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Tracheal intubation of outpatients with and without muscle relaxants.

PURPOSE: To compare intubating conditions and postoperative myalgias in outpatients after intubation with propofol/alfentanil compared with propofol/alfentanil/succinylcholine with and without precurarisation with d-tubocurarine. METHODS: 144 ASA I-II ambulatory patients for dental extraction under anesthesia were studied. Subjects received either 3 mg d-tubocurarine (Group II) or saline (Groups I, III) i.v. prior to induction of anesthesia with 20 microg x kg(-1) alfentanil and 2.5 mg x kg(-1) propofol followed by 1.5 mg x kg(-1) succinylcholine (II and III) or saline 0.9% (I) for muscle relaxation. The ease of airway management and the postoperative incidence, severity and distribution of muscle pains were examined. RESULTS: Intubation was successful in all patients and there were no differences in jaw mobility, ease of bag-mask ventilation, visualization of the vocal cords or cord position. Limb movement was more common during intubation in Group I (37.5%) than in Group III (8.3%) or Group II (2%), P < 0.05. At home, VAS scores for myalgia were higher in Group III than in Group I and II. Neck myalgia was more common in Group II (72%) than in Groups II (44%) and I (41%), P < 0.05. Myalgias were also more common in Group III patients (P < 0.05). CONCLUSION: Acceptable intubating conditions were achieved with propofol and alfentanil alone. Succinylcholine reduced limb movement during intubation but was associated with postoperative myalgias for up to five days. Precurarisation with tubocurarine reduced the severity of succinylcholine myalgia.

Adolescent↗

Decreased number of acetylcholine receptors is the mechanism that alters the time course of muscle relaxants in myasthenia gravis: a study in a rat model.

BACKGROUND: In myasthenic patients, the time course of action of non-depolarizing neuromuscular blocking agents is prolonged and the sensitivity is increased. We used our antegrade perfused rat peroneal nerve anterior tibialis muscle model to investigate if this altered time course of effect and sensitivity can be explained by the decreased acetylcholine receptor concentration that is caused by the disease. METHODS: Functional acetylcholine receptors were reduced by administration of alpha-bungarotoxin or by injecting monoclonal antibodies against rat acetylcholine receptors (experimental autoimmune myasthenia gravis). After induction of anaesthesia, the model was set up and perfusion of the tibialis anterior muscle with blood was started. After stabilization of the twitch, rocuronium or pancuronium were infused until 90% block was obtained. Twitch data and infusion data were recorded and used to calculate the time course of effect and potency. RESULTS: The potency of neuromuscular blocking agents was increased and the offset of the neuromuscular block was prolonged in both the alpha-bungarotoxin groups and the experimental autoimmune myasthenia gravis groups compared to controls. CONCLUSION: This study shows that the increased sensitivity to neuromuscular-blocking agents in myasthenia gravis can be accounted for by a decreased number of acetylcholine receptors. It also shows that the antegrade perfused rat peroneal nerve anterior tibialis muscle model is a suitable model to study the effects of myasthenia gravis on the time course of effect of neuromuscular blocking agents.

Androstanols↗

Inhibition of endothelium-dependent smooth muscle relaxation by calmodulin antagonists.

By using the calmodulin antagonists, calmidazolium and N-(6-aminohexyl)-5-chloro-1-naphthalene-sulfonamide (W-7), the hypothesis was investigated as to whether calmodulin is involved in the sequence of events leading to the endothelium-dependent vascular smooth muscle relaxation. Endothelium-dependent relaxations were studied on two different preparations, the rabbit aorta and the pulmonary artery of the guinea pig. Relaxations were produced in the precontracted rings (noradrenaline 3 X 10(-6) mol/l) in response to acetylcholine, 10(-8) to 10(-6) mol/l (aorta), histamine, 3 X 10(-8) to 1 X 10(-6) mol/l (pulmonary artery) or the calcium ionophore A 23187, 1 X 10(-8) to 3 X 10(-7) mol/l (aorta and pulmonary artery). In the presence of calmidazolium and W-7 the endothelium-dependent relaxation was inhibited in a dose dependent manner. This inhibition was seen in a concentration range that coincides with calmodulin inhibition. The half maximal concentrations of calmidazolium for the inhibition of the relaxation of the aorta induced by acetylcholine and A 23187 were 3 X 10(-6) mol/l and 1.4 X 10(-6) mol/l and that of W-7 were 3.1 X 10(-5) and 3.6 X 10(-5) mol/l, respectively. Complete inhibition was obtained both for acetylcholine-and for A 23187-induced relaxations by preincubation with 1 X 10(-5) mol/l calmidazolium or 1 X 10(-4) mol/l W-7. The half maximal concentrations of calmidazolium for the inhibition of the relaxation of the pulmonary artery in response to histamine and A 23187 were 2.7 X 10(-6) mol/l and 3 X 10(-6) mol/l and complete inhibition was achieved at 1 X 10(-5) mol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

Interaction of muscle relaxant effect of gallamine with ethanol: in vivo mammalian model.

Ethanol produces alterations in muscular contraction and neuromuscular function both in vitro and in vivo in mammalian and amphibian tissues in dose dependent manner. It is not very well known whether gallamine, a commonly used muscle relaxant produces any interaction with ethanol. Hence in the present study, interactions of ethanol with gallamine are undertaken using rabbit head drop method. The latency time to produce head drop by gallamine in the absence and presence of ethanol (dose which produce ataxia) was insignificantly different (P > 0.05). It may be due to fact that ataxic dose may not be affecting neuromuscular transmission a significant manner. It, therefore, does not warrant to adjust the dose of gallamine in alcoholic persons.

Animals↗

The variability of inter-spike intervals of human spindle afferents in relaxed muscles.

The impulse discharge in single afferent units was recorded in waking human subjects. Tungsten needle electrodes were percutaneously inserted in the left radial nerve, and activity in muscle spindle afferents from the extensor muscles of the forearm were studied while the subjects remained relaxed. Thirty-six spontaneously discharging single units were studied, 16 primaries, 10 secondaries and 10 non-classified. The regularity of afferent discharge and the shape of the inter-spike interval histograms was assessed by off-line statistical analysis of stationary segments of afferent discharge. The mean discharge rate of both primary and secondary afferents was generally low. Secondaries predominantly fired with low variability, whereas primaries showed high as well as low variability, but the median values for the two groups differed significantly. However, the individual unit values of coefficient of variation showed a considerable overlap between the two groups. The size of the coefficient of variation in the human spindle afferents was between that of de-efferented and of intact afferents in decerebrated cats. Determination of the coefficient of variation may therefore help, as a complementary criterion, to differentiate between primary and secondary afferents in man.

Adult↗

[Anaphylactoid reactions to muscle relaxants].

Anaphylactoid (i. e. anaphylactic-like) reactions have been estimated to occur in between one in 600 and one in 1,000 general anaesthesias. Two thirds of these reactions are caused by neuromuscular blocking drugs used during anaesthesia. An anaphylactoid potential is inherent in all muscle relaxants, albeit to a varied extent, reflecting an obligatory feature of their molecular structure (quaternary ammonium groups) and common physicochemical characteristics. Hence, also newer relaxants are not void of anaphylactoid risk. In Britain, the recent availability of drug-specific radioallergosorbent tests (RAST) has initiated much controversy on preanaesthetic antibody screening and possible medicolegal consequences. Since every anaesthetist must expect to be faced with such an unforeseen and occasionally life-threatening reaction, the characteristic clinical manifestations, basic therapeutic strategies and current opinion on underlying pathophysiological mechanisms are summarized in this review article. Based on the recommendations of the British National Adverse Anaesthetic Reaction Advisory Service (NAARAS), essential diagnostic procedures during and after anaphylactoid events are discussed. Finally, prophylactic precautions including the preoperative administration of H1- and H2-antihistamines are recommended.

Anaphylaxis↗