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tubocurarine/inflamação

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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)
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
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
Under physiological conditions, the small intestine represents a barrier against harmful antigens and pathogens. Maintaining of the intestinal barrier depends largely on cell⁻cell interactions (adherent-junctions) and cell⁻matrix interactions (tight-junctions). Inflammatory bowel disease is

Pharmacological characterization of conotoxin lt14a as a potent non-addictive analgesic.

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Conotoxin lt14a is a small peptide consisting of 13 amino acids. It was originally identified from the cDNA of Conus litteratus in the South China Sea. Previous reports showed lt14a exhibited antinociceptive activity using a hot plate-induced pain mouse model and acted as an antagonist of neuronal

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
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
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)

Acetylcholine beyond neurons: the non-neuronal cholinergic system in humans.

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Animal life is controlled by neurons and in this setting cholinergic neurons play an important role. Cholinergic neurons release ACh, which via nicotinic and muscarinic receptors (n- and mAChRs) mediate chemical neurotransmission, a highly integrative process. Thus, the organism responds to external
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