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PubMed2000

[Acute low back pain: activity, NSAID's and muscle relaxants effective; bedrest and targeted exercise not effective; results of systematic reviews].

OBJECTIVE: To inventory the current state of the art regarding the effectiveness of conservative treatment of acute low back pain. DESIGN: Systematic reviews. METHOD: The relevant literature from the period January 1966-September 1999 was retrieved via Medline, Embase, Psychlit and the Cochrane Library and via reference lists in the articles found. The methodological quality of the studies was assessed using criteria for internal validity. On the basis of the number of examinations, their quality and the consistency of the findings, conclusions were subdivided into four levels of strength of scientific evidence. RESULTS: Approximately two-thirds of the randomised trials in the field of back pain were of poor methodological quality. There was strong evidence that advice to stay active, non-steroidal anti-inflammatory drugs (NSAIDs) and muscle relaxants were effective in acute low back pain. There was also strong evidence that bed rest and specific exercises were not effective in acute low back pain. Strong evidence for effectiveness of many other commonly used interventions was lacking.

Acute Disease↗
PubMed1991

Vascular smooth muscle relaxation by alpha 1-adrenoceptor blocking action of denopamine in isolated rabbit aorta.

We investigated the mechanism of vascular relaxation by denopamine (Deno), an oral positive inotropic agent that has selective beta 1-adrenergic action. Deno relaxed, dose-dependently (0.1-30 microM), ring segments of rabbit aorta, which were partially precontracted with 1 microM phenylephrine (Phe) or norepinephrine (NE), but did not relax those precontracted with 5 microM prostaglandin F2 alpha or 40 mM K+. The relaxation was not significantly inhibited by pretreatment with 10 microM propranolol or metoprolol. Deno produced parallel shifts in concentration-response curves to Phe, but this was not true for clonidine. The Schild plot analysis resulted in a linear regression of a slope of 1.075 +/- 0.063, which was not significantly different from unity, and the pA2 value of Deno against Phe was 5.57 +/- 0.02. The specific binding of [3H]prazosin to a rabbit aorta membrane preparation was displaced in a concentration-dependent manner by the simultaneous addition of Deno. The slope of a Hill plot was not significantly different from unity (1.102 +/- 0.147). The pK1 value for Deno calculated from the displacement curve was 5.29 +/- 0.17, which was not significantly different from the pA2 value of Deno. In conclusion, vascular smooth muscle relaxation by Deno was mediated by the blocking effect of alpha 1-adrenoceptors. Thus, these findings suggest that Deno may be effective in the treatment of congestive heart failure because it elicits a positive inotropic effect by beta 1-adrenergic action and vasodilation by alpha 1-adrenergic blocking action.

Adrenergic alpha-Antagonists↗
PubMed2000

Nitric oxide-induced cGMP accumulation in the mouse bladder is not related to smooth muscle relaxation.

The functional role of nitric oxide (NO) and the guanylate cyclase/cGMP second messenger system was investigated in the mouse bladder. Electrical field stimulation and the NO-donor 3-morpholino-sydnonimin hydrochloride (SIN-1) did not induce relaxation of the carbachol-precontracted bladder. However, sodium nitroprusside (10(-3) M) was found to enhance the contractile response to electrical field stimulation by 24+/-6% (n=8; P<0.05) without affecting the contractile response to carbachol. The enhancement of bladder contractility evoked by sodium nitroprusside was inhibited by the guanylate cyclase inhibitor 1H-[1,2, 4]oxadiazolo[4,3-a]quinoxalime-1-one (ODQ; 10(-6) M). Incubation of bladder strips with SIN-1 and sodium nitroprusside caused an increase in cGMP accumulation as measured by radioimmunoassay. Immunohistochemical studies showed cGMP-immunoreactivity in nerve fibres and in stromal cells, but not in smooth muscle bundles after exposure to NO-donors. The results show that NO-donors have no inhibitory effect on smooth muscle tone in the mouse bladder, but that NO may have a functional role as an excitatory neuromodulator. The targets of endogenous NO in the bladder may be the demonstrated cGMP-positive structures, i.e., nerves and stromal cells.

Animals↗
PubMed1992

Prolonged exposure to catecholamines enhances sensitivity of smooth muscle relaxation induced by sodium nitroprusside and atriopeptin.

Desensitization of alpha-1 adrenergic receptor-mediated contraction occurs in aortic smooth muscle from rats after in vitro exposure to norepinephrine (NE). The purpose of this study was to examine effects of pretreatment of blood vessels with catecholamines on relaxant responses of the vessels to sodium nitroprusside (SNP) and atriopeptin III (ANF). Vessels preincubated with NE for 4 hr had a markedly increased sensitivity to relaxation induced by SNP as compared to controls. The concentration of SNP giving half-maximal relaxation (log EC50) was -8.78 +/- 0.09 in the vessels pretreated with NE and -7.40 +/- 0.18 in controls (P less than .001). NE-treated vessels also had an increased sensitivity to ANF (EC50 -8.23 +/- 0.11 vs. -7.03 +/- 0.31, respectively; P less than .01). However, both desensitized and control vessels had similar sensitivity to relaxation induced by 8-bromo-cyclic GMP. The capacity of SNP to stimulate intracellular cyclic GMP accumulation in vessels pretreated with NE was greater than controls at a high concentration of SNP (10(-5) M.). However, there was no correlation between vasodilation induced by lower concentrations of SNP and stimulation of cyclic GMP accumulation in these blood vessels. Activity of soluble and particulate guanylate cyclase in NE-treated vessels was increased compared to controls. Changes in sensitivity of smooth muscle relaxation to SNP and ANF after prolonged exposure to catecholamines may relate to changes in capacity of the cyclic GMP system.

Animals↗
PubMed1999

The smooth muscle relaxant effects of venom from the inland taipan (Oxyuranus microlepidotus).

Venom (10 microg/ml) relaxed phenylephrine-precontracted aortae. This relaxation was unaffected by removal of the endothelium or a combination of N(G)-nitro-L-arginine (L-NOARG; 0.1 mM), oxyhaemoglobin (10 microM) and indomethacin (10 microM). 4-BPB (0.78 mM), propranolol (1 microM), or a combination of apamin (0.1 microM), charybdotoxin (0.1 microM) and glibenclamide (10 microM) did not effect endothelium-independent relaxation, suggesting a lack of PLA2 activity or an effect at beta-adrenoceptors or K+ channels. Venom (10 microg/ml) reversed Bay K 8644 (0.1 microM)-induced contraction indicating the venom may have an effect on L-type Ca2+ channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1992

Peripheral acting muscle relaxants alter the effects of baclofen on the electrocorticograms in the rat.

The effects of intraperitoneally administered baclofen on behavior and electrocorticograms (ECoG) were studied in freely moving and paralyzed rats. In the freely moving rats, 10 mg/kg of baclofen suppressed ECoGs with behavioral sedation, and 20 mg/kg caused whole body twitching accompanied with spike discharges in low voltage slow waves background. In the freely moving rats, baclofen acted as depressant in low dose and convulsant in high dose. In the paralyzed rat, 10 mg/kg of baclofen first suppressed ECoGs. Though fast waves components recovered with slow waves background in the ECoGs of rats paralyzed with gallamine (50 mg/kg) 3 hours after the baclofen injection, fast waves activities were not observed in the ECoG of rats paralyzed with succinylcholine (50 mg/kg), d-tubocurarine (3 mg/kg) or pancuronium (1 mg/kg). Under paralysis with d-tubocurarine, baclofen suppressed ECoG first, and then spike discharges started 90 min after the injection. These results suggest that the effects of baclofen on ECoG were different depending on the muscle relaxant used.

Animals↗
PubMed2002

Neuromuscular pharmacology of TAAC3, a new nondepolarizing muscle relaxant with rapid onset and ultrashort duration of action.

UNLABELLED: We selected bis [N-(3,4-diacetoxybenzyl) tropanium-3alpha-yl] glutarate dibromide (TAAC3) from many new tropinyl diester derivatives to evaluate its neuromuscular blocking (NMB) and autonomic side effects on anesthetized rats, rabbits, guinea pigs, cats, pigs, dogs, and monkeys. NMB potency, onset, recovery index, and duration of action were determined. Comparisons of these pharmacologic variables were made between TAAC3 and rocuronium. In the cat, the degrees of train-of-four and tetanic fade, posttetanic potentiation, and pharmacologic antagonism were evaluated. For determination of the NMB maintenance dose, TAAC3 was also given to rabbits and pigs in the initial dose/maintenance infusion mode. Cardiac vagal block was evaluated in the rat, pig, cat, and guinea pig on the basis of the inhibition of the bradycardia to stimulation of the vagus nerve. Sympathetic ganglion block was studied on the superior cervical ganglion-nictitating membrane preparation of the cat. TAAC3 produced nondepolarizing NMB. Its NMB 90% effective doses ranged from 90 to 425 microg/kg, depending on the species. TAAC3 had a faster onset (0.8-1.0 min), shorter recovery index (0.6-1.1 min), and shorter duration of action (1.8-3.5 min) than rocuronium. It produced a slight cumulative effect on infusion, but not on repeated single-dose administration. Cardiac vagal block was present at doses exceeding the NMB 90% effective dose. In the cat and pig at equipotent NMB doses, the degree of cardiac vagal block was similar to that of rocuronium. There was no demonstrable sympathetic ganglion block in the cat. In view of its favorable NMB characteristics, TAAC3 is now undergoing detailed preclinical studies. IMPLICATIONS: We developed a new nondepolarizing muscle relaxant, TAAC3, and investigated it in several animal models. TAAC3 has shown a very rapid onset and an ultrashort duration of neuromuscular blocking action. A minor degree of cardiac vagal block was observed. TAAC3 is promising for further studies.

Androstanols↗
PubMed1980

Apamin, a nonspecific antagonist of smooth muscle relaxants.

Apamin, a peptide of bee venom, was shown to inhibit the relaxant responses of guinea-pig taenia caeci to ATP, noradrenaline, adenosine and, less effectively, to stimulation of noradrenergic inhibitory nerves. Thus apamin acts nonspecifically and, contrary to the suggestion of Vladimirova and Shuba (1978), the fact that inhibitory responses due to nerve stimulation and ATP are blocked by the toxin does not allow conclusions as to the possible transmitter role of ATP in these nerves.

Adenosine↗