Home oximetry studies for diagnosis of sleep apnea/hypopnea syndrome: limitation of memory storage capabilities.

BACKGROUND: Memory oximeters enable diagnostic studies for sleep apnea hypopnea syndrome (SAHS) to be performed in the home. However, memory capabilities may be limited. STUDY OBJECTIVES: To compare a pulse oximeter used at home with an 8-h memory, storing data every 12 s, and in the laboratory, with on-line recording every 2 s. DESIGN: Prospective cohort study. SETTING: Patients' homes and a sleep laboratory. PATIENTS: One hundred patients with suspected SAHS. MEASUREMENTS: Home oximetry and a laboratory full polysomnography. The number of >/= 4% dips in pulse oximetric saturation (SpO(2)) was calculated for each study. Daytime sleepiness was assessed by the Epworth Sleepiness Scale (ESS) score. RESULTS: The mean dips per hour were 5.3/h (range, 0 to 53/h) for home studies and 13.4/h (range, 0 to 106/h) for laboratory studies; the relationship between home and laboratory studies was as follows: home = (0.4 x laboratory) - 0.01 +/- 11.2; r(2) = 0.64. Mean difference was 8.4/h (- 2.5 to + 77.9/h), which correlated with the mean of the measurements. At a cutoff point of 10/h, 52 studies were both negative and 13 studies were both positive. Nineteen home studies were false-negatives. Sensitivity was 0.41, and specificity was 1.0. In these 19 studies, 7 patients had an ESS score > 10 and 4 patients had an ESS score > 14. To confirm that differences were due to different sampling rates, 16 additional patients had on-line data and stored data collected simultaneously in the laboratory. Mean dips per hour were 3.2/h (range, 0.1 to 18.3/h) for the stored data and 8.34/h (0.2 to 22.8/h) for on-line data; the relationship being stored was as follows: 0.5 on-line - 1.17 +/- 2.6; r(2) = 0.69. Mean difference was 5.2/h (0.04 to 15.4 h), which correlated with the mean of the measurements. CONCLUSION: Home studies using a memory storage pulse oximeter may underestimate the number of hypoxic dips, probably due to sampling rates. Clinically significant hypoxic SAHS may therefore be missed.

The distribution of [125I]ricin in mice following aerosol inhalation exposure.

Studies were conducted to examine the uptake and redistribution of [125I]ricin from the lungs of mice following nose-only aerosol inhalation exposure. Radiolabelled contents were measured in lung and various extra-pulmonary tissues 15 min through 30 h following 10 min aerosol exposures. Pharmacokinetic analyses were performed on whole-organ data obtained for lungs, stomach, liver and spleen. Radioactivity within the lungs, maximal at 15 min post-exposure, was eliminated in a biexponential fashion with a long beta half-life (approximately 40 h). Large amounts of radiolabel were also found within the gastrointestinal tract. Radiolabel within the stomach exhibited an absorption phase and two-compartment elimination. Radiolabel content of many other tissues, including known accumulation sites for intravenously administered toxin, was significantly (p < 0.05) increased (relative to 15 min post-exposure) in association with the early elimination of radiolabel from the lungs, but levels in these tissues were very low and did not increase after 4 h post-exposure. The only exception was our sample of trachea, which showed delayed elevations in radiolabel (peak at 24 h); this pattern was attributable to the contained thyroid (not removed at necropsy) and its trapping of free [125I] released upon tissue [125I]ricin degradation. The overall data indicate that ricin administered by aerosol inhalation is delivered to both respiratory and gastrointestinal tracts; however, it is not extensively transported from either tract to other potential target sites. Ricin delivered to the lungs is primarily sequestered within the lungs until degradation. Only small amounts of ricin delivered to the gastrointestinal tract are absorbed into the circulation.

Evaluation of a new electronic spirometer: the vitalograph "Escort" spirometer.

BACKGROUND: The "Escort" spirometer is a lightweight, hand held spirometer employing a Fleisch pneumotachograph. Measurements of forced expiratory volume in one second (FEV1), forced vital capacity (FVC), and peak expiratory flow (PEF) are obtained from a single FVC manoeuvre. Results are displayed on a small liquid crystal display, but there is no graphical display. The performance of the Escort spirometer has been compared with that of a wedge bellows spirometer (Vitalograph S model) and a Wright PEF meter. METHODS: One hundred and thirteen subjects performed three FVC manoeuvres on the wedge bellows and Escort spirometers and three PEF manoeuvres on the Wright meter. The best reading for each index was recorded. In 21 of the subjects comparison of a Wright manoeuvre with an FVC manoeuvre on the Escort spirometer was performed, whilst in three subjects the effect of repeated blows was studied. RESULTS: The FEV1 ranged from 0.5 to 5.4 litres, FVC from 1.05 to 6.2 litres, and PEF from 100 to 725 l/min. The mean (SD) difference for the FEV1 was -0.05 (0.15) (95% confidence interval (95% CI) -0.07 to -0.02) litres, for FVC 0.03 (0.28) (95% CI -0.02 to +0.08) litres, and for PEF 1.68 (50.6) (95% CI -7.7 to +11.1) l/min. The differences were positively correlated with the mean reading for PEF and FVC but not for FEV1. The Wright PEF manoeuvre performed on the Escort produced significantly higher PEF readings (mean difference -22.9 litres). There was no significant effect of repeated FVC manoeuvres on any of the indices. CONCLUSIONS: The Escort spirometer compares extremely well with a wedge bellows spirometer for measurement of FEV1 and FVC, whilst yielding results of PEF from an FVC manoeuvre which are comparable to those obtained from a Wright meter. It can be recommended for use as a portable hand held spirometer.

Proadifen-induced production of prostacyclin by equine peritoneal macrophages.

A study was performed to determine the effect of proadifen hydrochloride on prostacyclin (prostaglandin I2 [PGI2]) and thromboxane A2 (TxA2) synthesis by equine peritoneal macrophages and the effect of proadifen on endotoxin-induced synthesis of PGI2 and TxA2 by equine macrophages. Peritoneal macrophages (2.5 x 10(6)/ml) were incubated for 6 hours in tissue culture media containing 1) nothing (nontreated control), 2) proadifen hydrochloride (20, 100, 250, and 500 mumol/L, 3) endotoxin (5 ng/ml), or 4) the calcium ionophore A23187 (0.95 mumol/L). In a second series of experiments, peritoneal macrophages were incubated with endotoxin (5 ng/ml) and proadifen (250 umol/L), for 6 hours. Concentrations of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2, the stable metabolites of PGI2 and TxA2, were determined in the incubation media by radioimmunoassay. Proadifen caused increased synthesis of PGI2 by equine macrophages, without affecting TxA2 production. The increased PGI2 production was similar to that induced by endotoxin and calcium ionophore; however, the latter 2 agents significantly stimulated TxA2 production as well (P less than 0.05). There were no significant differences among mean concentrations of 6-keto-PGF1 alpha in media from macrophages treated with 100, 250, or 500 mumol/L proadifen, but there was a significant curvilinear regression between their concentrations. The ratio of thromboxane B2 to 6-keto-PGF1 alpha was significantly lower than baseline in incubation media from macrophages exposed to proadifen, endotoxin, and calcium ionophore. Proadifen hydrochloride did not significantly change equine peritoneal macrophage production of PGI2 or TxA2 in response to endotoxin.