Isolated Rectus Abdominis Muscle Research Articles

Isolated rectus abdominis muscle recurrence of endometrial cancer

Isolated rectus abdominis muscle recurrence of endometrial cancer

Effect of portulaca olearecea and its interaction with vecuronium on neuromuscular junction in experimental animals

Background: The extracts from the plant Portulaca oleracrea have been mentioned to have muscle relaxant properties in traditional medicine literatures and used as a food supplement. The site of therapeutic action is directly on muscle fibres rather than neuromuscular transmission.The muscle relaxant property is found to be similar with dantrolene in frog rectus abdominis .So objectives of our study to analyze the effect of Portulaca oleracea and its interaction with vecuronium on the neuromuscular junction in experimental animal.Methods: The study was conducted in two parts i.e. study 1 and study 2. In study 1:2 ml and 4 ml Portulaca oleracea fresh aqueous leave juice was given orally to 12 number rabbits and vecuronium 5 microgram/ml was given intravenously to all 6 rats through marginal ear vein with the help of scalp vein attached with 10 ml syringe. The head drop time is recorded and reversal of neuromuscular blockade was done with neostigmine (0.25 mg/kg) along with atropine (2 mg). Study 2: 2 ml and 4 ml of Portulaca oleracea fresh aqueous leave juice was tested on frog's isolated rectus abdominis muscle in Dales’s isolated organ bath and its interaction with vecuronium (1 mmole-32 mmole) was recorded.Results: Portulaca oleracea has muscle relaxant properties, which was recorded which was indicated by decreasing the time of head drop and complete block in study 1. In study 2, it also decreased the Ach induced contraction in presence of vecuronium.Conclusions: The results indicate the muscle relaxant properties fresh juice of Portulac Oleracea probably due to high content of potassium.

Rectus Abdominis Endometrioma after Caesarean Section.

Isolated rectus abdominis muscle endometriosis is very uncommon with less than 20 case reports being published to date since its first description in 1984 by Amato and Levitt. We report another case of isolated rectus abdominis endometriosis in a 37-year-old patient with a previous caesarian section. We also discuss the diagnostic and treatment particularities in these patients. In our case, the treatment was only surgical and currently the patient is disease-free during the 24-month follow-up.

Action of mefloquine on toad isolated rectus abdominis muscle.

The effects of mefloquine and quinine on acetylcholine-induced contractures of the toad rectus abdominis muscle have been investigated. Both drugs depressed acetylcholine-induced contractures in a dose-related and non-competitive manner. A partial reversal of the block was observed in the presence of 4-aminopyridine (10, 50 microM) and increased Ca2+ content (1.25x) of the Ringer solution. In both cases, the mefloquine-induced blockade was more readily reversed than that induced by quinine. Mefloquine and quinine at concentrations greater than 100 and 500 microM, respectively, also elicited a direct contractile response on the muscle. Quantitative differences in their contractile activity have been attributed to the greater lipid solubility and tissue binding affinity of mefloquine.

Pharmacological activity of N-methyl-carbamylcholine, a novel acetylcholine receptor agonist with selectivity for nicotinic receptors

N-Methyl-carbamylcholine (also called N-methyl-carbachol) is an analogue of the mixed muscarinic-nicotinic acetylcholine receptor agonist, carbachol. Previous studies have provided evidence that radiolabelled N-methyl-carbachol can bind selectively to nicotinic acetylcholine receptors in rat brain. To determine whether N-methyl-carbachol acts as an agonist or an antagonist at nicotinic and/or muscarinic receptor sites, the present study examined the pharmacological activity of this compound on some cholinergically innervated tissues. N-Methyl-carbachol, like carbachol, depolarized rat isolated sympathetic ganglia and these effects were inhibited by a nicotinic antagonist, d-tubocurarine, but not by a muscarinic antagonist, atropine. Exposure of rat sympathetic ganglia to N-methyl-carbachol blocked the compound action potential generated in ganglia by stimulation of the pre-ganglionic trunk; this effect of N-methyl-carbachol was likely due to desensitization of the nicotinic response. N-Methyl-carbachol, like carbachol, stimulated the release of [ 3H]noradrenaline from cultured adrenal medullary cells that had been pre-loaded with [ 3H]noradrenaline; these effects were largely inhibited by a nicotinic antagonist, mecamylamine, while atropine produced less blockade. N-Methyl-carbachol contracted the frog isolated rectus abdominis muscle and the effect was completely blocked by d-tubocurarine. By contrast, contracture of the rectus abdominis produced by carbachol was partially inhibited by either atropine or d-tubocurarine. N-Methyl-carbachol, like carbachol, contracted the rat isolated ileum and these effects were completely blocked by atropine; however, N-methyl-carbachol was about 42 times less potent than carbachol for this effect. Intravenous injection of N-methyl-carbachol, like nicotine, to the rat produced a transient decrease followed by a more sustained rise in blood pressure while carbachol produced only a sustained decrease in blood pressure. The effects of N-methyl-carbachol and nicotine on blood pressure were blocked by pretreatment of the animal with a nicotinic antagonist, hexamethonium. N-Methyl-carbachol, like nicotine, stimulated the release of [ 3H]dopamine from rat striatal synaptosomes, pre-loaded with [ 3H]dopamine; release induced by either N-methyl-carbachol or nicotine was inhibited by mecamylamine but not by atropine. In rat cerebral cortical slices pre-loaded with [ 3H]inositol, carbachol, but not N-methyl-carbachol, stimulated the accumulation of [ 3H]inositol-1-phosphate, an effect blocked by atropine but not by mecamylamine. Behavioural effects of intracerebroventricular administration of N-methyl-carbachol to rats included reversible hind-limb splaying, impaired gait, respiratory depression and hypoactivity at early times after drug injection; these effects were blocked by pretreatment of animals with mecamylamine but were unaffected by pretreatment with a muscarinic antagonist, scopolamine. Thus the overall profile of activity indicates that N-methyl-carbachol is a relatively selective agonist acting at nicotinic acetylcholine receptors. These results suggest that the structures of muscarinic and nicotinic receptors may differ in the regions which recognize the amino terminal end of compounds such as carbachol or N-methyl-carbachol.

A comparison of the actions of 4-aminopyridine, caffeine and quinine on the toad isolated rectus abdominis muscle

1. 4-Aminopyridine (4-AP)-induced contractures have been compared with those evoked by caffeine and quinine on the toad rectus abdominis muscle. 2. All three compounds produced slowly-developing sustained contractures. The time to half maximal contracture and relaxation was significantly longer for 4-AP than for caffeine or quinine. 3. Verapamil and manganese inhibited 4-AP, caffeine and quinine-induced contractures. 4. Ca 2+-free-EGTA Ringer and procaine severely inhibited caffeine and quinine responses, but 4-AP contractures were relatively unaffected. 5. In depolarizing (100 mM K +) Ringer solution, caffeine and quinine responses were reduced to 6–9% of their controls. 4-AP responses were reduced by about 25%. 6. It is concluded that in the toad rectus muscle, 4-AP-induced contractures differ from those produced by caffeine and quinine, and appear to rely mainly on the release of intracellular located Ca 2+, while caffeine and quinine are considered to act predominantly on plasma membrane sites.

CIMETIDINE AND RANITIDINE: A STUDY OF COMPETITIVE AND ION‐CHANNEL BLOCKADE IN THE TOAD ISOLATED RECTUS ABDOMINIS MUSCLE

Responses of the toad isolated rectus abdominis muscle to cumulative doses of carbachol were recorded in the absence or presence of varying concentrations of cimetidine or ranitidine. The corresponding cumulative log concentration-response curves for carbachol were then plotted for each antagonist studied. Cimetidine (1 mmol/l) produced a straight and parallel 1.8-fold shift of the carbachol curve to the right of the corresponding control curve with no significant change in the maximal response. Cimetidine, at doses of 2.5 mmol/l and 5 mmol/l, and ranitidine, at doses of 0.1 mmol/l, 0.25 mmol/l and 0.5 mmol/l, produced a concentration-dependent and non-parallel shift of the carbachol curve to the right of the corresponding control curve accompanied by a marked decline of maximal responses. The results provide further evidence that ion-channel block may be involved in the neuromuscular blockade produced by cimetidine or ranitidine, the latter being more potent in this respect. Competitive antagonism may also be partly responsible for cimetidine-induced neuromuscular blockade, especially at lower drug concentrations.

ANTICHOLINESTERASE ACTIVITY OF AND POSSIBLE ION‐CHANNEL BLOCK BY CIMETIDINE, RANITIDINE AND OXMETIDINE IN THE TOAD ISOLATED RECTUS ABDOMINIS MUSCLE

Responses of the toad isolated rectus abdominis muscle to cumulative doses of acetylcholine were recorded in the absence or presence of varying concentrations of cimetidine, ranitidine or oxmetidine. The corresponding cumulative log concentration-response curves for acetylcholine were then plotted for each antagonist studied. Cimetidine (5 mmol/l), ranitidine (1 mmol/l) and oxmetidine (0.02 mmol/l) potentiated the effect of acetylcholine by 4-fold, 2.6-fold and 1.3-fold, respectively. At higher concentrations all three histamine H2-receptor antagonists produced a concentration-dependent and non-parallel shift of the acetylcholine curve to the right of the corresponding control curve accompanied by a depression of the maximal response. The results provide further evidence that the H2-antagonists studied possess anticholinesterase activity and also suggest that the H2-antagonists may produce neuromuscular blockade by ion-channel block. The clinical implications of the results obtained are also discussed.

Morphine-induced supersensitivity to acetylcholine in skeletal muscle and its mechanism of action

The effect of in vitro morphine pretreatment (250 μM) on the sensitivity of skeletal muscle to acetylcholine (ACh) was investigated using the isolated rectus abdominis muscle of frog. Morphine (15 or 120 min) significantly increased the sensitivity of the tissue to ACh. This increase in the sensitivity was found to be the greatest after 120 min. Morphine significantly increased the sensitivity of the tissue to carbachol only after 120 min. In the presence of physostigmine, morphine did not cause further augmentation of responses to ACh. Potassium chloride-induced contractile responses were not influenced by morphine. In the presence of morphine, maximum contractile responses to ACh were significantly decreased. Highly calcium (1.62 mM) in the medium decreased the magnitude of the morphine-induced supersensitivity to ACh at 120 min and antagonised the decrease in maximum contractile responses to ACh. These results suggest that morphine is causing supersensitivity by both its anticholinesterase activity and its inhibitory action on presynaptic nerve terminals.

Antioxotremorine action of propranolol.

1. The influence of propranolol on the neuromuscular, tremor-producing and muscarinic effects of oxotremorine was examined. 2. In the isolated rat phrenic nerve-diaphragm preparation the neuromuscular blocking effect of oxotremorine was inhibited by propranolol in a dose-dependent manner. 3. Propranolol intensified the paralytic effect of tubocurarine in the rat diaphragm and prevented antagonism of tubocurarine paralysis by tetraethylammonium. 4. Propranolol was devoid of any curare-like effect in the isolated rectus abdominis muscle of the frog. 5. Vasodepressor responses to oxotremorine in rats and spasmogenic responses to oxotremorine in guinea-pig ileum were not antagonized by propranolol. 6. A dose-dependent antagonism of oxotremorine-induced tremor in mice was observed after pretreatment with propranolol and it is suggested that this effect is due to an antagonism of a presynaptic effect of oxotremorine at skeletal neuromuscular junctions.

The effect of metronidazole on striated muscle

Metronidazole potentiated contractions of the frog isolated rectus abdominis muscle to acetylcholine but it did not potentiate contractions of the muscle to carbachol. It was shown on the same preparation that metronidazole prevented the destruction of acetylcholine by sheep serum cholinesterase. Metronidazole potentiated the contractions of the rat isolated diaphragm to stimulation of teh phrenic nerve. It also antagonised tubocurarine-induced neuromuscular blockade to stimulation of the phrenic nerve. It si suggested that metronidazole produces these effects by acting as an anticholinesterase.

The effect of antiadrenaline compounds on acetylcholine responses of frog rectus abdominis muscle.

1. Nine antiadrenaline compounds and ergometrine have been examined for their effect on acetylcholine (ACh)-induced contractures of the frog isolated rectus abdominis muscle.2. Tolazoline caused potentiation (pP(2)=4.14 at 7 min). Slightly higher concentrations of tolazoline caused antagonism (pA(2)=3.68 at 37 min).3. No potentiation of ACh responses was seen with any of the remaining compounds, which all antagonized ACh responses. Phenoxybenzamine gave the highest, and ergometrine the lowest, pA(2) values.4. In the concentrations needed to determine pA(2), yohimbine and ergometrine also had other effects on the muscle.5. These results are discussed in the context of previous findings.

RELATIVE ACTIONS OF QUATERNARY METHYL DERIVATIVES OF TYRAMINE, DOPAMINE AND NORADRENALINE.

Tyramine methiodide and dopamine methobromide have greater pressor effect (three- to five-times) in the spinal cat than the parent amines. Noradrenaline methochloride has little pressor effect. Dopamine methobromide is about four times as potent as nicotine; tyramine methiodide is about equiactive to nicotine; and noradrenaline methochloride has only one-tenth the potency of nicotine. Their pressor effects are usually abolished by hexamethonium but in some experiments the effect of noradrenaline methochloride persisted and was then abolished by tolazoline. Injected intravenously into the cat anaesthetized with chloralose, each of the three quaternary derivatives contracts the nictitating membrane; dopamine methobromide is again the most active, having more than six times the potency of nicotine. When the contractions of the nictitating membrane are induced by continuous stimulation of the preganglionic fibres of the cervical sympathetic nerve, intravenous injection of the quaternary derivatives of tyramine and dopamine has a biphasic effect; there is a block on which a contraction of the membrane appears to be superimposed. Noradrenaline methochloride produces only a further contraction of the membrane. On the isolated rectus abdominis muscle preparation of the frog, dopamine methobromide is the most active in contracting the muscle, being about twelve times as active as nicotine; noradrenaline methochloride is weakest, having only one-hundredth the activity of nicotine. These effects are antagonized by hexamethonium. On the isolated phrenic nerve-diaphragm preparation of the rat, the quaternary derivatives of tyramine and dopamine each have neuromuscular blocking properties, 0.7- and 3-times respectively that of nicotine. Noradrenaline methochloride has no effect. In the sciatic nerve-tibialis preparation of the cat, the quaternary derivatives of tyramine and dopamine are approximately equipotent in producing neuromuscular paralysis, having about three times the activity of nicotine and one-fifth that of suxamethonium. These effects are not antagonized either by neostigmine or by edrophonium. Noradrenaline methochloride has no neuromuscular blocking effect. The nicotine-like properties of these quaternized sympathomimetic amines are discussed. It is of interest that the presence of an hydroxyl group attached to the beta-carbon atom of the side-chain greatly reduces nicotine-like activity. By comparison, choline had about one forty-fifth the pressor activity of ethyltrimethylammonium.

Assay of suxamethonium and laudexium on the frog rectus abdominis.

Suxamethonium, like acetylcholine, causes contracture of the isolated rectus abdominis muscle of the frog, whereas laudexium antagonizes this effect. These actions may be used to assay both drugs with reasonable speed and fiducial limits, provided that changes in responsiveness of the preparation during the course of assay are met by suitable design and analysis. Small quantities of suxamethonium and laudexium may be assayed in certain body fluids.