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Journal articles on the topic 'Tubocurarina'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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Kopman, Aaron F. "Pancuronium, Gallamine, and d-Tubocurarine Compared." Anesthesiology 70, no. 6 (June 1, 1989): 915–20. http://dx.doi.org/10.1097/00000542-198906000-00006.

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12

KNILL, R. L. "D-Tubocurarine and Upper Airway Obstruction." Anesthesiology 71, no. 3 (September 1, 1989): 480. http://dx.doi.org/10.1097/00000542-198909000-00051.

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13

PAVLIN, EDWARD G. "D-Tubocurarine and Upper Airway Obstruction." Anesthesiology 71, no. 3 (September 1, 1989): 480. http://dx.doi.org/10.1097/00000542-198909000-00052.

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14

Devlin, E., and I. Bali. "Accidental intra-arterial injection of tubocurarine." Anaesthesia 46, no. 1 (January 1991): 75–76. http://dx.doi.org/10.1111/j.1365-2044.1991.tb09336.x.

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15

Bradley, Ronald J. "Prejunctional action of tubocurarine-like fade." Trends in Pharmacological Sciences 9, no. 6 (June 1988): 200–201. http://dx.doi.org/10.1016/0165-6147(88)90083-1.

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16

KURAS, A., and N. GUTMANIENĖ. "N-cholinergic facilitation of glutamate release from an individual retinotectal fiber in frog." Visual Neuroscience 18, no. 4 (July 2001): 549–58. http://dx.doi.org/10.1017/s0952523801184051.

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Nicotinic acetylcholine receptors are localized on retinotectal axons' terminals in lower vertebrates. The effects of activation of these receptors by endogenous acetylcholine were observed under stimulation of mass optic fibers. This study was designed to determine whether endogenous acetylcholine facilitates frog retinotectal transmission, provided only the synapses of an individual optic axon are activated, and to evaluate the feasible extent of nicotinic facilitation in these synapses by applied agonist. To this end, the effects of cholinergic drugs on the extracellular action and synaptic potentials recorded from the terminal arborization of a separate retinotectal fiber (in layer F of the tectum) were investigated in vivo. Glutamatergic nature of retinotectal synapses was reexamined by treatment with kynurenic acid. Both kynurenic acid (0.25–1 mM) and d-tubocurarine chloride (10–15 μM) significantly depressed the synaptic potentials. Carbamylcholine chloride (50–150 μM) evoked a large augmentation of the synaptic potentials and a slight but statistically significant decrease of the action potentials. D-tubocurarine reduced the effect of carbamylcholine. Pilocarpine hydrochloride (50 μM) had only a weak effect. The paired-pulse facilitation of the synaptic potentials changed significantly under the action of carbamylcholine and d-tubocurarine. The obtained results suggest that the glutamate release from activated synapses of individual retinotectal axons is facilitated by endogenous acetylcholine via presynaptic nicotinic receptors. Under used stimulation conditions, this modulation mechanism was employed only partially since its activation by applied carbamylcholine could enhance synaptic transmission up to 2.8 times.

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Dujic, Z., D. L. Roerig, H. K. Schedewie, J. P. Kampine, and Z. J. Bosnjak. "Presynaptic modulation of ganglionic ACh release by muscarinic and nicotinic receptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 259, no. 2 (August 1, 1990): R288—R293. http://dx.doi.org/10.1152/ajpregu.1990.259.2.r288.

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The present experiments were undertaken to investigate the effects of atropine and d-tubocurarine on acetylcholine (ACh) release and ganglionic synaptic transmission in the isolated cat stellate ganglion. Ganglionic release of picomole amounts of ACh was measured by radioenzymatic assay, and ganglionic transmission was estimated on the basis of the compound action potential recorded from the postganglionic stellate cardiac nerve. Atropine (5 microM) produced a significant increase in both spontaneous and evoked ACh release from the ganglion while depressing synaptic transmission. d-Tubocurarine (20 microM) also caused a significant, though smaller, increase in spontaneous release of ACh but had little effect on evoked release of ACh. These results suggest that ACh release and synaptic transmission in the cat stellate ganglion are subject to cholinergic feedback regulation, which appears to be mediated predominantly via muscarinic presynaptic receptors.

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18

Perrins, R., and A. Roberts. "Cholinergic contribution to excitation in a spinal locomotor central pattern generator in Xenopus embryos." Journal of Neurophysiology 73, no. 3 (March 1, 1995): 1013–19. http://dx.doi.org/10.1152/jn.1995.73.3.1013.

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1. We have investigated whether in Xenopus embryos, spinal interneurons of the central pattern generator (CPG) receive cholinergic or electrical excitatory input during swimming. The functions of cholinergic excitation during swimming were also investigated. 2. Intracellular recordings were made from rhythmically active presumed premotor interneurons in the dorsal third of the spinal cord. After locally blocking inhibitory potentials with 2 microM strychnine and 40 microM bicuculline, the reliability of spike firing and the amplitude of fast, on-cycle, excitatory postsynaptic potentials (EPSPs) underlying the single on-cycle spikes were measured during fictive swimming. 3. The nicotinic antagonists d-tubocurarine and dihydro-beta-erythroidine (DH beta E, both 10 microM) reversibly reduced the reliability of the spike firing during swimming and reduced the amplitude of the on-cycle EPSP by 16%. DH beta E also reduced the EPSP amplitude in spinalized embryos by 22%. These results indicate that interneurons receive rhythmic cholinergic excitation from a source within the spinal cord. 4. Combined applications of nicotinic and excitatory amino acid (EAA) antagonists or cadmium (Cd2+, 100-200 microM) resulted in complete block of the fast EPSP, suggesting that interneurons do not receive electrical excitation. 5. The nicotinic antagonists mecamylamine and d-tubocurarine (both 5 microM) reduced the duration of episodes of fictive swimming recorded from the ventral roots, in spinal embryos. When applied in the middle of a long episode, d-tubocurarine decreased the swimming frequency, ruling out an effect on the initiation pathway. The cholinesterase inhibitor eserine (10 microM) increased the duration of swimming episodes.(ABSTRACT TRUNCATED AT 250 WORDS)

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19

Lavery, G. G., R. S. J. Clarke, and J. Watkins. "Histaminoid responses to atracurium, vecuronium and tubocurarine." Annales Françaises d'Anesthésie et de Réanimation 4, no. 2 (January 1985): 180–83. http://dx.doi.org/10.1016/s0750-7658(85)80196-9.

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20

Nott, M. R., and B. J. Pollard. "Atracurium block prolonged by low dose tubocurarine." Anaesthesia 47, no. 9 (September 1992): 819–20. http://dx.doi.org/10.1111/j.1365-2044.1992.tb03288.x.

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21

Nott, M. R., and V. Tanner. "Reversal of atracurium after low dose tubocurarine." Anaesthesia 48, no. 7 (July 1993): 644–45. http://dx.doi.org/10.1111/j.1365-2044.1993.tb07154.x.

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22

STEINBERG, D., RI GERENSTEIN, and J. CHALITA. "DELAYED EFFECT OF PRIMING WITH d-TUBOCURARINE." Anesthesia & Analgesia 86, Supplement (February 1998): 505S. http://dx.doi.org/10.1097/00000539-199802001-00503.

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23

Kressin, N. A., A. M. Nielsen, G. E. Bisgard, and R. B. Laravuso. "D-TUBOCURARINE - EFFECTS ON RESPIRATORY CONTROL MECHANISMS." Anesthesiology 63, Supplement (September 1985): A510. http://dx.doi.org/10.1097/00000542-198509001-00510.

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24

Zorko, Matjaž, and MiloŠR Pavlič. "Multiple binding of D-tubocurarine to acetylcholinesterase." Biochemical Pharmacology 35, no. 14 (July 1986): 2287–96. http://dx.doi.org/10.1016/0006-2952(86)90453-3.

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25

Cox, T. C. "Low-affinity mixed acetylcholine-responsive receptors at the apical membrane of frog tadpole skin." American Journal of Physiology-Cell Physiology 264, no. 3 (March 1, 1993): C552—C558. http://dx.doi.org/10.1152/ajpcell.1993.264.3.c552.

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The larval frog skin has a very high electrical resistance and a corresponding low rate of transepithelial ion transport. Amiloride, a blocker of sodium transport in adult skin, transiently stimulates rather than inhibits short-circuit current (Isc) across larval skin through nonselective cation channels. Acetylcholine (ACh) stimulates Isc like amiloride, although the response is more prolonged. Pretreatment with ACh markedly suppressed amiloride stimulation of Isc; amiloride pretreatment also suppressed ACh stimulation. Half-maximal stimulation of Isc by ACh occurred at 347 microM. Stimulation by ACh was inhibited by both d-tubocurarine [dissociation constant (Kd) = 57 microM] and atropine (Kd = 49 microM). The specific nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium and the specific muscarinic agonist oxotremorine-M both stimulated Isc and were blocked by either atropine or d-tubocurarine. Reciprocal desensitization and blocker cross-reactivity suggest that ACh activates the same population of receptors as amiloride. This ACh-responsive receptor has characteristics of both nicotinic and muscarinic receptors found in other tissues.

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Maggi, C. A., S. Giuliani, P. Santicioli, and A. Meli. "Analysis of factors involved in determining urinary bladder voiding cycle in urethan-anesthetized rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 251, no. 2 (August 1, 1986): R250—R257. http://dx.doi.org/10.1152/ajpregu.1986.251.2.r250.

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The mechanism(s) involved in determining the voiding cycle of the rat urinary bladder have been investigated in urethan-anesthetized animals. Fluid emission is almost confined to that phase of the voiding cycle which is characterized by the presence of a series of high-frequency oscillations in intraluminal pressure (IPHFO). During this phase the mean urethral flow rate reached a maximum and fluid was expelled in a stream-like fashion. The index obtained by multiplying the amplitude of IPHFO by their duration was significantly related to the maximal value of urethral flow rate. The IPHFO were selectively abolished by administration of d-tubocurarine at a dose that barely affects detrusor contractility. Moreover, d-tubocurarine reduced mean urethral flow rate and increased residual volume. The reflex (hexamethonium sensitive) mechanism(s) responsible for the generation of IPHFO is more developed in male than female rats. This mechanism, which involves activation of skeletal muscle, plays a significant role in determining bladder voiding in this species.

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Dilger, James P., Ana Maria Vidal, Man Liu, Claire Mettewie, Takahiro Suzuki, Anh Pham, and Deeptankar Demazumder. "Roles of Amino Acids and Subunits in Determining the Inhibition of Nicotinic Acetylcholine Receptors by Competitive Antagonists." Anesthesiology 106, no. 6 (June 1, 2007): 1186–95. http://dx.doi.org/10.1097/01.anes.0000267602.94516.7f.

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Background Binding sites for agonists and competitive antagonists (nondepolarizing neuromuscular blocking agents) are located at the alpha-delta and alpha-epsilon subunit interfaces of adult nicotinic acetylcholine receptors. Most information about the amino acids that participate in antagonist binding comes from binding studies with (+)-tubocurarine and metocurine. These bind selectively to the alpha-epsilon interface but are differentially sensitive to mutations. To test the generality of this observation, the authors measured current inhibition by five competitive antagonists on wild-type and mutant acetylcholine receptors. Methods HEK293 cells were transfected with wild-type or mutant (alphaY198F, epsilonD59A, epsilonD59N, epsilonD173A, epsilonD173N, deltaD180K) mouse muscle acetylcholine receptor complementary DNA. Outside-out patches were excised and perfused with acetylcholine in the absence and presence of antagonist. Concentration-response curves were constructed to determine antagonist IC50. An antagonist-removal protocol was used to determine dissociation and association rates. Results Effects of mutations were antagonist specific. alphaY198F decreased the IC50 of (+)-tubocurarine 10-fold, increased the IC50 of vecuronium 5-fold, and had smaller effects on other antagonists. (+)-Tubocurarine was the most sensitive antagonist to epsilonD173 mutations. epsilonD59 mutations had large effects on metocurine and cisatracurium. deltaD180K decreased inhibition by pancuronium, vecuronium, and cisatracurium. Inhibition by these antagonists was increased for receptors containing two delta subunits but no epsilon subunit. Differences in IC50 arose from differences in both dissociation and association rates. Conclusion Competitive antagonists exhibited different patterns of sensitivity to mutations. Except for pancuronium, the antagonists were sensitive to mutations at the alpha-epsilon interface. Pancuronium, vecuronium, and cisatracurium were selective for the alpha-delta interface. This suggests the possibility of synergistic inhibition by pairs of antagonists.

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Odierna, Gianmaria Lorenzo, and William Donald Phillips. "The Safety Factor for Neuromuscular Transmission: Effects of Dimethylsulphoxide, Cannabinoids and Synaptic Homeostasis." Journal of Neuromuscular Diseases 8, no. 5 (September 14, 2021): 831–44. http://dx.doi.org/10.3233/jnd-210654.

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Background In myasthenia gravis, impaired postsynaptic sensitivity to acetylcholine results in failure of neuromuscular transmission and fatiguing muscle weakness. Objective Develop an ex vivo muscle contraction assay to test cannabinoids and other substances that might act on the myasthenic neuromuscular junction to restore control of the muscle. Methods Tubocurarine was added to an ex vivo, mouse phrenic nerve-hemidiaphragm muscle preparation to reduce acetylcholine sensitivity. This produced a myasthenia-like decrement in twitch force during a train of 10 nerve impulses (3 / sec). Endplate potential (EPP) recordings were used to confirm and extend the findings. Results Surprisingly, addition to the bath of dimethylsulphoxide (DMSO), at concentrations as low as 0.1%(v/v), partially reversed the decrement in nerve-evoked force. Intracellular electrophysiology, conducted in the presence of tubocurarine, showed that DMSO increased the amplitudes of both the spontaneous miniature EPP (MEPP) and the (nerve-evoked) EPP. In the absence of tubocurarine (synaptic potentials at physiological levels), an adaptive fall in quantal content negated the DMSO-induced rise in EPP amplitude. The effects of cannabinoid receptor agonists (solubilized with DMSO) in the contraction assay do not support their further exploration as useful therapeutic agents for myasthenia gravis. CP 55,940 (a dual agonist for cannabinoid receptor types 1 and 2) reversed the beneficial effects of DMSO. Conclusions: We demonstrate a powerful effect of DMSO upon quantal amplitude that might mislead pharmacological studies of synaptic function wherever DMSO is used as a drug vehicle. Our results also show that compounds targeting impaired neuromuscular transmission should be tested under myasthenic-like conditions, so as to avoid confounding effects of synaptic homeostasis.

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Fortier, L. Philippe, Richard Robitaille, and François Donati. "Increased Sensitivity to Depolarizing and Nondepolarizing Neuromuscular Blocking Agents in Young Rat Hemidiaphragms." Anesthesiology 95, no. 2 (August 1, 2001): 478–84. http://dx.doi.org/10.1097/00000542-200108000-00033.

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Background Newborn neuromuscular junctions are more sensitive to d-tubocurarine than more mature preparations. It is unclear whether the same modifications occur with newer nondepolarizing agents and depolarizing agent succinylcholine. The purpose of this study was to determine the relative sensitivity of newborn neuromuscular junctions to succinylcholine and five nondepolarizing agents. Methods The phrenic nerve-hemidiaphragm preparation from 60 rats was used, 30 aged 9-12 days (newborn) and 30 aged 27-33 days (adult). Five rats from each group were exposed to one of six neuromuscular blocking agents (d-tubocurarine, cisatracurium, atracurium, vecuronium, rocuronium, and succinylcholine). Indirectly elicited twitch tension was measured during control conditions in the absence of blocking agent, followed by four concentrations of one of the six agents. Concentration-response curves were constructed and the EC50 (concentration required to produce 50% depression of twitch tension) was obtained. Potency ratios (EC50adult/EC50newborn) were derived for each agent. Results Newborn preparations were significantly (P < 0.001) more sensitive than their adult counterparts for all six agents tested. For nondepolarizing agents, the potency ratio was in the 6-12 range. The EC50adult/EC50newborn were as follows, in decreasing potency order: d-tubocurarine, 1.68/0.23 microM; cisatracurium, 2.73/0.47 microM; vecuronium, 5.47/0.59 microM; rocuronium, 9.7/0.78 microM; and atracurium, 12.3/1.9 microM. Succinylcholine was three times as potent in newborn rats, with an EC50adult/EC50newborn of 21.3/7.3 microM. The ratio for succinylcholine was significantly less than for all nondepolarizing drugs (P < 0.02). Conclusion The newborn neuromuscular junction of the rat shows an increased sensitivity to all neuromuscular blocking agents tested, including succinylcholine. However, the potency ratio was greater for nondepolarizing than depolarizing drugs. The optimal dose of these agents for certain situations such as cesarean section and anesthesia in neonates should be reassessed.

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30

Hart, Paul S., Peter M. C. Wright, Ronald Brown, Marie Lau, Manohar L. Sharma, Ronald D. Miller, Larry Gruenke, and Dennis M. Fisher. "Edrophonium Increases Mivacurium Concentrations during Constant Mivacurium Infusion, and Large Doses Minimally Antagonize Paralysis." Anesthesiology 82, no. 4 (April 1, 1995): 912–18. http://dx.doi.org/10.1097/00000542-199504000-00014.

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Background Mivacurium, a nondepolarizing muscle relaxant, is metabolized by plasma cholinesterase. Although edrophonium does not alter plasma cholinesterase activity, we have observed that doses of edrophonium that antagonize paralysis from other nondepolarizing muscle relaxants are less effective with mivacurium. We speculated that edrophonium might after metabolism of mivacurium, thereby hindering antagonism of paralysis. Accordingly, we determined the effect of edrophonium on neuromuscular function and plasma mivacurium concentrations during constant mivacurium infusion. Methods We infused mivacurium to maintain 90% depression of adductor pollicis twitch tension and then gave edrophonium in doses ranging from 125-2,000 micrograms/kg without altering the mivacurium infusion. Peak twitch tension after edrophonium was determined to estimate the dose of edrophonium antagonizing 50% of twitch depression for antagonism of mivacurium; plasma cholinesterase activity and mivacurium concentrations before and after edrophonium were measured. Additional subjects were given 500 micrograms/kg edrophonium to antagonize continuous infusions of d-tubocurarine and vecuronium. Results With mivacurium, edrophonium increased twitch tension in a dose-dependent manner: the dose of edrophonium antagonizing 50% of twitch depression was 2,810 micrograms/kg. The largest dose of edrophonium (2,000 micrograms/kg) produced only 45 +/- 7% antagonism. Edrophonium, 500 micrograms/kg, antagonized mivacurium markedly less than it antagonized d-tubocurarine and vecuronium. Edrophonium increased plasma concentrations of the two potent stereoisomers of mivacurium 48% and 79%, these peaking at 1-2 min; plasma cholinesterase activity was unchanged. Conclusions Edrophonium doses that antagonize d-tubocurarine and vecuronium are less effective in antagonizing the neuromuscular effects of mivacurium during constant infusion. Edrophonium increases plasma mivacurium concentrations, partly or completely explaining its limited efficacy; the mechanism by which edrophonium increases mivacurium concentrations remains unexplained. Our results demonstrate that antagonism of mivacurium by edrophonium is impaired, and therefore we question whether edrophonium should be used to antagonize mivacurium.

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Lu, G. P., M. R. Seidel, J. A. Gibson, C. Monell, E. A. M. Frost, and P. L. Goldiner. "CEREBRAL VASCULAR EFFECT OF VECURONIUM, PIPECURONIUM, AND TUBOCURARINE." Journal of Neurosurgical Anesthesiology 4, no. 4 (October 1992): 314. http://dx.doi.org/10.1097/00008506-199210000-00048.

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32

Fuke, N., J. Martyn, C. S. Kim, and S. Basta. "Concentration-dependent interaction of theophylline with d-tubocurarine." Journal of Applied Physiology 62, no. 5 (May 1, 1987): 1970–74. http://dx.doi.org/10.1152/jappl.1987.62.5.1970.

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The interaction of theophylline with d-tubocurarine chloride (dTC) was examined in rabbits. After steady-state subtherapeutic (less than 10 mg/l), therapeutic (10–20 mg/l), and toxic (greater than 20 mg/l) concentrations of theophylline, dose-response curves for dTC were determined and compared with controls that received no theophylline. At therapeutic concentrations of theophylline the effective dose for 50% inhibition of twitch (ED50) for dTC (mean +/- SE, 0.115 +/- 0.016 mg/kg) was significantly shifted to the left in comparison with the control (0.165 +/-0.008 mg/kg). The ED50 of dTC for the subtherapeutic group was 0.143 +/- 0.011 mg/kg, which was less than the control but not of statistical significance (P = 0.1). The ED50 for the toxic theophylline group was 0.168 +/- 0.003 mg/kg, which was not significantly different from controls but significantly different from the theophylline therapeutic and subtherapeutic groups. Thus, toxic concentrations of theophylline reversed the potentiating effects of therapeutic and subtherapeutic concentrations of dTC dose-response curves. Therefore, depending on concentration, theophylline exhibits a biphasic interaction with dTC. Surgical patients on theophylline may require less dTC intraoperatively. More importantly, the use of theophylline in the postoperative period to reverse anesthetic effects may result in recurarization.

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WALKER, J. S., C. A. SHANKS, and K. F. BROWN. "Altered d.d- Tubocurarine Disposition During Cardiopulmonary Bypass Surgery." Survey of Anesthesiology 29, no. 1 (February 1985): 11. http://dx.doi.org/10.1097/00132586-198502000-00010.

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34

Kelly, S. S., G. P. Morgan, and J. W. Smith. "The origin of (+)-tubocurarine resistance in dystrophic mice." British Journal of Pharmacology 89, no. 1 (September 1986): 47–53. http://dx.doi.org/10.1111/j.1476-5381.1986.tb11119.x.

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35

Dain, Alexander C., Barry W. Madsen, and Robert O. Edeson. "Kinetics of (+)-tubocurarine blockade at the neuromuscular junction." British Journal of Pharmacology 103, no. 2 (June 1991): 1607–13. http://dx.doi.org/10.1111/j.1476-5381.1991.tb09835.x.

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Waud, Barbara E., Yoshikiyo Amaki, and Douglas R. Waud. "Disuse and d???Tubocurarine Sensitivity in Isolated Muscles." Anesthesia & Analgesia 64, no. 12 (December 1985): 1178???1182. http://dx.doi.org/10.1213/00000539-198512000-00008.

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Waud, Barbara E., and Douglas R. Waud. "Tubocurarine Sensitivity of the Diaphragm after Limb Immobilization." Anesthesia & Analgesia 65, no. 5 (May 1986): 493???495. http://dx.doi.org/10.1213/00000539-198605000-00011.

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38

Pedersen, Steen E., and Rao V. L. Papineni. "Interaction ofd-Tubocurarine Analogs with theTorpedoNicotinic Acetylcholine Receptor:." Journal of Biological Chemistry 270, no. 52 (December 29, 1995): 31141–50. http://dx.doi.org/10.1074/jbc.270.52.31141.

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39

Gerber, H. R., J. Romppainen, and W. Schwinn. "Potentiation of atracurium by pancuronium and d-tubocurarine." Canadian Anaesthetists’ Society Journal 33, no. 5 (September 1986): 563–70. http://dx.doi.org/10.1007/bf03014261.

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40

Stojan, Jure, and MilosˇR Pavlicˇ. "On the inhibition of cholinesterase by d-tubocurarine." Biochimica et Biophysica Acta (BBA) - Protein Structure and Molecular Enzymology 1079, no. 1 (August 1991): 96–102. http://dx.doi.org/10.1016/0167-4838(91)90029-y.

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41

Wang, Wei, Makino Watanabe, Takeshi Nakamura, Yoshihisa Kudo, and Rikuo Ochi. "Properties and expression of Ca2+-activated K+ channels in H9c2 cells derived from rat ventricle." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 5 (May 1, 1999): H1559—H1566. http://dx.doi.org/10.1152/ajpheart.1999.276.5.h1559.

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H9c2 is a clonal myogenic cell line derived from embryonic rat ventricle that can serve as a surrogate for cardiac or skeletal muscle in vitro. Using whole cell clamp with H9c2 myotubes, we observed that depolarizing pulses activated slow outward K+ currents and then slow tail currents. The K+ currents were abolished in a Ca2+-free external solution, indicating that they were Ca2+-activated K+ currents. They were blocked by apamin, a small-conductance Ca2+-activated K+ (SK) channel antagonist (IC50 = 6.2 nM), and by d-tubocurarine (IC50 = 49.4 μM). Activation of SK channels exhibited a bell-shaped voltage dependence that paralleled the current-voltage relation for L-type Ca2+ currents ( I Ca,L). I Ca,L exhibited a slow time course similar to skeletal I Ca,L, were unaffected by apamin, and were only slightly depressed by d-tubocurarine. RT-PCR analysis of the mRNAs revealed that rSK3, but not rSK1 or rSK2, was expressed in H9c2 myotubes but not in myoblasts. These results suggest that rSK3 channels are expressed in H9c2 myotubes and are primarily activated by I Ca,L directly or indirectly via Ca2+-induced Ca2+ release from sarcoplasmic reticulum.

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42

ANCTIL, MICHEL. "Cholinergic and Monoaminergic Mechanisms Associated with Control of Bioluminescence in the Ctenophore Mnemiopsis Leidyi." Journal of Experimental Biology 119, no. 1 (November 1, 1985): 225–38. http://dx.doi.org/10.1242/jeb.119.1.225.

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1. The effects of cholinergic and monoaminergic drugs and blocking agents on luminescence responses of the comb-jelly Mnemiopsis leidyi were investigated, using isolated strips of meridional cells. 2. Catecholamines elicited dose-dependent flash activity and adrenalin was the most patent. The adrenalin response was abolished by propranolol (0.1 mmol l−1), but not phentolamine. Reserpine (0.1 mmol l−1) suppressed the flash response to electrical stimulation without affecting the adrenalin response. 3. Acetylcholine (ACh) elicited flash activity which was propagated along the meridional canals. Eserine (0.01 mmol l−1) potentiated the flash response to either ACh or electrical stimulation. 4. Tubocurarine reduced or abolished responses to either ACh or electrical stimulation. Atropine elicited intense flash activity and potentiated the response to electrical stimulation, but failed to block the ACh response. 5. Prolonged exposure of meridional canals to serotonin (5-HT) depressed or abolished flash responses to ACh, adrenalin and electrical stimulation. 6. The ACh flash response was abolished by propranolol but the response to adrenalin was not altered by tubocurarine. It is concluded that nicotinic cholinergic and beta-adrenergic mechanisms are interrelated and indirectly involved in excitation of luminescence in Mnemiopsis.

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Park, Chang Kil, and Ik Soo Kim. "Pancuronium Effect on d-Tubocurarine Induced Hypotension in Rabbit." Korean Journal of Anesthesiology 18, no. 2 (1985): 150. http://dx.doi.org/10.4097/kjae.1985.18.2.150.

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Hill, Susan A., Ralph P. F. Scott, and John J. Savarese. "Structure-activity relationships: from tubocurarine to the present day." Baillière's Clinical Anaesthesiology 8, no. 2 (June 1994): 317–48. http://dx.doi.org/10.1016/s0950-3501(05)80096-0.

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45

Szeto, Hazel H., and Donald J. Hinman. "Differential sensitivities of fetal muscle groups to d-tubocurarine." American Journal of Obstetrics and Gynecology 163, no. 1 (July 1990): 202–9. http://dx.doi.org/10.1016/s0002-9378(11)90699-1.

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SIMPSON, D. A., D. J. WRIGHT, and J. E. HAMMOND. "INFLUENCE OF TUBOCURARINE, PANCURONIUM AND ATRACURIUM ON BRONCHOMOTOR TONE." British Journal of Anaesthesia 57, no. 8 (August 1985): 753–57. http://dx.doi.org/10.1093/bja/57.8.753.

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47

Hogue, Charles W., and J. A. Jeevendra Martyn. "LOWER MOTOR NEURON INJURY INDUCES RESISTANCE TO d-TUBOCURARINE." Anesthesiology 69, no. 3A (September 1, 1988): A501. http://dx.doi.org/10.1097/00000542-198809010-00501.

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48

Yan, Dong, Steen E. Pedersen, and Michael M. White. "Interaction of d-tubocurarine analogs with the 5HT3 receptor." Neuropharmacology 37, no. 2 (February 1998): 251–57. http://dx.doi.org/10.1016/s0028-3908(98)00010-0.

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Fishleder, R. I., and C. K. Buckner. "DIFFERENTIAL RESPONSE OF GUINEA PIG AIRWAYS TO D-TUBOCURARINE." Anesthesiology 63, Supplement (September 1985): A292. http://dx.doi.org/10.1097/00000542-198509001-00292.

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Vizi, E. S., G. T. Somogyi, H. Nagashima, D. Duncalf, I. A. Chaudry, and F. F. Foldes. "d-TUBOCURARINE AND PANCURONIUM INHIBIT EVOKED RELEASE OF ACETYLCHOLINE." Anesthesiology 63, Supplement (September 1985): A328. http://dx.doi.org/10.1097/00000542-198509001-00328.

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