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Biomedical subjects

R R Mercer

Publications and source records attributed to R R Mercer.

42 records · Page 3Linked to original sources
PubMed1984

Alterations in lung structure caused by inhalation of oxidants.

Morphometric and morphologic methods have been used to evaluate changes in rat lungs caused by the inhalation of a variety of oxidants. Exposure to 100% oxygen causes diffuse pulmonary injury and leads to death after 66-72 h of exposure. The primary insult leading to death in rats exposed to hyperoxia is injury to pulmonary capillary endothelium. Sublethal exposure to hyperoxia was found to cause diffuse injury to all major components of the alveolar septum and was associated with destruction of approximately 50% of the pulmonary capillary endothelial cells. A corresponding decrease in pulmonary capillary surface area and capillary lumen volume also occurred. Exposure to ozone and to nitrogen dioxide in low concentrations did not cause a diffuse injury throughout the alveolar region of the lung, but rather led predominantly to structural alterations in terminal bronchioles and in their adjacent alveoli. Morphometric evaluation of animals exposed to 0.25 ppm ozone and to 2 ppm NO2 demonstrated quantitatively and qualitatively similar lesions. These lesions primarily involve injury and remodelling of the alveolar epithelium. These changes in the alveolar epithelium were also associated with the recruitment of increased numbers of alveolar macrophages to the proximal alveolar region. The different types of lung injury caused by various oxidants are most likely to be related to differences in their reactivity with tissue components and to differences in concentration, distribution, and diffusion characteristics of the oxidant gases.

Animals↗
PubMed1983

Effects of prenatal nitrofen exposure on postnatal lung function in the rat.

The herbicide Nitrofen was administered by gavage to pregnant F-344 rats during Days 10 through 13 of gestation. Postnatal lung function was measured in male progeny at 3 and 6 weeks of age. There were no differences in body weight or wet and dry lung weights between control and Nitrofen-exposed rats in either age group. Nitrofen produced no observable effects on lung function at 3 weeks of age. However, by 6 weeks of age the Nitrofen-exposed animals had significant decreases in tidal volume (p less than 0.01), vital capacity (p less than 0.01), total lung capacity (p less than 0.05), and quasi-static lung compliance (p less than 0.01). There was also a mild ventilation inhomogeneity, as indicated by significant increases in the nitrogen washout slope (p less than 0.01) and the moment ratio (p less than 0.05). Histopathology of lung, liver, kidney, and testes was not significantly altered by Nitrofen exposure. These data suggest that prenatal Nitrofen exposure may have an effect on postnatal lung maturation in the rat and could potentially be useful as a model of pulmonary hypoplasia.

Aging↗
PubMed1982

Oxygen consumption measured with microcomputer-assisted Warburg manometry.

We have developed and tested an automated system that measures in vitro oxygen consumption by Warburg manometry in as many as 16 units that are under the simultaneous control of a microcomputer which requires attention at the beginning of the study only. The all-glass Submarine Volumometers used are readily adapted to automation using a microcomputer that interacts with an infrared photodetector sensitive to manometric changes in the reaction vessel and a stepper motor that can advance the calibrated micrometer in response to these changes. The microcomputer interacts with the user at the start of the study during data entry and subsequently determines volume changes related to oxygen consumption, calculates respiration rates, and prints or graphs the results without further user interaction. We compared this automated system with manual methods by measuring the oxygen consumption of lung tissue slices and by determining the ability of the system to match known volumes entered manually. We found that the results obtained using the automated system were not significantly different from known manual methods (P less than 0.05).

Animals↗
PubMed1982

Dose response of elastase-induced emphysema in hamsters.

Elastase-induced emphysema in hamsters was studied using pulmonary function tests in an effort to develop techniques for determining the effects of air pollutants on the progression of this disease. Single intratracheal injections of 6, 12, or 24 units of porcine pancreatic elastase produced dose-related changes in pulmonary function after 4 wk when compared with sham-injected control animals. Boyle's law end-expiratory volume and residual volume, measured by gas dilution, increased (p less than 0.05) at 12 and 24 units, respectively, whereas vital capacity, determined plethysmographically, and total lung capacity wee increased (p less than 0.05) at all 3 elastase doses. Respiratory system compliance, calculated by a nonlinear least squares regression fit of the deflation pressure-volume curve, increased (p less than 0.05) at 24 units only. The multiple-breath nitrogen washout slope (N2 slope) and the single-breath diffusing capacity for carbon monoxide (DLCO) decreased (p less than 0.05) at all 3 doses of elastase. Both histologic and physiologic evaluation showed dose-related pulmonary impairment. It appears, therefore, that as little as 6 units of elastase produces mild emphysema in hamsters, which is detectable by pulmonary function testing. Of these tests, the DLCO and N2 slope were the most effective in detecting the degree of impairment.

Animals↗
PubMed1978

Servo control of end-tidal CO2 in paralyzed animals.

We are reporting an electronic circuit which uses the peak end-tidal CO2 signal from a rapid infrared CO2 analyzer to vary the motor rate of a fixed volume respirator. It contains variable gain and a lag compensation network which permits critical damping to prevent oscillation. The CO2 analyzer, circuitry, and respirator are connected in a closed-loop servo system that allows automatic control of the CO2 level. The system's gain and performance are such that it can accommodate large changes of CO2 return to the lungs with no more than +/- 0.5 Torr carbon dioxide pressure (PCO2) error signal. It has proved useful in experiments on neural respiratory control in paralyzed animals where it is desired to keep PCO2 constant despite changes in cardiac output and venous and CO2 return to the lungs, and to monitor the approximate magnitude of these changes.

Carbon Dioxide↗