We applied a dialysis technique to the hearts of anesthetized cats and examined whether the concentration of dialysate norepinephrine (NE) reflected NE disposition at the cardiac sympathetic nerve terminals. Dialysis probes were implanted in the left ventricular wall, and dialysate NE concentrations were measured as an index of myocardial interstitial NE levels. Stimulation of stellate ganglia significantly increased dialysate NE responses that were suppressed by local administration of an NE-releasing inhibitor (omega-conotoxin GVIA, 10 microM). Increments in basal dialysate NE levels were correlated with concentrations of a locally administered neuronal uptake blocker (desipramine; 1, 10, and 100 microM). Desipramine (100 microM) augmented stimulation-induced dialysate NE responses. Local administration of a neuronal vesicle uptake blocker (reserpine, 1 and 10 microM) did not alter dialysate NE levels but increased dialysate dihydroxyphenylglycol levels. An NE-releasing amine (tyramine, 100 microg/ml) was locally administered to examine NE storage capacity at the nerve terminal. The tyramine-induced NE-releasing response was completely abolished by pretreatment with reserpine (1 mg/kg i.p.). Thus cardiac dialysis with local administration of a pharmacological tool offers a new, concise approach to assessment of neuronal NE release, uptake, vesicle uptake, and storage capacity by cardiac sympathetic nerve terminals.

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During controlled mechanical ventilation, minute ventilation rather than tidal volume affected the accuracy of cardiac output measurement using the partial carbon dioxide rebreathing technique. When spontaneous breathing is present, the carbon dioxide rebreathing technique is less accurate and increases spontaneous tidal volume and respiratory rate.

In this study, we compared three gas compositions to determine if the duration of apnoea for SpO2 to decrease is proportionate to the oxygen fraction of the gas prior to apnoea. Twenty-five patients ASA physical status 1-2 aged two months to 12 years were included in the study. Anaesthesia was induced via a mask with 5% sevoflurane and 66% N2O in oxygen. After paralysis with vecuronium (0.12 mg.kg-1, i.v.) the trachea was intubated and anaesthesia was maintained with sevoflurane and N2O in oxygen. When cardiovascular stability was obtained, the patient was randomly set to breathe one of three gas compositions: 1. oxygen (FiO2 1.0), 2. N2O/O2 (FiO2 0.4), and 3. air/O2 (FiO2 0.4). All three gas compositions included 2-4% of sevoflurane to maintain anaesthesia. After more than eight min of each gas breathing, apnoea was begun by disconnecting the breathing circuit from the tracheal tube. The time from the start of apnoea (SpO2 100%) to SpO2 of 95% (T95) was measured. T95 measured after breathing N2O/O2 and air/O2 were 34.6 +/- 5.7 and 28.8 +/- 4.7% of that measured after oxygen breathing (P < 0.001 vs oxygen breathing, P < 0.001 vs oxygen and N2O/O2 breathing), respectively. Preoxygenation before intubation was validated to delay the haemoglobin desaturation brought about by apnoea. An induction technique using a low FiO2 will allow rapid haemoglobin desaturation.

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