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Carbon monoxide diffusion

Fiber R and M Karplus 1990. Enhanced Sampling in Molecular Dynamics Use of the Time-Dependent Hartree Approximation for a Simulation of Carbon Monoxide Diffusion through Myoglobin. Journal of the American Chemical Society 112 9161-9175. [Pg.650]

Chest constriction impaired carbon monoxide diffusion capacity decrease in lung function without exercise... [Pg.373]

Elber, R. Karplus, M., Enhanced sampling in molecular-dynamics - use of the time-dependent Hartree approximation for a simulation of carbon-monoxide diffusion through myoglobin, J. Am. Chem. Soc. 1990,112, 9161-9175... [Pg.319]

Changes in pulmonary function have been observed in a variety of species after short-term exposure to ozone, including alterations in the elastic behavior of the lungs, increased resistance to flow, and decreased carbon monoxide diffusion capacity. [Pg.332]

A short-term study of guinea pigs exposed to zinc oxide fume 3 hours/day for 6 days at the threshold limit value (TLV) of 5mg/m revealed pulmonary function changes and morphologic evidence of small airway inflammation and edema. Pulmonary flow resistance increased, compliance decreased, and lung volumes and carbon monoxide diffusing capacity decreased. Some of these changes persisted for the 72-hour duration of postexposure follow-up. [Pg.751]

Carbon monoxide is produced by the incomplete combustion of fuel, and since it readily diffuses through heated iron, it frequently happens that iron stoves, used for heating purposes in large buildings, constitute a source of this gas m the air, the carbon monoxide diffusing into the building, instead of being earned up the chimney or burned. [Pg.180]

More sophisticated techniques than the ones used by Haldane have estabhshed that CO binds to hemoglobin with an affinity 200 times greater than that of oxygen (Ernst and Zibrak, 1998 Roughton and Darling, 1944 Sendroy et al, 1930). Carbon monoxide diffuses from the alveoh to the blood in pulmonary capillaries across the alveoh-capillary membrane, which is composed of pulmonary epithelium, the capillary epithelium, and the fused basement membranes of the two. The uptake of CO by Hb is very rapid and the transfer of CO is diffusion limited (Prockop and Chichkoa, 2007). [Pg.277]

A 77-year-old man who had taken amiodarone 400 mg/day for 11 months developed crackles at the lung bases and scattered respiratory wheeze (76). His leukocyte count was raised at 13.5 x 109/1 and he had progressive reduction in carbon monoxide diffusing capacity, serially measured. A chest X-ray showed bilateral opacities in the upper zones, peripheral in distribution, and a CT scan showed dense bilateral lung parenchjmal opacities. The symptoms of dyspnea on exertion, cough with minimal sputum, pleuritic chest pain, and low-grade fever abated after withdrawal, and the upper lobe densities resolved. [Pg.153]

In 25 patients, three had proven interstitial pneumonitis and KL-6 serum concentrations of 414, 848, and 1217 U/ ml in contrast, all of the other 22 patients had normal CT scans and normal KL-6 concentrations (under 500 U/ml) (82). In the same study the limitations of carbon monoxide diffusing capacity in the diagnosis of amiodarone-induced lung disease (SEDA-15, 168) were again demonstrated. [Pg.154]

Beryllium compromises the immune system. Enzymes catalyzed by magnesium or calcium can be inhibited by beryllium succinic dehydrogenase is activated. Beryllium exposure leads to a deficiency in lung carbon monoxide diffusing capacity. Hypercalcemia (excess of calcium in the blood) can occur. [Pg.266]

Diffusion Carbon monoxide diffusing capacity Measurement of efficiency of alveolar gas exchange decreases with thickening of alveolar blood-air barrier... [Pg.2270]

The majority of patients with pulmonary hypertension are largely asymptomatic until marked vascular alterations have developed. When blood flow through the pulmonary artery is obstructed over a long period of time, however, the clinical picture is predictable and markedly uniform. In general, the patients exhibit normal pulmonary function measurements, a low carbon monoxide diffusion capacity (DlCO), and marked hyperventilation that leads to hypocapnia and decreased serum bicarbonate concentrations. Additional symptoms include weakness, fatigue, exertional dyspnea, and chest pains upon exertion due to low cardiac output and hypoxemia. Occasionally, hoarseness, hemoptysis, and cyanosis occur. [Pg.373]

Several animal inhalation toxicity studies have been conducted on various jet fuels (summarized in Table 4-2). In one study, male F344 rats were exposed to shale-oil-derived JP-4 continuously for 90 days by inhalation at 1,000 mg/m3. The exposure resulted in no effects on lung volumes, dynamic resistance and compliance, quasistatic compliance, partial and full forced vital capacities, carbon monoxide diffusion capacity, and closing volume. There... [Pg.45]

IV. Diagnosis is based on a history of exposure to asbestos (usually at least 15-20 years before onset of symptoms) and clinical presentation of one or more of the syndromes described above. Chest x-ray typically shows small, irregular, round opacities distributed primarily in the lower lung fields. Pleural plaques, diffuse thickening, or calcification may be present. Pulmonary function tests reveal decreased vital capacity and total lung capacity and impairment of carbon monoxide diffusion. [Pg.122]

An experimental human exposure study titled Tetrachloroethylene Development of a biologic standard for the industrial worker by breath analysis, completed by Stewart and colleagues, was first published by NIOSH in 1974. This publication can now be obtained from the National Technical Information Service (NTIS) with a 1981 date, and is cited as Stewart et al. (1981) throughout this Profile. In this study, four male volunteers were sequentially exposed to 0, 20, 100, or 150 ppm tetrachloroethylene vapor for 7.5 hours/day, 5 days/week (Stewart et al. 1981). The men were exposed to each concentration for 1 week. Once each week, pulmonary function was assessed at both rest and during two levels of exercise with forced maximum expiratory flow measurements, while alveolar-capillary gas exchange was measured by single breath carbon monoxide diffusion. The exposures to tetrachloroethylene at these vapor concentrations and time intervals had no effect on the pulmonary function measurements. [Pg.44]

American Association for Respiratory Care, 1999, Clinical Practice Guideline Single-breath Carbon Monoxide Diffusing Capacity, Respir. Care, 44(5) 539-546. [Pg.565]

American Thmacic Society, 1995, Single Breath Carbon Monoxide Diffusing Capacity (transfer factor), Am. Rev. Respir. Dis., 152 2185-2198. [Pg.566]

Inhaled insulin In 251 patients with type 1 diabetes who used insulin lispro and insulin glargine, compared with 249 patients using AIR inhaled insulin and insulin glargine in a 6-month randomized trial, nocturnal hypoglycemia was more frequent in those who used AIR insulin, especially in the first month [12 ]. Those who used AIR insulin also had more frequent cough (28 patients compared with 14), dyspnea (5 patients compared with 0), and reduced carbon monoxide diffusing capacity in the lungs. More of those who used insulin lispro completed the study (217 versus 192). [Pg.686]


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See also in sourсe #XX -- [ Pg.545 ]




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