d tubocurarine/възпаление

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Indomethacin/ibuprofen-like anti-inflammatory agents selectively potentiate the gamma-aminobutyric acid-antagonistic effects of several norfloxacin-like quinolone antibacterial agents on [35S]t-butylbicyclophosphorothionate binding.

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Four piperazinoquinolone antibacterial drugs (norfloxacin, ciprofloxacin, enoxacin, and pipemidic acid), known to be gamma-aminobutyric acid (GABA) antagonists, fully reversed the inhibitory effect of GABA on [35S]t-butylbicyclophosphorothionate ([35S] TBPS) binding to rat brain membranes in vitro.

Propofol enhances a d-tubocurarine-induced twitch depression in septic rat diaphragm.

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We estimated the effect of d-tubocurarine (dTc) on neuromuscular transmission and the action of propofol on dTc-induced twitch depression by using sham control and septic rat nerve-hemidiaphragm preparations in vitro. Isometric twitch tension elicited by indirect (phrenic nerve) or direct (muscle)

Chronic intraperitoneal endotoxin treatment in rats induces resistance to d-tubocurarine, but does not produce up-regulation of acetylcholine receptors.

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BACKGROUND Chronic systemic inflammation resulting from intraperitoneal Eschevichia coli endotoxin administration or Corynebacterium injections induces tolerance to non-depolarizing neuromuscular blockers in rodents. Although this has been explained as up-regulation of muscle acetylcholine receptors

Sepsis attenuates the intensity of the neuromuscular blocking effect of d-tubocurarine and the antagonistic actions of neostigmine and edrophonium accompanying depression of muscle contractility of the diaphragm.

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BACKGROUND Prolonged effects of non-depolarizing muscle relaxants in septic patients have been reported, although the influence of sepsis on neuromuscular transmission has not yet been clarified satisfactorily. These studies were intended to elucidate the influence of sepsis on neuromuscular

Neuromuscular dysfunction in burns and its relationship to burn size, hypermetabolism, and immunosuppression.

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The etiology of neuromuscular (NM) dysfunction following burn injury has not been characterized. NM deficits, together with hypermetabolism and immunosuppression, are debilitating processes which play a key role in the morbidity and mortality of burned patients. This study examined the usefulness of

Cecal ligation and puncture peritonitis model shows decreased nicotinic acetylcholine receptor numbers in rat muscle: immunopathologic mechanisms?

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BACKGROUND Although systemic inflammation is believed to cause upregulation of nicotinic acetylcholine receptors (nAchRs) in muscle, chronic infections such as Chagas' disease occasionally are complicated by myasthenia gravis. The authors investigated how a nonlethal cecal ligation and puncture

Acetylcholine stimulates bronchial epithelial cells to release neutrophil and monocyte chemotactic activity.

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Bronchial asthma is accompanied by inflammatory cell infiltration in the airway. Increased bronchial reactivity to cholinergic stimulation is well recognized in patients with bronchial asthma. Thus, we postulated that acetylcholine (ACh) stimulates bronchial epithelial cells (BEC) to release

[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

Effect of Bothrops insularis venom on the mouse and chick nerve-muscle preparation.

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The effects of Bothrops insularis venom were examined in vivo in mice and chicks and in vitro using the mouse phrenic nerve diaphragm and chick biventer cervicis muscle preparations. Incubation of the indirectly or directly stimulated mouse preparation with B. insularis venom (20-80 micrograms/ml)

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