 30 patients [11 (37.7%) males, 19 (63.3%) females, mean age 52.3±7.18 years] who underwent laparoscopic surgery and general anesthesia associated with skeletal muscles relaxation, were examined. The degree of neuromuscular transmission recovery and time to trachea extubation performed by an anesthetist after the end of surgery (like laparoscopic cholecystectomy, appendectomy) and general anesthesia associated with skeletal muscles relaxation were assessed using quantitative monitoring of neuromuscular transmission and «blind» control. Results. In 21 patients no drugs were used to reverse the skeletal muscles relaxation. Trachea extubation in this group was performed 10.5 minutes after the end of surgery in average at the neuromuscular transmission Train of Four (TOF) level of 43-81% for 15 patients and at the TOF level over 90% in 6 patients. In 9 patients, sugammadex (2 mg/kg) was used for neuromuscular transmission reversal, the average level of neuromuscular blockade (TOF) in those patients was 41±6.5%. TOF average recovery time up to 90% was 1 minute 48 seconds. Trachea extubation was performed no later than 4 minutes after the sugammadex administration. Conclusion. The subjective assessment of neuromuscular transmission recovery, based on the assessment of clinical signs, is not able to completely exclude the residual muscle relaxation. Objective monitoring of neuromuscular transmission is required to determine the time of intubation, administration of maintenance doses of muscle relaxants, and for assessment of efficacy of reversal and possibility for trachea extubation.
38

Fogarty, Matthew J., Maria A. Gonzalez Porras, Carlos B. Mantilla und Gary C. Sieck. „Diaphragm neuromuscular transmission failure in aged rats“. Journal of Neurophysiology 122, Nr. 1 (01.07.2019): 93–104. http://dx.doi.org/10.1152/jn.00061.2019.

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In aging Fischer 344 rats, phrenic motor neuron loss, neuromuscular junction abnormalities, and diaphragm muscle (DIAm) sarcopenia are present by 24 mo of age, with larger fast-twitch fatigue-intermediate (type FInt) and fast-twitch fatigable (type FF) motor units particularly vulnerable. We hypothesize that in old rats, DIAm neuromuscular transmission deficits are specific to type FInt and/or FF units. In phrenic nerve/DIAm preparations from rats at 6 and 24 mo of age, the phrenic nerve was supramaximally stimulated at 10, 40, or 75 Hz. Every 15 s, the DIAm was directly stimulated, and the difference in forces evoked by nerve and muscle stimulation was used to estimate neuromuscular transmission failure. Neuromuscular transmission failure in the DIAm was observed at each stimulation frequency. In the initial stimulus trains, the forces evoked by phrenic nerve stimulation at 40 and 75 Hz were significantly less than those evoked by direct muscle stimulation, and this difference was markedly greater in 24-mo-old rats. During repetitive nerve stimulation, neuromuscular transmission failure at 40 and 75 Hz worsened to a greater extent in 24-mo-old rats compared with younger animals. Because type IIx and/or IIb DIAm fibers (type FInt and/or FF motor units) display greater susceptibility to neuromuscular transmission failure at higher frequencies of stimulation, these data suggest that the age-related loss of larger phrenic motor neurons impacts nerve conduction to muscle at higher frequencies and may contribute to DIAm sarcopenia in old rats. NEW & NOTEWORTHY Diaphragm muscle (DIAm) sarcopenia, phrenic motor neuron loss, and perturbations of neuromuscular junctions (NMJs) are well described in aged rodents and selectively affect FInt and FF motor units. Less attention has been paid to the motor unit-specific aspects of nerve-muscle conduction. In old rats, increased neuromuscular transmission failure occurred at stimulation frequencies where FInt and FF motor units exhibit conduction failures, along with decreased apposition of pre- and postsynaptic domains of DIAm NMJs of these units.
39

Krivoi, Igor, und Alexey Petrov. „Cholesterol and the Safety Factor for Neuromuscular Transmission“. International Journal of Molecular Sciences 20, Nr. 5 (28.02.2019): 1046. http://dx.doi.org/10.3390/ijms20051046.

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A present review is devoted to the analysis of literature data and results of own research. Skeletal muscle neuromuscular junction is specialized to trigger the striated muscle fiber contraction in response to motor neuron activity. The safety factor at the neuromuscular junction strongly depends on a variety of pre- and postsynaptic factors. The review focuses on the crucial role of membrane cholesterol to maintain a high efficiency of neuromuscular transmission. Cholesterol metabolism in the neuromuscular junction, its role in the synaptic vesicle cycle and neurotransmitter release, endplate electrogenesis, as well as contribution of cholesterol to the synaptogenesis, synaptic integrity, and motor disorders are discussed.
40

Ermilov, Leonid G., Juan N. Pulido, Fawn W. Atchison, Wen-Zhi Zhan, Mark H. Ereth, Gary C. Sieck und Carlos B. Mantilla. „Impairment of diaphragm muscle force and neuromuscular transmission after normothermic cardiopulmonary bypass: effect of low-dose inhaled CO“. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, Nr. 3 (März 2010): R784—R789. http://dx.doi.org/10.1152/ajpregu.00737.2009.

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Cardiopulmonary bypass (CPB) is associated with significant postoperative morbidity, but its effects on the neuromuscular system are unclear. Recent studies indicate that even relatively short periods of mechanical ventilation result in significant neuromuscular effects. Carbon monoxide (CO) has gained recent attention as therapy to reduce the deleterious effects of CPB. We hypothesized that 1) CPB results in impaired neuromuscular transmission and reduced diaphragm force generation; and 2) CO treatment during CPB will mitigate these effects. In adult male Sprague-Dawley rats, diaphragm muscle-specific force and neuromuscular transmission properties were measured 90 min after weaning from normothermic CPB (1 h). During CPB, either low-dose inhaled CO (250 ppm) or air was administered. The short period of mechanical ventilation used in the present study (∼3 h) did not adversely affect diaphragm muscle contractile properties or neuromuscular transmission. CPB elicited a significant decrease in isometric diaphragm muscle-specific force compared with time-matched, mechanically ventilated rats (∼25% decline in both twitch and tetanic force). Diaphragm muscle fatigability to 40-Hz repetitive stimulation did not change significantly. Neuromuscular transmission failure during repetitive activation was 60 ± 2% in CPB animals compared with 76 ± 4% in mechanically ventilated rats ( P < 0.05). CO treatment during CPB abrogated the neuromuscular effects of CPB, such that diaphragm isometric twitch force and neuromuscular transmission were no longer significantly different from mechanically ventilated rats. Thus, CPB has important detrimental effects on diaphragm muscle contractility and neuromuscular transmission that are largely mitigated by CO treatment. Further studies are needed to ascertain the underlying mechanisms of CPB-induced neuromuscular dysfunction and to establish the potential role of CO therapy.
41

Grishin, S. N., A. E. Khairullin, A. Y. Teplov und M. A. Mukhamedyarov. „Neuromuscular Transmission in a Barium Environment“. Biophysics 67, Nr. 3 (Juni 2022): 457–60. http://dx.doi.org/10.1134/s000635092203006x.

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42

Stanec, A., und T. Baker. „Physiology and pharmacology of neuromuscular transmission“. Current Opinion in Anaesthesiology 2, Nr. 4 (August 1989): 470–73. http://dx.doi.org/10.1097/00001503-198908000-00018.

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43

Engbæk, J. „Measurement and monitoring of neuromuscular transmission“. Current Opinion in Anaesthesiology 3, Nr. 4 (August 1990): 625–29. http://dx.doi.org/10.1097/00001503-199003040-00022.

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44

Engbæk, J. „Measurement and monitoring of neuromuscular transmission“. Current Opinion in Anaesthesiology 3, Nr. 4 (August 1990): 625–29. http://dx.doi.org/10.1097/00001503-199008000-00022.

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45

Kopman, David, und Cynthia A. Lien. „Physiology and Pharmacology of Neuromuscular Transmission“. ASA Refresher Courses in Anesthesiology 37, Nr. 1 (Juli 2009): 107–17. http://dx.doi.org/10.1097/asa.0b013e3181a6898d.

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46

Ertas, Mustafa, und M. Baris Baslo. „Abnormal Neuromuscular Transmission in Cluster Headache“. Headache: The Journal of Head and Face Pain 43, Nr. 6 (Juni 2003): 616–20. http://dx.doi.org/10.1046/j.1526-4610.2003.03103.x.

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47

LOAN, P. B., L. D. PAXTON, R. K. MIRAKHUR, F. M. CONNOLLY und E. P. McCOY. „The TOF-Guard neuromuscular transmission monitor.“ Anaesthesia 50, Nr. 8 (August 1995): 699–702. http://dx.doi.org/10.1111/j.1365-2044.1995.tb06097.x.

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48

Ross, R. „Neuromuscular transmission in the 17th century“. Journal of Neurology, Neurosurgery & Psychiatry 51, Nr. 10 (01.10.1988): 1268. http://dx.doi.org/10.1136/jnnp.51.10.1268.

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49

Klose, M. K. „Stress-Induced Thermoprotection of Neuromuscular Transmission“. Integrative and Comparative Biology 44, Nr. 1 (01.02.2004): 14–20. http://dx.doi.org/10.1093/icb/44.1.14.

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50

Massey, Janice. „Electromyography in Disorders of Neuromuscular Transmission“. Seminars in Neurology 10, Nr. 01 (März 1990): 6–11. http://dx.doi.org/10.1055/s-2008-1041247.

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