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Nicotinic receptors anesthetics

Interestingly, one study has shown that cocaine may be a direct antagonist at nicotinic receptors (Damaj et al. 1999). Cocaine blocks several of nicotine s effects, including analgesia on the tail-flick test, independent of its monoamine activity or local anesthetic effects. [Pg.334]

No difference has been observed in the interactions of the two enantiomers of isoflurane with hpid bilayers. But the (5)-enantiomer of isoflurane is two times more active than the (7 )-enantiomer toward a calcium channel receptor, that is sensitive to volatile anesthetic agents, while nodifference in activity has been observed toward an anesthetic nonsensitive receptor. The (5)-enantiomer of isoflurane is also more active than the (R)-enantiomer toward acetylcholine nicotinic receptor and GABA receptor. These data strongly suggest that fluoroethers interact not only with cerebral membranous lipids but also with receptor proteins. [Pg.337]

In small doses, local anesthetics can depress posttetanic potentiation via a prejunctional neural effect. In large doses, local anesthetics can block neuromuscular transmission. With higher doses, local anesthetics block acetylcholine-induced muscle contractions as a result of blockade of the nicotinic receptor ion channels. Experimentally, similar effects can be demonstrated with sodium channel-blocking antiarrhythmic drugs such as quinidine. However, at the doses used for cardiac arrhythmias, this interaction is of little or no clinical significance. Higher concentrations of bupivacaine (0.75%) have been associated with cardiac arrhythmias independent of the muscle relaxant used. [Pg.589]

Belladonna alkaloids have an extremely broad pharmacological spectrum. In addition to their ability to block M-receptors, atropine and scopolamine also act on other receptors, thus showing corresponding effects. They can only block nicotinic cholinergic receptors, however, in significantly larger doses than those used in clinics. Atropine also exhibits properties of local anesthetics and histamine (Hj) receptor blockers. Atropine and... [Pg.196]

Figure 1. The evolutionary relationship between ligand-gated ion channels with four membrane spanning domains (modified from Flood, P. Effects of Volatile Anesthetics at Nicotinic Acetylcholine Receptors. In Molecular Bases of Anesthesia. (2001) Ed. E. Moody and P. Skolnick CRC Press, New York p. 306). Figure 1. The evolutionary relationship between ligand-gated ion channels with four membrane spanning domains (modified from Flood, P. Effects of Volatile Anesthetics at Nicotinic Acetylcholine Receptors. In Molecular Bases of Anesthesia. (2001) Ed. E. Moody and P. Skolnick CRC Press, New York p. 306).
Local anesthetics have poorly understood effects on inflammation at sites of injury, and these anti-inflammatory effects may contribute to improved pain control in some chronic pain syndromes. At the concentrations used in spinal anesthesia, local anesthetics can inhibit transmission via substance P (neurokinin-1), NMDA, and AMPA receptors in the secondary afferent neurons (Figure 26-1). These effects may contribute to the analgesia achieved by subarachnoid administration. Local anesthetics can also be shown to block a variety of other ion channels, including nicotinic acetylcholine channels in the spinal cord. However, there is no convincing evidence that this mechanism is important in the acute clinical effects of these drugs. High concentrations of local anesthetics in the subarachnoid space can interfere with intra-axonal transport and calcium homeostasis, contributing to potential spinal toxicity. [Pg.566]

Succinylcholine Agonist at nicotinic acetylcholine (ACh) receptors, especially at neuromuscular junctions depolarizes may stimulate ganglionic nicotinic ACh and cardiac muscarinic ACh receptors Initial depolarization causes transient contractions, followed by prolonged flaccid paralysis depolarization is then followed by repolarization that is also accompanied by paralysis Placement of tracheal tube at start of anesthetic procedure t rarely, control of muscle contractions in status epilepticus Rapid metabolism by plasma cholinesterase normal duration, 5 min Toxicities Arrhythmias hyperkalemia transient increased intraabdominal, intraocular pressure postoperative muscle pain... [Pg.595]

Unique General Anesthetic Binding Sites Within Distinct Conformational States of the Nicotinic Acetylcholine Receptor... [Pg.447]

Neuromuscular blockade is a rare side-effect of the aminoglycosides, related to blockade of acetylcholine at the nicotinic cholinergic receptor. This is most often seen as respiratory depression and apnea when anesthetic agents are administered... [Pg.31]

The molecular mechanism of action of inhalation anesthetics remains a matter of controversy. The classical view is that narcosis is induced by an unspecific disruption of cell membrane lipids by insertion of the lipophilic anesthetic [95]. Studies of enantiomerically pure analogs of several of the compounds depicted in Scheme 4.42 [96] have, however, revealed clear differences between the effects of enantiomers [97] (Scheme 4.43). There is also a growing body of evidence that the anesthetic effect is at least partly because of specific interaction with proteins [98], for example potassium ion channels and central nicotinic acetylcholine receptors [99]. [Pg.263]


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