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At least 73 records · Page 4Linked to original sources
PubMed1979

Effects of muscle relaxants on catecholamine release from adrenal medulla.

Bovine adrenals were perfused with secretagogues in the presence or absence of muscle relaxants. On a molar basis, Dially-nor-toxiferine was as potent as tubocurarine in inhibiting the catecholamine release induced by carbachol; pancuronium was about 100 times less potent than tubocurarine, whereas gallamine and succinylcholine produced no inhibition whatsoever. KCl-induced catechoamine release was not affected by any of these compounds. Nicotine-induced catecholamine release was inhibitedby diallyl-nor-toxiferine, tubocurarine and pancuronium, but not by gallamine or succinylcholine. Muscarine failed to stimulate the adrenal medulla to release catecholamines. The results show that the inhibition of catecholamine release is based on the specific block of the nicotinic receptor, whereas gallamine and succinylcholine possess no blocking action, and that diallyl-nor-toxiferine and tubocurarine might affect clinical symptoms under conditions in which catecholamine release from the adrenal is increased by a compensatory mechanism.

Adrenal Medulla↗
PubMed1969

The strychnine-like action of curare and related compounds on the somatosensory evoked response of the rat cortex.

1. Drugs were applied to the cerebral cortex of rats anaesthetized with pentobarbitone and changes measured in the somatosensory primary evoked response.2. Computer-derived averages of thirty-two consecutive responses yielded stable and consistent measurements of the potential changes comprising the evoked response, and comparable records from the opposite (non-drug treated) cortex provided an essential control for systemic actions of the drug.3. The modifications produced by curare and strychnine were indistinguishable. The first positive wave (peak latency 7 msec) was unaltered; the second positive wave (peak latency 11.5 msec) was variably enhanced, and the first and second negative waves (peak latencies 16 and 40 msec) were replaced by a much larger negative wave (peak latency 22 msec).4. The time of onset of the effect on the negative waves and the maximal amplitude attained by the abnormal negative wave were related to the log concentration of the drug used. Curare is approximately 10 times more potent than strychnine.5. Toxiferine I, di-allylnortoxiferine and atropine also produced this effect but were less potent than strychnine.6. Succinylcholine, dihydro-beta-erythroidine and gallamine triethiodide did not produce this effect (in concentrations up to 10(-3)M).7. The observations are consistent with an action of curare and strychnine on an intracortical cholinergic inhibitory system, but other possibilities including a "non-specific excitatory action" cannot be excluded.

Animals↗
PubMed1978

Actions of some transmitters and their antagonists on salivary secretion in a tick.

Cholinomimetics (pilocarpine, carbachol, physostigmine, acetylcholine, acetyl-beta-methylcholine) and sympathomimetics (dopamine, epinephrine), when injected into the hemolymph, provoked salivary fluid secretion in the female ixodid tick Amblyomma hebraeum Koch. Atropine, but not tubocurarine or toxiferine, abolished pilocarpine-induced secretion without reducing the response to dopamine. Reserpine and guanethidine likewise selectively attenuated pilocarpine-induced secretion. Following extirpation of the synganglion, pilocarpine no longer provoked a secretory response whereas dopamine did. Thus, the salivary gland appears to be innervated directly by catecholaminergic rather than cholinergic secretory nerves. It is suggested that pilocarpine elicits salivation by interacting with muscarinic-type cholinergic receptors situated either on the cell bodies of the secretory nerves, or alternatively in the integrative or sensory pathway.

Acetylcholine↗
PubMed2004

Bisquaternary caracurine V and iso-caracurine V salts as ligands for the muscle type of nicotinic acetylcholine receptors: SAR and QSAR studies.

The binding constants (K(i) values) of 24 caracurine V and 6 iso-caracurine V analogues for the muscle type of nicotinic ACh receptors (nAChR) from Torpedo californica were determined in a binding assay using (+/-)-[(3)H]epibatidine as a radioligand. The allyl alcohol group present in the iso-caracurine V ring system was found to be essential for high binding affinity. The most potent compounds are the dimethyl and di-(4-nitrobenzyl)-iso-caracurinium V salts 29 (18 nM), and 31 (79 nM), respectively. Compound 29 and the corresponding diallyl analogue 30 (350 nM) exhibited similar binding affinities as the equally substituted neuromuscular-blocking agents toxiferine I (14 nM) and alcuronium (234 nM), respectively. The SAR results were confirmed by QSAR studies, which additionally revealed that the presence of hydrogen-bond acceptor groups close to the quaternary nitrogen, is detrimental for the nicotinic binding affinity. The diallyl- and dimethylcaracurinium V salts 13 and 27, respectively, which are known to be among the most potent allosteric modulators of M(2) receptors (EC(50)=10 and 8nM, respectively), exhibited rather low nicotinic binding affinities for muscle type nAChR (K(i)=1.5 and 5.2 microM, respectively). Such a large difference in affinity suggests that it is possible to develop compounds with high muscarinic allosteric potency and low or negligible affinities for (alpha1)(2)beta1gammadelta nAChR. Additionally, the iso-caracurine V analogues with binding affinities comparable to those of (+)-tubocurarine and alcuronium could become a new class of neuromuscular-blocking agents.

Alkaloids↗
PubMed1977

Hemodynamic effects of locally applied epinephrine used with various general anesthetic techniques.

Halothane-nitrous oxide-oxygen (GOF), nitrous oxide-oxygen with diallyl-nor-toxiferine (Jackson-Rees method), or nitrous oxide-oxygen with droperidol-pentazocine (modified NLA) were administered in 190 instances of repair of cleft lips and cleft palates. Epinephrine, 1:30,000, 1:100,000, or 1:300,000, was injected as the vasoconstrictor around the operative field. Epinephrine concentration of 1:100,000 provided sufficient hemostasis, whereas 1:300,000 was insufficient. With the same concentration of epinephrine, GOF and modified NLA seemed to be better than the Jackson-Rees method, since the GOF and modified NLA groups showed less increase of pulse rate, blood pressure, and plethysmographic changes. A 1:30,000 concentration of epinephrine could be used safely with the Jackson-Rees method and the hemostasis with this concentration was superior to 1:100,000. However, it is recommended only for the cleft lip operation, since these patients are younger and need better hemostasis, and hypersalivation after reversal does not disturb the postoperative course. So-called epinephrine-induced arrhythmia with halothane anesthesia occurred in 1 of 34 instances with 1:300,000 solution and in 5 of 48 instances with 1:100,000 solution. Propranolol was given in only one instance. All others returned to normal rhythm with hyperventilation with pure oxygen. The use of 1:100,000 solution of epinephrine as an adjunct with modified NLA is the most satisfactory and safe method for cleft palate operations, and 1:30,000 with the Jackson-Rees is the better method for cleft lip repairs.

Alcuronium↗
PubMed1977

Intra-uterine growth retardation and limb deformities produced by neuromuscular blocking agents in the rat fetus.

Intra-uterine growth retardation and limb deformities, resembling clubfoot, were produced by tubocuararine chloride, and by toxiferine, when administered to the rat fetus between the 16th and 19th day of gestation. These effects were associated in some fetuses, but were not sex-linked. Fetuses in the middle part of the uterine horn were observed to be more vulnerable. Placentae of the affected fetuses were smaller in size and weight at birth. Direct toxic effects of the drug on the fetus and/or on the placenta, along with immobilization of the fetus in utero due to the neuromuscular blocking action of the drugs, seem responsible for these effects. These finding warrant proper caution and care in administering such drugs to women, even as late as the third trimester of pregnancy.

Abnormalities, Drug-Induced↗