[Anesthetic management of a patient with transfusion-related acute lung injury (TRALI)].

Transfusion-related acute lung injury (TRALI) is characterized by pulmonary edema and hypoxemia within 6 hours of transfusion in the absence of other causes of acute lung injury or circulatory overload and is now considered the leading cause of transfusion-related death. We report a female patient who showed hypoxemia after transfusion without any other causes of acute lung injury. The patient is a 43-year-old woman, who received emergency transurethral hemostasis for bladder hemorrhage with hematuria and low hemoglobin concentration (3.2 g x dl(-1)). General anesthesia was maintained with sevoflurane, remifentanil, and vecuronium. Two units of RBC were transfused during operation. Since she showed high blood pressure, tachycardia, and a painful expression after operation, we extubated her. Although we gave her O2 6 l x min(-1) after extubation, she showed low oxygen saturation (90%), thus we started bag-mask ventilation. However, she complained of dyspnea and the chest X-ray revealed bilateral diffuse pulmonary edema following hypoxemia (80%). Thus we inserted endotracheal tube and started positive pressure assist ventilation. The next day, hypoxemia was improved under PEEP therapy. The anti-HLA antibody in the transfused plasma was positive. We conclude that the early recognition and management of TRALI is essential during and after operation.

Muscarinic receptor subtypes modulate the release of [3H]-noradrenaline in rat spinal cord slices.

Spinal muscarinic receptors are involved in the mediation of antinociceptive effects. The modulation of noradrenaline (NA) release on muscarinic receptor subtypes in the rat spinal cord was investigated in in vitro perfusion experiments. After rat spinal cord slices were preincubated in [3H]NA, the slices were perfused with a superfusion apparatus. The slices were field stimulated during the 4th (S1) and 11th (S2) superfusion collection periods. Perfusion of drugs was initiated at the 8th collection period and was maintained until the 14th collection period. Fractional release was calculated as the percentage of the radioactivity present in the slices at the beginning of the stimulation period. Drugs were administered between S1 and S2. The following drugs were used: [3H]NA, neostigmine, pirenzepine (M1 antagonist), AFDX116 (M2 antagonist), atropine. Neostigmine significantly increased the release of [3H]NA in a concentration-dependent manner. Pirenzepine (1 microM) and atropine (0.3 microM) significantly reduced the release of [3H]NA, but AFDX116 (1 microM) did not significantly reduce release in the presence of neostigmine (1 microM). The results of this study indicate that neostigmine can enhance noradrenergic neurotransmission, and that acetylcholine can stimulate spinal cord NA release via M1 muscarinic receptor subtypes.

[A comparison of two methods for continuous cardiac output measurement: PulseCO VS CCO].

BACKGROUND: PulseCO (PulseCO) (PulseCO Hemodynamic Monitor, LiDCO Co., London, England) is a low invasive apparatus to measure cardiac output continuously from arterial pulse waveform. CCO (774 HF 75, Edwards Lifescience Co., California, USA) is a continuous cardiac monitor commonly used clinically. The purpose of this study is to compare the accuracy of these two methods for cardiac output measurement with the thermodilution technique (TDCO) as control. METHODS: To compare the accuracy of PulseCO with that of CCO, six patients with pulmonary-artery catheter inserted were recruited. PulseCO and CCO were measured continuously, and these CO values were compared with TDCO measurements every hour. RESULTS: Correlation with TDCO was examined in PulseCO (r=0.82) and CCO (r=0.80). CONCLUSIONS: PulseCO was low invasive, and showed a significantly better correlation with TDCO, compared with CCO.

[Determination of cotinine in human urine by gas chromatograph-mass spectrometry].

A gas chromatograph-mass spectrometric assay has been developed for the quantitation of cotinine, the major metabolite of nicotine, in human urine. Extraction or condensing procedure was not required and the method reduced time involved in sample preparation. The analytes were separated on the fused-silica capillary column. The operating conditions were: injector, 250 degrees C; detector, 280 degrees C; column, 50-250 degrees C. The total gas flow-rate of helium (carrier) was 50 ml.min-1 and the pressure of column inlet was 100-200 kPa. The retention time was 18.1 min and the limit of quantitation was 5 ng.ml-1. This method provides an easy and simple assay for the detection of cotinine in clinical settings.

Halothane attenuated haloperidol and enhanced clozapine-induced dopamine release in the rat striatum.

The effect of halothane anesthesia on changes in the extracellular concentrations of dopamine (DA) and its metabolites (3-methoxytyramine (3-MT), 3,4-dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA)) induced by neuroleptics was studied using in vivo microdialysis techniques. Halothane attenuated haloperidol-induced dopamine release and enhanced clozapine-induced dopamine release in the rat striatum.A microdialysis probe was implanted into the right striatum of male SD rats. Rats were given saline or the same volume of 200 microg kg(-1) haloperidol (D(2) receptor antagonist), 10 mg kg(-1) sulpiride (D(2) and D(3) antagonist), or 10 mg kg(-1) clozapine (D(4) and 5-HT(2) antagonist) intraperitoneally with or without 1-h halothane anesthesia (0.5 or 1.5%). Halothane anesthesia did not change the extracellular concentration of DA, but increased the metabolite concentrations in a dose-dependent manner. The increased DA concentration induced by haloperidol was significantly attenuated by halothane anesthesia, whereas the metabolite concentrations were unaffected. Halothane had no effect on the changes in the concentrations of DA or its metabolites induced by sulpiride. The clozapine-induced increases in DA and its metabolites were enhanced by halothane anesthesia. Our results suggest that halothane anesthesia modifies the DA release modulated by antipsychotic drugs in different ways, depending on the effects of dopaminergic or serotonergic pathways.