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PubMed1988

Histamine release by some new skeletal muscle relaxants studied at the rat ileum.

The effects of 6 non-depolarizing muscle relaxants on histamine release were investigated, pharmacologically, using histamine and histamine antagonists, e.g. mepyramine, clemastine, dimotane. The results showed that gallamine, pancuronium, vecuronium, atracurium, tubocurarine and alcuronium produced concentration-dependent contractions in the rat ileum, gallamine and pancuronium being the most effective agents in producing muscle contraction. The H1 blocker, mepyramine, reduced the contractions produced by the muscle relaxants, as well as that produced by histamine. However, there was always some residual contraction, not blocked by high concentrations of mepyramine in the case of the muscle relaxants, but not in the case of histamine, the contraction of which was totally blocked by high concentrations of mepyramine. These results also suggested that, in part, the contraction produced by muscle relaxants, may be due to a mechanism other than histamine release, e.g. release of other mediators and/or an effect on intracellular calcium ions. Since very high concentrations of atracurium and vecuronium (40-50 times higher than clinical concentrations) were used in this study to produce marked contractions, the implication is that in clinical concentrations, they have little effect on histamine release. In contrast, gallamine and pancuronium can release histamine even at low concentrations, i.e. at or near their clinical concentrations in man. These, therefore, are the cause of the adverse reactions seen after drug administration.

Animals↗
PubMed1988

The use of muscle relaxant to supplement local anaesthetics for Bier's blocks.

In searching for the 'ideal' muscle relaxant for use with intravenous regional anaesthesia, muscle relaxation was assessed with and without the addition of Atracurium to Bier's Block in four volunteers. This was followed by a clinical study of 36 patients with wrist fractures to confirm the drug's safety and examine the possible clinical advantages of using a muscle relaxant. The addition of 2 mg of Atracurium to the Bier's Block improved the ease of reduction (P less than 0.025) and the quality of analgesia (P less than 0.05) (Mann-Whitney U test). The authors conclude that the addition of Atracurium to a Bier's Block is useful in selected patients with a wrist fracture.

Anesthesia, Local↗
PubMed1995

Airway smooth muscle relaxant effects of the cocaine pyrolysis product, methylecgonidine.

Methylecgonidine (anhydroecgonine methylester; MEG) is produced when cocaine base ("crack") is heated. Since crack smoking can produce significant airway toxicity and the role of MEG in this toxicity is unknown, we determined the effects of MEG on guinea pig isolated tracheal rings. Trachea do not contract in response to MEG; rather, MEG (10(-9) to 10(-3) M) dose-dependently relaxed tissue precontracted with 2 x 10(-3) M acetylcholine (ACh). MEG (10(-9) to 10(-6) M) reduced the magnitude of contractions induced by ACh, carbachol, histamine and KCl in a nonsurmountable manner; the maximal response to these agents was not restored after repeated washing. MEG did not affect contractions induced by BaCl2. 4-Diphenyl acetoxymethyl piperidine methiodide (4-DAMP; 10(-7) M), in the presence or absence of MEG (10(-7) M), shifted the dose-effect curve for ACh 30-fold to the right. After washing, sensitivity to ACh was fully recovered in tissues exposed to 4-DAMP alone, but was still reduced to 50% of control in tissues exposed to 4-DAMP and MEG. The effects of MEG were unlike those of cocaine which, at 10(-7) to 10(-5) M, increased the magnitude of contractions induced by ACh (10(-9) to 2 x 10(-3) M); MEG (10(-7) M) abolished this increase. The mechanism by which MEG relaxes tracheal smooth muscle has not been established, but it is likely to be independent of direct interaction with sites that mediate the effects of the bronchoconstrictor agents used in this study.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1985

Muscle relaxants for out-patient procedures.

The requirements for muscle relaxation in out-patient anesthesia are: a short total relaxation enabling the induction of an endotracheal tube followed by a period of 15-20 minutes of clinical relaxation. Reversal should be spontaneous. The new short acting muscle relaxants vecuronium and atracurium enable such a procedure, provided small doses are used (0.045 mg/kg for vecuronium or 0.2 mg/kg for atracurium. These small doses require a longer waiting time before intubation is easily performed (5 min for vecuronium and 6 min for atracurium). Spontaneous reversal of these small doses is achieved within 20-30 minutes. Potentiation of the relaxation by inhalational agents is not recommended.

Ambulatory Surgical Procedures↗
PubMed2004

Simulation of interaction between two non-depolarizing muscle relaxants: generation of an additive or a supra-additive neuromuscular block.

GOAL: To examine in a model of neuromuscular transmission the interaction between two non-depolarizing muscle relaxants. An additive or a supra-additive interaction was evaluated as a function of the affinities of acetylcholine and the muscle relaxants for the two binding sites at a single receptor. METHODS: Affinity of acetylcholine for site1 was postulated to be higher than for site2. Muscle relaxants may display a similar pattern of affinities, a higher affinity for site2, or the affinities may be identical. Receptors with both sites occupied by acetylcholine are activated and, if their concentration at an end plate surpasses the critical threshold, initiate contraction of the associated muscle fiber. The number of contracting muscle fibers determines twitch strength of the whole muscle. Neuromuscular block (NMB) = 1--twitch. NMB was simulated for muscle relaxants acting as single agents or in three types of combinations. (a) Complementary fractions of equieffective concentrations. (b) Variable combinations of equieffective concentrations producing NMB equal to NMB produced by the single muscle relaxant (isobolographic analysis), and (c) NMB-vs.-concentration relationship of single agents and of their combination in a fixed ratio. RESULTS: Additive interaction was simulated for pairs of muscle relaxants displaying identical ratios of affinities. All other pairs produce a supra-additive interaction, more prominent, the more divergent the patterns of affinities. The slopes of NMB-vs.-concentration curves were steeper for supra-additive combinations than for single agents. CONCLUSION: The simulations define conditions leading to additive or supra-additive interaction and suggest an experimental design suitable to test the results.

Acetylcholine↗
PubMed1997

Influence of anaesthesia and muscle relaxation on intubating conditions and sympathoadrenal response to tracheal intubation.

BACKGROUND: The study aimed to assess the relative influence of anaesthesia and muscle relaxation on intubating conditions and the haemodynamic and catecholamine responses to tracheal intubation. METHODS: Sixty ASA 1 or 2 patients were randomly assigned to one of four groups (15 patients each) that differed in the depth of anaesthesia (thiopentone plus fentanyl 2.5 microg x kg(-1) or thiopentone alone) and the degree of vecuronium-induced neuromuscular block (100% or > or =65%) at intubation. Muscle relaxation was measured at 0.1 Hz by means of mechanomyography. Heart rate (HR) and mean arterial blood pressure (MAP) were measured before and after induction of anaesthesia, and 1 min and 5 min following intubation, while adrenaline (A) and noradrenaline concentrations (NA) were determined from arterial blood samples. RESULTS: Intubating conditions were improved primarily by providing complete muscle relaxation at the adductor pollicis muscle (P<0.001) and to a lesser extent by adding fentanyl to thiopentone (P=0.04). The response of HR and MAP to tracheal intubation was attenuated mainly by fentanyl (P<0.001). Complete muscle relaxation further diminished the response of MAP to intubation (P=0.03). Changes in A and NA were dependent on the depth of anaesthesia only (P < or =0.01). CONCLUSION: The results of the study demonstrate that the sympathoadrenal response to intubation is attenuated by adding fentanyl (2.5 X kg[-1]) to an induction regimen with thiopentone, whereas provision of complete muscle relaxation at the adductor pollicis muscle is necessary to attain smooth intubating conditions.

Adolescent↗
PubMed1989

[Anesthetic management of a patient with dermatomyositis--clinical observation of the effect of muscle relaxants].

A 58 year old woman suffering from dermatomyositis underwent elective surgery for spinal caries. Concerning the anesthetic management of patient suffering from dermatomyositis, there is little information on the appropriate use of muscle relaxants. It is generally suspected that the patient is sensitive to nondepolarizing muscle relaxants. Anesthesia was with oxygen-nitrous oxide and fentanyl. Pancuronium 6 mg was given intravenously after awake intubation and an additional dose of 2 mg was given after 7.3 hours. During anesthesia neuromuscular function was monitored by neuromuscular transmission monitor (Datex Relaxograph). Duration of neuromuscular block was defined as the time for the twitch height to recover from total paralysis to 25% of the control value. Duration in this patient was 3.1 hours and this was longer as compared with the values of 1.1-1.8 hours obtained in 7 control patients. It is suggested that a usual dose of muscle relaxants results in a relatively higher effect in the patients with dermatomyositis because of their diminished muscle mass. The anesthetist should be careful in using muscle relaxants. The muscle relaxants should be given to such a patient with monitoring closely the neuromuscular function using a neuromuscular transmission monitor.

Anesthesia↗
PubMed1992

A primary role for protein kinase A in smooth muscle relaxation induced by adrenergic agonists and neuropeptides.

Many studies suggest that smooth muscle relaxation caused by beta-adrenergic agents and various neuropeptides occurs as a result of an increase in cellular adenosine 3',5'-cyclic monophosphate (cAMP). However, the evidence is indirect, and furthermore does not demonstrate that an increase in cAMP is essential for mediating relaxation. To define more clearly the role of cAMP in receptor-mediated smooth muscle relaxation, we used a specific competitive antagonist of the action of cAMP on protein kinase A, (R)-p-adenosine 3',5'-cyclic phosphorothioate [(R)-p-cAMPS], and its S isomer, (S)-p-cAMPS, which functions as a cAMP agonist. In gastric smooth muscle cells from guinea pig, (S)-p-cAMPS caused a dose-related relaxation [50% inhibitory concentration (IC50) 86 +/- 59 nM]. Vasoactive intestinal peptide (VIP) produced smooth muscle cell relaxation (IC50 2.3 +/- 0.8 nM) through occupation of specific VIP receptors. (R)-p-cAMPS inhibited VIP-induced relaxation, with a rightward shift in the VIP dose-response curve, suggesting competitive antagonism. Furthermore, (R)-p-cAMPS inhibited relaxation induced by other agents that increase cellular cAMP (isoproterenol, calcitonin gene-related peptide, and glucagon) but not that induced by ATP or sodium nitroprusside. (R)-p-cAMPS had no effect on contraction stimulated by carbachol, cholecystokinin, or substance P. These data demonstrate that activation of protein kinase A is primarily responsible for mediating gastrin smooth muscle relaxation produced by adrenergic agents and various neuropeptides.

Animals↗
PubMed1987

[Central muscle relaxant activities of 2-methyl-3-aminopropiophenone derivatives].

In this experiment, we synthetized new 2-methyl-3-aminopropiophenone (MP) derivatives, whose structure is known to have central muscle relaxant activities, and quinolizidine and indan . tetralin derivatives derived from MP by cyclization, and we investigated the central muscle relaxant activity. Among the quinolizidine derivatives, there was a very strong central depressant agent, trans (3H, 9aH)-3-(p-chloro) benzoyl-quinolizidine (HSR-740), and among the indan . tetralin derivatives, there was an excitant agents, trans (1H, 2H)-5-methoxy-3, 3-dimethyl-2-piperidinomethyl indan-1-ol (HSR-719). From the results, these derivatives were not considered to be adequate for central muscle relaxant. Among the MP derivatives, (4'-chloro-2'-methoxy-3-piperidino) propiophenone HCl (HSR-733) and (4'-ethyl-2-methyl-3-pyrrolidino) propiophenone HCl (HSR-770) strongly inhibited the cooperative movement in the rotating rod method using mice, and it exerted almost the same depressant activity on the cross extensor reflex using alpha-chloralose anesthetized rats. However, the inhibitory effects of HSR-733 on the anemic decerebrate rigidity and the rigidity induced by intracollicular decerebration in rats were weaker than those of HSR-770 and eperisone. In spinal cats, at a low dose (5 mg/kg, i.v.), HSR-733 depressed monosynaptic and dorsal root reflex potentials as compared with polysynaptic reflex potentials, and inhibitory effects of HSR-733 on these three reflex potentials were more potent than those of eperisone and HSR-770. Although HSR-770 acts on the spinal cord and supraspinal level on which eperisone has been reported to act, HSR-733 may mainly act on the spinal cord. These results indicate that the MP derivative with a 2-methyl group may be suitable as a central muscle relaxant. HSR-770, which has equipotent muscle relaxant activity to eperisone, exerted strong inhibitory effects on oxotremorine-induced tremor and weak inhibitory effects on spontaneous motor activity in the Animex method using mice, as compared with eperisone.

Animals↗
PubMed2003

Comparative analysis of nitric oxide and SALMFamide neuropeptides as general muscle relaxants in starfish.

Previous studies have established that the gaseous signalling molecule nitric oxide (NO) and the SALMFamide neuropeptides S1 and S2 cause cardiac stomach relaxation in the starfish Asterias rubens. Here we show that S1, S2 and the NO donor SNAP also cause relaxation of two other preparations from Asterias - tube feet and the apical muscle of the body wall. The rank order of effectiveness as muscle relaxants when tested at a concentration of 10 micro mol l(-1) was SNAP>S2>S1 for both tube feet and apical muscle whereas for cardiac stomach it was S2>S1>SNAP. Significantly, these data indicate that NO and SALMFamide neuropeptides function as general muscle relaxants in starfish but vary in their relative importance in different organ systems. The molecular mechanisms by which NO and SALMFamides cause muscle relaxation in starfish are not known, but previous pharmacological studies on the cardiac stomach using the soluble guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazol[4,3-a]quinoxalin-1-one (ODQ) indicate that the cyclic nucleotide second messenger cGMP may mediate effects of NO. Consistent with this hypothesis, here we report that ODQ also causes partial inhibition of the relaxing effect of SNAP on tube foot and apical muscle preparations. To further investigate the involvement of cyclic nucleotides as mediators of the effects of NO and SALMFamides on starfish muscle, we have measured both cGMP and cAMP in cardiac stomach and in apical muscle after treatment with S1, S2 or SNAP. However, no significant changes in cyclic nucleotide content were observed compared with controls. Further experiments were performed on apical muscle tissue in the presence of the cyclic-nucleotide-phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), a drug that also causes cardiac stomach relaxation in starfish. Treatment with IBMX caused a 2-3-fold increase above basal levels for cGMP and cAMP, but co-treatment with IBMX and S1 or S2 or SNAP resulted in no significant further increase above the level observed with IBMX alone. We conclude from these data that the relaxing action of NO on starfish muscle may be mediated by both cGMP-dependent and cGMP-independent pathways. However, the mechanisms by which SALMFamides cause muscle relaxation in starfish remain unknown and, although our results do not rule out the involvement of cGMP or cAMP, other signalling pathways may now need to be investigated.

1-Methyl-3-isobutylxanthine↗
PubMed1997

[Muscle relaxants. New substances and neuromuscular monitoring].

INTRODUCTION: Recent developments in both the quantitative evaluation of neuromuscular blockade and new muscle relaxants are reviewed. With respect to nerve stimulation, neuromuscular recording, and definition of parameters, the results of the 1994 Copenhagen International Consensus Conference are highlighted. Future clinical studies should adhere to these standards. MUSCLE RELAXANTS: Rocuronium, cisatracurium, and mivacurium are new muscle relaxants that were released for clinical use in 1995/1996. Of these, rocuronium has the shortest time of onset, whereas its recovery characteristics closely resemble those of vecuronium. Rocuronium is five times less potent than vecuronium. Twice the ED95 of rocuronium provides good or excellent intubating conditions within 60 to 90 s. Slight vagolytic effects were reported following injection of 0.6 mg/kg rocuronium, while histamine release was not observed. Cisatracurium is one of the ten steroisomers of atracurium. It is five times as potent as the chiral mixture while having a similar pharmacodynamic and -kinetic profile. Up to eight times the ED95 did not cause significant histamine release or clinically relevant cardiovascular effects. Mivacurium is a short-acting nondepolarizing benzylisoquinoline muscle relaxant that undergoes rapid break-down by plasma cholinesterase (PChE). Its duration of action is about one-half as long as that of equipotent doses of atracurium and vecuronium and three times as long as succinylcholine. Mivacurium has a moderate histamine-releasing potential. In patients with atypical or reduced PChE activity, the duration of action of mivacurium is prolonged.

Anesthesia↗
PubMed1991

Evaluation of a new reactive solid phase for radioimmunoassay of serum specific IgE against muscle relaxant drugs.

Until now, immunoassays for detection of anti-muscle relaxant IgE in serum have been performed with the drug coupled to epoxy-activated Sepharose or to RAST papers dics. In the present work we have used a quaternary ammonium-Sepharose in which the quaternary ammonium reactive group (choline chloride) was directly coupled to Sepharose via an ether linkage. 50 microliters of the quaternary ammonium solid phase (QAS) was incubated with 50 microliters of serum for 3 h, washed, incubated 18 h with 125I-anti-IgE and washed again. The results were expressed as the percentage of 125I-anti-IgE absorbed onto the solid phase. The results were at 1.3 +/- 0.5% for 20 control sera, with an upper normal limit estimated to 2.3%. The within-run reproducibility ranged from 3.2% to 10.0%. The results were significantly correlated with those obtained with either alcuronium-epoxy-Sepharose, choline-epoxy-Sepharose, the RAST-alcuronium or with the RAST-succinyl choline (respectively, r = 0.66, r = 0.80, r = 0.81, r = 0.40 and r = 0.85). The values obtained with the sera of 83 patients ranged from 0.3 to 38.5%. The sensitivity was estimated at 87.9%, 66.7% and 40.7% with the QAS-RIA, the RAST-succinyl choline and the RAST-alcuronium, respectively. The inhibition of adsorption of specific IgE onto the gel ranged from 13.0 to 90.6% in presence of 130 nmol of soluble muscle relaxants. In 83.3% of 30 cases, the highest inhibition was obtained with the muscle relaxant which was clinically incriminated.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcuronium↗
PubMed1998

Human supplementary motor area is active in preparation for both voluntary muscle relaxation and contraction: subdural recording of Bereitschaftspotential.

Bereitschaftspotentials (BPs) preceding muscle relaxation and contraction were compared by using subdural electrodes which were implanted onto the right medial frontal surface in two patients with supplementary motor area (SMA) seizure. The applied movement paradigm (muscle relaxation and contraction tasks) was completely the same as employed in our previous study [Terada, K., Ikeda, A., Nagamine, T. and Shibasaki, H., Electroenceph. clin. Neurophysiol., 95 (1995) 335-345]. In both patients, either negative or positive BPs were observed in the SMA-proper and supplementary negative motor area (SNMA) starting at 1.2-1.8 prior to both movements. In one patient, BP was more widespread in the relaxation task whereas more restricted to the hand area in the contraction task. In the other patient, the BPs were observed in the cortical area rostral to SNMA (pre-SMA), in addition to the SMA-proper, in both tasks. It is concluded that SMA-proper and SNMA, and probably pre-SMA as well, in humans are similarly active in preparation for both voluntary muscle contraction and relaxation.

Adult↗
PubMed2003

Conformation, action, and mechanism of action of neuromuscular blocking muscle relaxants.

Since curare was introduced into clinical anaesthesia in 1942, efforts to create better neuromuscular blocking (NMB) muscle relaxants have continued. Today, muscle relaxation remains a mainstay of modern anaesthesia and intensive care. Through manipulation of the traditional structure-action relationships, many new and improved muscle relaxants have been created, and several have been brought to clinical use. However, structure-action relationship is inconsistent and has its limits. Using computer-aided molecular conformational analyses, the conformation-action relationships of NMB agents of various chemical classes have been explored. Conformation, no less than structure, of the NMB agents has shed new light on their mechanisms of action. By reflection, the conformations also suggest new details of the topology of the receptive sites of the nicotinic acetylcholine receptor modeled for the motor endplate of the skeletal muscle.

Computer Simulation↗
PubMed2005

Inhibitors of prostaglandin transport and metabolism augment protease-activated receptor-2-mediated increases in prostaglandin E2 levels and smooth muscle relaxation in mouse isolated trachea.

Stimulants of protease-activated receptor-2 (PAR(2)), such as Ser-Leu-Ile-Gly-Arg-Leu-NH(2) (SLIGRL), cause airway smooth muscle relaxation via the release of the bronchodilatory prostanoid prostaglandin E(2) (PGE(2)). The principal aim of the current study was to determine whether compounds that inhibit PGE(2) reuptake by the prostaglandin transporter [bromocresol green and U46619 (9,11-dideoxy-9alpha,11alpha-methanoepoxy PGF2alpha) and PGE(2) metabolism by 15-hydroxyprostaglandin dehydrogenase (thiazolidenedione compounds rosiglitazone and ciglitazone) significantly enhanced the capacity of SLIGRL to elevate PGE(2) levels and produce relaxation in isolated segments of upper and lower mouse trachea. SLIGRL produced concentration-dependent increases in PGE(2) levels and smooth muscle relaxation, although both effects were significantly greater in lower tracheal segments than in upper tracheal segments. SLIGRL-induced increases in PGE(2) levels were significantly enhanced in the presence of ciglitazone and rosiglitazone, and these effects were not inhibited by GW9662 (2-chloro-5-nitrobenzanilide), a peroxisome proliferator-activated receptor-gamma antagonist. SLI-GRL-induced relaxation responses were also significantly enhanced by ciglitazone and rosiglitazone, whereas responses to isoprenaline, a PGE(2)-independent smooth muscle relaxant, were unaltered. Ciglitazone and rosiglitazone alone produced concentration-dependent increases in PGE(2) levels and smooth muscle relaxation, and these responses were inhibited by indomethacin, a cyclooxygenase inhibitor. Bromocresol green, an inhibitor of prostaglandin transport, significantly enhanced SLIGRL-induced increases in PGE(2) levels and relaxation. Immunohistochemical staining for 15-hydroxyprostaglandin dehydrogenase was relatively intense over airway smooth muscle, as was staining for the prostaglandin transporter over both airway smooth muscle and epithelium. In summary, inhibitors of PGE(2) reuptake and metabolism significantly potentiate PAR(2)-mediated increases in PGE(2) levels and smooth muscle relaxation in murine-isolated airways.

Animals↗
PubMed1999

Activities of the primary and supplementary motor areas increase in preparation and execution of voluntary muscle relaxation: an event-related fMRI study.

Brain activity associated with voluntary muscle relaxation was examined by applying event-related functional magnetic resonance imaging (fMRI) technique, which enables us to observe change of fMRI signals associated with a single motor trial. The subject voluntarily relaxed or contracted the right upper limb muscles. Each motor mode had two conditions; one required joint movement, and the other did not. Five axial images covering the primary motor area (M1) and supplementary motor area (SMA) were obtained once every second, using an echoplanar 1.5 tesla MRI scanner. One session consisted of 60 dynamic scans (i.e., 60 sec). The subject performed a single motor trial (i.e., relaxation or contraction) during one session in his own time. Ten sessions were done for each task. During fMRI scanning, electromyogram (EMG) was monitored from the right forearm muscles to identify the motor onset. We calculated the correlation between the obtained fMRI signal and the expected hemodynamic response. The muscle relaxation showed transient signal increase time-locked to the EMG offset in the M1 contralateral to the movement and bilateral SMAs, where activation was observed also in the muscle contraction. Activated volume in both the rostral and caudal parts of SMA was significantly larger for the muscle relaxation than for the muscle contraction (p < 0.05). The results suggest that voluntary muscle relaxation occurs as a consequence of excitation of corticospinal projection neurons or intracortical inhibitory interneurons, or both, in the M1 and SMA, and both pre-SMA and SMA proper play an important role in motor inhibition.

Adult↗
PubMed1996

Cyclobenzaprine, a centrally acting muscle relaxant, acts on descending serotonergic systems.

The centrally acting muscle relaxant cyclobenzaprine was thought to be an alpha 2-adrenoceptor agonist that reduced muscle tone by decreasing the activity of descending noradrenergic neurons. In the present study, we examined the effects of cyclobenzaprine on descending neurons by measuring the monosynaptic reflex in rats. Cyclobenzaprine reduced the monosynaptic reflex amplitude dose dependently and this effect was not inhibited by the alpha 2-adrenoceptor antagonists idazoxan and yohimbine. Cyclobenzaprine-induced monosynaptic reflex depression was not attenuated by noradrenergic neuronal lesions produced by 6-hydroxydopamine. However, cyclobenzaprine inhibited monosynaptic reflex facilitation induced by (+/-)-1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane, a 5-HT2 receptor agonist, in spinalized rats markedly, and 5-HT depletion by DL-p-chlorophenylalanine inhibited the depressive effect of cyclobenzaprine on the monosynaptic reflex. These results suggest that cyclobenzaprine is a 5-HT2 receptor antagonist and that its muscle relaxant effect is due to inhibition of serotonergic, not noradrenergic, descending systems in the spinal cord.

Adrenergic alpha-2 Receptor Antagonists↗