Relevant bibliographies by topics / Tubocurarina

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  1. Journal articles
  2. Dissertations / Theses
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  4. Book chapters

Academic literature on the topic 'Tubocurarina'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Tubocurarina"

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Taveira, Eleusa F., José A. Rizzo, Joaquim Τ. Sousa, Lelia S. Fernandes, Wagner F. Torres, Maria C. M. Pereira, Ricardo F. Ansorval, and Antonio J. Lapa. "Atividade farmacológica dos extratos da casca do caule do tropeiro. O Connarus fulvus, Planch." Acta Amazonica 18, suppl 1-2 (1988): 231–40. http://dx.doi.org/10.1590/1809-43921988185240.

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O Cannarus fulvus Planch é utilizado em Goiás por ser "bom para o coração". Este trabalho estudou, a atividade farmacológica do extrato bruto etanólico (EE) do pó da casca do caule e da fração hidrossolúvel (FH) obtida após partição benzina/água. O EE e a FH produziram em ratos e camundongos diminuição da motilidade, sonolência sem hipnose, dificuldade respiratória, analgésia e arrastamento do trem posterior; estes proporcionais às doses. As DL50 em camundongos foram 210+/-22 e 310+/-52mg/kg, i.p. para o EE e FH respectivamente. A FH prolongou o sono barbitúrico, o tempo de reação ao calor na placa, quente e antagonizou (80%) as ações convulsivantes do pentilenotetrazol, mas não as da estricnina. Protegeu (100%) camundongos contra a ação letal do pancurônio e potencializou a ação da succinilcolina. Em preparações isolada, a FH potencializou (20%) a contração do diafragma em resposta ao estímulo elétrico do nervo frênico de ratos e reverteu o bloqueio neuromuscular produzido pela d-tubocurarina, em átrios de ratos e cobaias a freqüência e a força de contração não foram alteradas. As injeções do EE e FH em ratos anestesiados produziram hipotensão (5 a 100mg/kg); doses maiores foram letais. Os dados obtidos não confirmaram ação cardiativa direta. A planta apresentou ações depressões do S.N.C., analgésica, anticonvulsivante e descurarizante.
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Kim, C., M. Hirose, and J. A. J. Martyn. "d-Tubocurarine Accentuates the Burn-induced Upregulation of Nicotinic Acetylcholine Receptors at the Muscle Membrane." Anesthesiology 83, no. 2 (August 1, 1995): 309–15. http://dx.doi.org/10.1097/00000542-199508000-00011.

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Background Increases in acetylcholine receptors (AChRs) at the muscle membrane, induced by burn injury, have been associated with a hyperkalemic response to succinylcholine and resistance to d-tubocurarine-like drugs. Muscle relaxants often are administered to burn-injured patients in the intensive care unit to facilitate mechanical ventilation. This study in rats tested whether continuous administration of d-tubocurarine in subparalytic doses exaggerates the upregulation of AChRs induced by burn trauma. Subparalytic doses were used to avoid the confounding effects of immobilization. Methods Three days after an approximate 50% body surface area burn or sham injury, the animals received an infusion of 3.03 +/- 0.05 micrograms/h of d-tubocurarine or equal volume of saline directly to the left gastrocnemius muscle via catheter connected to a subcutaneously implanted osmotic pump. After 7 days of d-tubocurarine or saline infusion, the AChRs were quantitated using 125I-alpha-bungarotoxin. The AChRs on the d-tubocurarine or saline-infused left gastrocnemius were compared to the contralateral gastrocnemius in the same group. The right or left gastrocnemius AChRs were compared to the ipsilateral muscles between groups. These intra- and intergroup comparisons allowed the delineation of the effects of catheter irritation, burns, or d-tubocurarine on AChRs. Results Daily examination of the withdrawal response to toe-pinch revealed no evidence of paralysis. Weight loss in the burn-injury animals receiving d-tubocurarine or saline was similar, confirming that the infusion of d-tubocurarine did not impair the mobility of the animals to move and feed. The plasma d-tubocurarine concentration after 7 days of infusion was 26.0 +/- 12 ng/ml (mean +/- SE). Regardless of burn or sham injury or of d-tubocurarine or saline infusion, the concentration of AChRs on the left was consistently greater than in the contralateral right gastrocnemius muscles within the same group, indicating that manipulation of the area alone can result in upregulation of AChRs. The AChRs in the right gastrocnemius of burn-injured animals were greater than those in the same muscle of sham-injured animals, regardless of saline (7.24 +/- 0.9 vs. 5.7 +/- 0.5 fmoles/mg protein, P = 0.06) or d-tubocurarine (7.3 +/- 0.4 vs. 5.7 +/- 0.5, P < 0.05) infusion to the burn-injury groups. AChRs in the left gastrocnemius of burn-injury animals receiving d-tubocurarine were significantly greater than those in burn- or sham-injury animals receiving saline (13.9 +/- 1.1 vs. 9.8 +/- 1.2 and 7.1 +/- 0.5 fmoles/mg protein, respectively, P < 0.05). Conclusions Burn-induced upregulation of AChRs is accentuated by infusion of subparalytic doses of d-tubocurarine. Concomitant administration of d-tubocurarine to burn-injured patients may result in further exaggeration of the aberrant responses to neuromuscular relaxants.
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Nguyen-Huu, Tu, Alexandre Dobbertin, Julien Barbier, Jasmina Minic, Eric Krejci, Philippe Duvaldestin, and Jordi Molgó. "Cholinesterases and the Resistance of the Mouse Diaphragm to the Effect of Tubocurarine." Anesthesiology 103, no. 4 (October 1, 2005): 788–95. http://dx.doi.org/10.1097/00000542-200510000-00017.

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Background The diaphragm is resistant to competitive neuromuscular blocking agents. Because of the competitive mechanism of action of tubocurarine, the rate of hydrolysis of acetylcholine at the neuromuscular junction may modulate its neuromuscular blocking effect. The authors compared the neuromuscular blocking effect of tubocurarine on isolated diaphragm and extensor digitorum longus (EDL) muscles and quantified the acetylcholinesterase activity in hetero-oligomers. Methods Adult Swiss-Webster and collagen Q-deficient (ColQ) mice were used. The blocking effect of tubocurarine on nerve-evoked muscle twitches was determined in isolated diaphragm and EDL muscles, after inhibition of acetylcholinesterase by fasciculin-1, butyrylcholinesterase by tetraisopropylpyro-phosphoramide, or both acetylcholinesterase and butyrylcholinesterase by neostigmine, and in acetylcholinesterase-deficient ColQ muscles. The different acetylcholinesterase oligomers extracted from diaphragm and EDL muscles were quantified in sucrose gradient. Results The EC50 for tubocurarine to decrease the nerve-evoked twitch response was four times higher in the diaphragm than in the EDL. The activity of the different acetylcholinesterase oligomers was lower in the diaphragm as compared with the EDL. Inhibition of acetylcholinesterase by antagonists resulted in an increased dose of tubocurarine but an unchanged resistance ratio between the diaphragm and the EDL. A similar diaphragmatic resistance was found in ColQ muscles. Conclusion The current study indicates that, despite differences in acetylcholinesterase activity between the diaphragm and EDL, the diaphragmatic resistance to tubocurarine cannot be explained by the different rate of acetylcholine hydrolysis in the synaptic cleft.
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Coleman, William F. "Molecular Model of Tubocurarine." Journal of Chemical Education 83, no. 12 (December 2006): 1831. http://dx.doi.org/10.1021/ed083p1831.

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Ball, C., and R. Westhorpe. "Muscle Relaxants—d-tubocurarine." Anaesthesia and Intensive Care 33, no. 4 (August 2005): 431. http://dx.doi.org/10.1177/0310057x0503300401.

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Scott, Pr J. E., Marion Haigh, Geok-Eng Neo, and Sarah Gibson. "The effect of muscle paralysis on the radial growth of collagen fibrils in developing tendon." Clinical Science 72, no. 3 (March 1, 1987): 359–63. http://dx.doi.org/10.1042/cs0720359.

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1. Voluntary muscle activity in chick embryos was paralysed by administration in ovo of tubocurarine hydrochloride, administered in single or multiple doses, from day 9 to day 13 after fertilization. Control eggs were given saline instead of tubocurarine or were simply incubated without operative interference. Embryos were killed at 9, 13, 14, 16 and 19 days after fertilization. Flexor digitorum tendons were removed, fixed in glutaraldehyde, embedded in plastic, sectioned, and stained with phosphotungstic acid for electron microscopy. The diameters of the tendon collagen fibrils were measured, on electron micrographs, using a Magiscan Mk II programme. 2. Tendon collagen fibril expansion was not inhibited by tubocurarine treatment. It is concluded that the rapid increase of collagen fibril diameters, which coincides in the normal embryo with the first onset of use of the associated muscle, is not dependent on muscle activity. There remains a possibility that other ways of producing tension in the tendon could provide sufficient stimulus to fibril expansion.
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von der Weid, P. Y., and J. L. Beny. "Effect of Ca2+ ionophores on membrane potential of pig coronary artery endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 6 (June 1, 1992): H1823—H1831. http://dx.doi.org/10.1152/ajpheart.1992.262.6.h1823.

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Ca2+ ionophores (A23187 and ionomycin) were used to determine whether an increase in cytosolic Ca2+ plays a direct role in pig coronary endothelial cell hyperpolarization. Ionophores induced concentration-dependent hyperpolarizations that were not altered by the presence of N omega-nitro-L-argnine (L-NNA), and inhibitor of nitric oxide synthesis. d-Tubocurarine decreased by 65-89% the A23187- and substance P (SP)-generated hyperpolarization of endothelial cells. To study the role of endothelial cell hyperpolarization in the endothelium-dependent relaxation of precontracted coronary artery strips, A23187 and SP concentration-response curves were built up in the presence of d-tubocurarine and/or L-NNA. A decrease in the maximal response was observed only when both d-tubocurarine and L-NNA were present. Our direct in situ approach gives results in agreement with a gating of Ca(2+)-activated K+ channels during A23187- and SP-induced hyperpolarizations of endothelial cells. We suggest that these hyperpolarizations play a role in the endothelial cell-dependent relaxation induced by A23187 and SP in the pig coronary artery.
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Mirakhur, Rajinder K., Fiona M. Gibson, and Christopher J. Ferres. "Vecuronium and d-Tubocurarine Combination." Anesthesia & Analgesia 64, no. 7 (July 1985): 711???714. http://dx.doi.org/10.1213/00000539-198507000-00011.

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Beaufort, Ton M., Johannes H. Proost, Martin C. Houwertjes, Jan Roggeveld, and Mark J. K. H. Wierda. "The Pulmonary First-pass Uptake of Five Nondepolarizing Muscle Relaxants in the Pig." Anesthesiology 90, no. 2 (February 1, 1999): 477–83. http://dx.doi.org/10.1097/00000542-199902000-00023.

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Background It is not known whether the lungs influence the early pharmacokinetics of muscle relaxants and, if they do, whether differences in pulmonary uptake contribute to the differences in potency and/or onset time among muscle relaxants. Because the lungs are uniquely positioned, receive the entire cardiac output, have a large capillary surface area, and can temporarily store various basic drugs, the authors determined whether substantial pulmonary first-pass uptake of muscle relaxants occurs. Methods In 14 pigs, rocuronium, vecuronium, Org 9487, Org 7617, or d-tubocurarine were administered simultaneously with indocyanin green within 1 s into the right ventricle, and then arterial blood was sampled every 1.2 s (in the first min). The tibialis muscle response was registered mechanomyographically. Results The maximum block was 93% (68-100% [median and range]). Onset times ranged from 83 s (78-86 s) for rocuronium to 182 s (172-192 s) for d-tubocurarine. Fraction-versus-time outflow curves showed that the peak of muscle relaxants and indocyanin green occurred almost simultaneously. Pulmonary first-pass retention was negligible. The retention of muscle relaxants at 95% passage of indocyanin green was -9% (-31 to 18%). The difference in the mean transit time between muscle relaxant and indocyanin green was 1.0 (0.8 to 1.4), 0.2 (-0.8 to 0.3), 0.3 (0.2 to 0.4), 0.5 (0.2 to 1.3), and -2.2 s for rocuronium, vecuronium, Org 9487, Org 7617, and d-tubocurarine, respectively. Conclusions There is no substantial pulmonary first-pass uptake of rocuronium, vecuronium, Org 9487, Org 7617, or d-tubocurarine in pigs. Therefore, differences in pulmonary first-pass uptake do not contribute to the differences in potency and/or onset time among muscle relaxants.
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Boothby, K. M., and A. Roberts. "The stopping response of Xenopus laevis embryos: pharmacology and intracellular physiology of rhythmic spinal neurones and hindbrain neurones." Journal of Experimental Biology 169, no. 1 (August 1, 1992): 65–86. http://dx.doi.org/10.1242/jeb.169.1.65.

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1. Xenopus laevis embryos stop swimming in response to pressure on the cement gland. This behaviour and ‘fictive’ stopping are blocked by bicuculline (10 mumol 1(−1)), tubocurarine (110 mumol 1(−1)) and kynurenic acid (0.5 mmol 1(−1)). 2. Intracellular recordings from spinal neurones active during swimming have shown that pressure on the cement gland evokes compound, chloride-dependent inhibitory postsynaptic potentials (IPSPs). These are blocked by bicuculline, tubocurarine and kynurenic acid, but are unaffected by strychnine (2 mumol 1(−1)). 3. When the cement gland is pressed, trigeminal ganglion activity precedes both the IPSPs and the termination of ‘fictive’ swimming activity recorded in rhythmic spinal neurones. The trigeminal discharge is unaffected by the antagonists bicuculline, tubocurarine, kynurenic acid and strychnine. 4. Intracellular recordings from the hindbrain have revealed neurones that are normally silent, but rhythmically inhibited during ‘fictive’ swimming. In these neurones pressure on the cement gland evokes depolarising potentials, often with one or more spikes. 5. We propose that the stopping response depends on the excitation of pressure-sensitive trigeminal receptors which innervate the cement gland. These release an excitatory amino acid to excite brainstem GABAergic reticulospinal neurones, which inhibit spinal neurones to turn off the central pattern generator for swimming. There may also be a less direct pathway.
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Dissertations / Theses on the topic "Tubocurarina"

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Loyola, Yolanda Christina de Sousa. "Influencia dos anestesicos locais no bloqueio neuromuscular produzido por diferentes bloqueadores neuromusculares : estudo experimental." [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310900.

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Orientador: Angelica de F. de Assunção Braga
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-06T23:53:56Z (GMT). No. of bitstreams: 1 Loyola_YolandaChristinadeSousa_D.pdf: 22412843 bytes, checksum: 64766635e73a046988de0b090a234fe6 (MD5) Previous issue date: 2006
Resumo: Os anestésicos locais comumente empregados na prática clínica podem interagir com os bloqueadores neuromusculares e potencializar seus efeitos. Muitos autores estudaram esta interação mas o mecanismo envolvido na potencialização do bloqueio neuromuscular e a ação dos anestésicos locais nos sítios pré e pós juncionais não foram completamente elucidados. Neste trabalho através de experimentos específicos na junção neuromuscular foram estudados os seguintes parâmetros: o efeito dos anestésicos locais procaína e lidocaína na transmissão neuromuscular; a sua influência no bloqueio neuromuscular produzido pela d-tubocurarina e pelo rocurônio; a eficácia da neostigmina e da 4-aminopirídina na reversão do bloqueio produzido pela associação anestésicos locais - bloqueadores neuromusculares; os efeitos dos anestésicos locais nos potenciais de membrana e potenciais de placa terminal em miniatura. Avaliou-se também em preparações diafragma de rato cronicamente desnervado e biventer cervicis de pintainho os efeitos dos anestésicos locais na ação contraturante da acetilcolina. Os resultados foram expressos em médias e desvios padrão e analisados através dos testes de Wilcoxon e Mann-Witney, adotando-se um nível de significância de 5% (p < 0,05). Nas preparações nervo frênico - diafragma de rato, sob estimulação elétrica indireta, os anestésicos locais nas concentrações empregadas, não alteraram a amplitude das respostas musculares mas potencializaram os efeitos da d- tubocurarina e do rocurônio.. Este bloqueio foi parcialmente e totalmente revertido pela neostigmina e pela 4-aminopiridina, respectivamente. A procaína e a lidocaína não causaram alteração significativa nos potenciais de membrana, não demonstrando ação despolarizante na fibra muscular. A procaína causou diminuição na amplitude e na freqüência dos potenciais de placa terminal em miniatura (pptms) e a lidocaína, ao contrário, promoveu um aumento inicial na freqüência dos pptms seguida de bloqueio. Nas preparações biventer cervicis de pintainho e diafragma de rato cronicamente desnervado, a procaína e a lidocaína promoveram diminuição significativa na resposta contraturante da acetilcolina evidenciando um efeito pós-juncional. Os resultados obtidos demonstram um sinergismo entre as drogas devido principalmente a um efeito pós-juncional
Abstract: Local anesthetics commonly used in clinical practice can interact with neuromuscular blockers and potentiate their effects. Many authors studied this interaction, but the mechanism involved in the potentiation of neuromuscular blockers and the action of local anesthetics in the pre and postjunctional sites were not completely elucidated- In this study, in specific experiments in the neuromuscular junction the following parameters were studied: the effects of the local anesthetics procaine and lidocaine in the neuromuscular transmission; its influence on the neuromuscular blockade produced by d-tubocurarine and by rocuronium; the efficacy of neostigmine and of 4-aminopyhdine in the reversion of the blockade produced by the association of local anesthetics - neuromuscular blockers; the effects of local anesthetics on the membrane potentials and miniature end - plate potentials. It was also evaluated in chronically denervated rat diaphragm preparation and chick biventer cervicis preparation the effects of local anesthetics on acetylcholine contracture. The results were expressed in average and standard deviation and analyzed through the Wilcoxon and Mann-Witney tests, adopting a level of significance of 5% (p <0.05). In rat phrenic nerve diaphragm preparations under indirect electric stimulation, local anesthetics in the concentrations used did not change the amplitude of the muscle response but potentiated the effects of d-tubocurarine and of rocuronium. This blockade was partially and totally reverted by neostigmine and by 4-aminopyridine, respectively. Procaine and lidocaine caused no significant alteration in the membrane potentials, not demonstrating depolarizing action in the muscle fiber. Procaine caused a decrease in the amplitude and frequency of the miniature end - plate potentials {meps) and lidocaine, in contrast, promoted an initial increase in the frequency of meps followed by blockade. In chick biventer cervicis preparations and chronically denervated rat diaphragm, procaine and lidocaine promoted a significant decrease in the response to acetylcholine contracture evidencing a post-junctional effect. The results obtained demonstrate a synergism among the drugs mainly due to a postjunctional effect
Doutorado
Doutor em Farmacologia
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Brier, Timothy James. "The interaction of polyamine-amides with the nicotinic acetylcholine receptor of the TE671 cell lines." Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247142.

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Rametti, Larry Bertram. "On-line control of d-tubocurarine induced muscle relaxation.Volume1." Thesis, University of Cape Town, 1985. http://hdl.handle.net/11427/23351.

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Maskell, Peter D. "Pharmacological analysis of recombinant human GABA←A receptors expressed in Xenopus oocytes." Thesis, Oxford Brookes University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367392.

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CHEN, SHU-MIN, and 陳淑敏. "Neostigmine,d-Tubocurarine,Choline及Carbachol 在小鼠膈神經--膈肌所引起終板電位衰減之研究." Thesis, 1986. http://ndltd.ncl.edu.tw/handle/26466341060168909036.

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Books on the topic "Tubocurarina"

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Hunter, Jennifer M., and Thomas Fuchs-Buder. Neuromuscular blockade and reversal. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0016.

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Over the past 70 years since the introduction of d-tubocurarine, the search for an ideal neuromuscular blocking agent has led to the development of the depolarizing drug, succinylcholine (suxamethonium), with its rapid onset of action and plasma metabolism, and a series of non-depolarizing agents of which there are two groups: benzylisoquinoliniums (e.g. atracurium, cisatracurium and mivacurium) and aminosteroidal agents (e.g. pancuronium, vecuronium and rocuronium). The need to monitor neuromuscular block perioperatively to ensure the appropriate dose of any neuromuscular blocking drug is given has led to the development of several nerve stimulation techniques. Particularly useful clinically are the train-of-four twitch response, double-burst stimulation, and the post-tetanic count. Their benefits and limitations are considered in this chapter. The most suitable equipment to monitor neuromuscular block and the appropriate anatomical sites for stimulation are discussed. To prevent residual block with its pathophysiological consequences such as upper airway and pharyngeal dysfunction and potential respiratory failure at the end of surgery, antagonizing agents are used. These are of two types: anticholinesterases such as neostigmine and edrophonium, and the γ‎-cyclodextrin, sugammadex. The pharmacodynamics and pharmacokinetics of neuromuscular blocking drugs and their antagonists are altered by the extremes of age, obesity, and several disease states including renal and hepatic failure, neuromuscular disorders, and critical illness. The altered response to all these drugs in these pathologies, which is related to their metabolism and excretion, is considered in detail, together with their other side-effects including the particular disadvantages to the use of succinylcholine.
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Book chapters on the topic "Tubocurarina"

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Wang, Shou-Bao, Xiu-Ying Yang, and Guan-Hua Du. "Tubocurarine." In Natural Small Molecule Drugs from Plants, 337–41. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-8022-7_56.

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Taverner, D. "The Action of d-Tubocurarine and Strychnine on the Spinal Cord of the Cat." In Ciba Foundation Symposium - The Spinal Cord, 231–46. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470718827.ch17.

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Ueda, E., J. Takeda, J. Takahashi, and K. Fukushima. "Comparative Studies of Pipecuronium and Tubocurarine on Releases of Histamine and N-Methylhistamine in Surgical Patients." In Muscle Relaxants, 373. Tokyo: Springer Japan, 1995. http://dx.doi.org/10.1007/978-4-431-66896-1_74.

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Ward, Joanna M., Hassan Fajrak, and Chris Prior. "Time Course of Neuromuscular Block of Vecuronium Analogues and d-Tubocurarine in the Chick Biventer Cervicis Muscle." In Muscle Relaxants, 365. Tokyo: Springer Japan, 1995. http://dx.doi.org/10.1007/978-4-431-66896-1_66.

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"Tubocurarine." In Meyler's Side Effects of Drugs, 222–27. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-444-53717-1.01607-3.

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Clarke, Zoe. "Tubocurarine." In xPharm: The Comprehensive Pharmacology Reference, 1–4. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.61618-6.

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Furman, Brian L. "Tubocurarine ☆." In Reference Module in Biomedical Sciences. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-801238-3.97634-7.

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"Tubocurarine." In Meyler's Side Effects of Drugs: The International Encyclopedia of Adverse Drug Reactions and Interactions, 3532–36. Elsevier, 2006. http://dx.doi.org/10.1016/b0-44-451005-2/00253-9.

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Burr, S. A., and Y. L. Leung. "Curare (d-Tubocurarine)." In Encyclopedia of Toxicology, 1088–89. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-386454-3.00482-6.

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Prior, C., T. Searl, K. Pemberton, W. C. Bowman, and I. G. Marshall. "Combined Effect of (–)-Vesamicol and (+)-Tubocurarine on Endplate Current Amplitude in Rat Skeletal Muscle at High Frequencies of Nerve Stimulation." In Presynaptic Receptors and Neuronal Transporters, 343–44. Elsevier, 1991. http://dx.doi.org/10.1016/b978-0-08-041165-1.50118-6.

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