Accuracy of the Dinamap 1846 XT automated blood pressure monitor.

Accurate blood pressure (BP) measurement is important for the detection and treatment of hypertension. Despite widespread use of automated devices, there is limited published evidence for their reliability and accuracy. To determine the reliability and accuracy of the Dinamap 1846XT (Critikon Corporation, Tampa, FL, USA), a commonly used non-invasive oscillometric BP monitor The Dinamap was evaluated against the mercury manometer in 70 randomly selected adult hospitalised medical patients. Each individual underwent three sets of standardised BP measurement by automated method and three sets by mercury manometer by two independent observers. Reliability of BP measurement was assessed by repeated measures analysis. Dinamap accuracy was evaluated according to the American Association of Medical Instrumentation (AAMI) and British Hypertension Society (BHS) guidelines. Most patients were either normotensive or had stage I hypertension. The Dinamap tended to overestimate lower diastolic BP, and displayed poor reliability (P < 0.05). despite meeting aami guidelines, only 59% of systolic and 56% of diastolic dinamap readings were within 5 mm hg of the mercury manometer and 84% of systolic and 80% of diastolic readings were within 10 mm hg (bhs grade c). systolic and diastolic accuracy were worse with pressures >160/90 mm Hg (grade D) although these measures were based on a smaller sample of subjects. In conclusion the Dinamap yields inaccurate estimates of both systolic and diastolic BP even under standardised, and thus optimal conditions. This inaccuracy is exaggerated at higher BP (>160/90 mm Hg), although the number of measurements at higher pressures was small. We recommend that this device not be used when accurate BP measurement is needed for therapeutic decision-making.

Constrictive bronchiolitis and ulcerative colitis.

Pulmonary complications occur in an estimated 0.21% of patients with inflammatory bowel disease. The most common presentation of pulmonary manifestations is large airway disease, such as tracheobronchitis, chronic bronchitis or bronchiectasis. Small airway disease, such as constrictive bronchiolitis or bronchiolitis obliterans with organizing pneumonia, is less frequently reported, and is described as occurring in isolation from large airway disease. A case of a postcolectomy ulcerative colitis in a patient who has both large airway involvement, tracheobronchitis and bronchiectasis, and constrictive bronchiolitis is presented.

Ontogeny of the activity of alcohol dehydrogenase and aldehyde dehydrogenases in the liver and placenta of the guinea pig.

The objectives of this study were to elucidate the ontogeny of the activity of alcohol dehydrogenase (ADH), low Km aldehyde dehydrogenase (ALDH) and high Km ALDH in the liver and placenta of the guinea pig, and to determine the relationship between the relative activity of each enzyme in the guinea pig maternal-placental-fetal unit and the disposition of ethanol and its proximate metabolite, acetaldehyde. The enzyme activities were determined in maternal liver, fetal liver, and placenta of the guinea pig at 34, 50, 60 and 65 days of gestation (term, about 66 days), in the liver of the 2-day-old neonate, and in adult liver. There was low ADH activity in fetal liver and placenta throughout gestation and in neonatal liver. The fetal liver low Km ALDH activity increased progressively and, at 60 days of gestation, was similar to adult liver activity, as was also the case for neonatal liver enzyme activity. Placental low Km ALDH activity was less than adult liver activity throughout gestation. Fetal hepatic high Km ALDH activity increased during gestation, but was less than adult liver activity, as was also the case for neonatal liver enzyme activity. Placental high Km ALDH activity was low throughout gestation. For oral administration of 0.5 g ethanol/kg maternal body weight to pregnant guinea pigs at mid-gestation (34 days), the maternal blood and fetal body ethanol concentration-time curves were similar. Acetaldehyde was measurable in maternal blood and fetal body at similar concentrations, which were 100- to 1000-fold less than the respective ethanol concentrations. The major difference in the disposition of ethanol and acetaldehyde at near-term pregnancy, compared with mid-gestation, was the lack of measurable acetaldehyde in fetal blood. These results indicate that the guinea pig fetus throughout gestation has virtually no capacity to oxidize ethanol, and its duration of exposure to ethanol is regulated by maternal hepatic ADH-catalyzed biotransformation of ethanol. The fetus, however, appears to have increasing low Km ALDH-dependent capacity to oxidize ethanol-derived acetaldehyde during development, and would appear to be increasingly protected from exposure to acetaldehyde as gestation progresses.

No effect of chronic ethanol administration on the activity of alcohol dehydrogenase and aldehyde dehydrogenases in the near-term pregnant guinea pig.

The objective of this study was to determine the effect of chronic maternal administration of moderate-dose ethanol on alcohol dehydrogenase, low Km aldehyde dehydrogenase, and high Km aldehyde dehydrogenase activities in the guinea pig at near-term pregnancy. The activity of each enzyme in the maternal liver, fetal liver, and placenta of the guinea pig at 59 days of gestation (term, 66 days) was determined spectrophotometrically following chronic daily oral administration of two doses of 1 g ethanol/kg maternal body weight or isocaloric sucrose solution. There was no experimental evidence of ethanol-induced malnutrition in the mother or growth retardation in the fetus. There was a statistically significant increase (65%) in the microsomal cytochrome P-450 content of the maternal liver for the ethanol treatment compared with the sucrose treatment. The alcohol dehydrogenase, low Km aldehyde dehydrogenase, and high Km aldehyde dehydrogenase activities in the maternal liver, fetal liver, and placenta were not statistically different for the ethanol-treated compared with the sucrose-treated animals. This also was the case for the maternal blood and fetal blood ethanol and acetaldehyde concentrations, determined at 2h after maternal administration of 1 g ethanol/kg maternal body weight. These data demonstrate that the ethanol- and acetaldehyde-oxidizing enzyme activities in the maternal-placental-fetal unit of the guinea pig at near-term pregnancy were not changed by chronic administration of moderate-dose ethanol.