d tubocurarine/hypersensitivitet

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Intradermal histamine releasing effect caused by Org-NC 45. A comparison with pancuronium, metocurine and d-tubocurarine.

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Histamine release caused by Org-NC 45, pancuronium, metocurine and d-tubocurarine was determined by measuring the diameter of the redness and skin induration following the intradermal injection of these drugs. d-Tubocurarine and metocurine caused the largest diameter of redness and induration,

Positive intradermal tests to D-tubocurarine in patients with cholinergic urticaria.

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Patients with cholinergic urticaria exhibit increased hypersensitivity to cholinergic drugs. In the present study, an attempt was made to determine whether these patients would also cross-react to various neuromuscular blocking agents having structures analogous with acetylcholine. The four patients

Developmentally delayed sensitivity of acetylcholine receptor in myotubes of nerve-muscle cocultures from genetically diabetic mouse embryos.

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The neuromuscular junctions of genetically diabetic KK-CAy mice are reported to be hypersensitive to succinylcholine (SuCh) but not to d-tubocurarine (d-TC). Spinal cord-muscle cocultures from normal ddY and diabetic KK-CAy mouse embryos were studied to examine the involvement of genetic factors in

Intradermal histamine release by 3 muscle relaxants.

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The induration and redness caused by intradermal injections of equipotent doses of atracurium, vecuronium and d-tubocurarine were measured in six healthy, male volunteers. Atracurium and d-tubocurarine were almost indistinguishable in their reactions. Vecuronium caused a significantly smaller

[Histamine release due to ganglion blocking agent and muscle relaxants from rat mast cells].

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The mechanisms of histamine release due to d-tubocurarine from rat mast cells have long been known to anesthesiologists, such as degranulatory process, Ca++ dependent process and energy coupled process. However, not much is known about histamine release due to some drugs such as trimethaphan and

Diabetic state-induced modifications of succinylcholine binding mode in the microsomal fractions of mouse skeletal muscles.

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The skeletal muscles of alloxan-induced diabetic mice and genetically diabetic KK-CAY mice are hypersensitive to a depolarizing blocker, succinylcholine (SuCh) but not to the competitive antagonist, d-tubocurarine (d-TC). The mechanism by which the action of the depolarizing blocker is modified in

Reaginic antibodies to drugs used in anesthesia.

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Twenty-four patients survived life-threatening clinical anaphylaxis due to anesthesia. In each case the diagnosis of anaphylaxis was confirmed and the responsible drug was found by intradermal testing. To determine whether the reactions were anaphylactic or anaphylactoid, serum from each patient was

Anaphylaxis to muscle relaxants: cross sensitivity between relaxants.

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Two patients are described who had clinical anaphylaxis due to muscle relaxants. One patient had systemic hypersensitivity and positive intradermal tests to d-tubocurarine and alcuronium. The second had systemic hypersensitivity to d-tubocurarine and positive intradermal tests to d-tubocurarine,

Effects of atropine and neostigmine on receptor interaction at the neuromuscular junction.

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Rats treated chronically with atropine or atropine and neostigmine showed marked alterations in the responsiveness of receptors at the neuromuscular junction. Receptors in the phrenic nerve-hemidiaphragm interacting with d-tubocurarine were unaffected by atropine but exhibited a supersensitivity

[Prevention of the unwanted action of hydrocortisone on the growth and development of rat pups with cholinolytic preparations].

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Experiments on young rats have shown that diplacin and d-tubocurarine in doses amounting to 1/15-1/20 of LD50 lower the ability of hydrocortisone to interfere with the physical development of the animals. Metamisyl, metacin, gangleron and benzohexonium have no such properties. In adult rats and

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