British journal of anaesthesia
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Randomized Controlled Trial Clinical Trial
Effect of nitrous oxide on cerebrovascular reactivity to carbon dioxide in children during sevoflurane anaesthesia.
Sevoflurane and nitrous oxide have intrinsic cerebral vasodilatory activity. To determine the effects of nitrous oxide on cerebrovascular reactivity to carbon dioxide (CCO(2)R) during sevoflurane anaesthesia in children, middle cerebral artery blood flow velocity (V(mca)) was measured over a range of end-tidal carbon dioxide concentrations (E'(CO(2))), using transcranial Doppler (TCD) ultrasonography. ⋯ Cerebrovascular carbon dioxide reactivity is reduced at and above an E'(CO(2)) of 45 mm Hg during 1.0 and 1.5 MAC sevoflurane anaesthesia. The addition of nitrous oxide to 1.5 MAC sevoflurane diminishes CCO(2)R in the hypocapnic range. This should be taken into consideration when hyperventilation techniques for reduction of brain bulk are being contemplated in children with raised intracranial pressure.
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Randomized Controlled Trial Clinical Trial
Effect of intravenous alizapride on spinal morphine-induced pruritus.
This double-blind study was undertaken to determine whether alizapride inhibits spinal morphine-induced pruritus. ⋯ Alizapride reduced the severity of morphine-induced pruritus.
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The pathophysiology of the serotoninergic system in malignant hyperthermia (MH) is not completely understood. The serotonin-2 (5HT(2A)) receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI) induces typical MH symptoms, including skeletal muscle rigidity, an increase in body temperature, hyperventilation and acidosis in conscious MH-susceptible (MHS) pigs. Whether these symptoms are directly generated in skeletal muscle, result from central serotonergic overstimulation or from a porcine stress syndrome remains unresolved. In this study the in vivo effects of DOI on anaesthetized (and thus stress-protected) MHS and MH-normal (MHN) pigs were investigated. ⋯ The comparability of the clinical presentation following DOI administration in MHS and MHN animals and the order of the development of MH-like symptoms favour the hypothesis of a central serotonergic overstimulation, leading to a serotonin syndrome.