PubMed Health⌕ Search

Biomedical subjects

J D Crapo

Publications and source records attributed to J D Crapo.

At least 163 records · Page 9Linked to original sources
PubMed1982

Lung tissue and capillary blood volumes by rebreathing and morphometric techniques.

Gas rebreathing measurements of lung tissue volume (Vt) and pulmonary capillary blood volume (Vc) were made in five anesthetized dogs. After the rebreathing measurements, the lungs were inflation fixed with glutaraldehyde and analyzed morphometrically. Each lung was morphometrically divided into alveolar and nonalveolar compartments and each compartment was divided into its air, tissue and blood components. Average rebreathing and morphometric measurements of Vc were 42 and 84 ml, respectively. The reasons for this difference remain unclear. The rebreathing Vt (198 ml) was 40 ml (25%) greater than the morphometric alveolar tissue and blood components (158 ml). Assuming that the rebreathing technique measures all of the alveolar compartment, the rebreathing measurement includes a significant fraction of the nonalveolar compartment.

Animals↗
PubMed1982

A copper-deficient, zinc-supplemented diet produces emphysema in pigs.

A mild form of emphysema was produced in pigs raised on a copper-deficient, zinc-supplemented diet. The copper-requiring enzyme, lysyl oxidase, catalyzes the cross-linking of tropoelastin into mature elastin. Zinc further inhibits the activity of lysyl oxidase. Lungs from animals raised on copper-deficient, zinc-supplemented diets of demonstrate perforations in alveolar walls and diminished amounts of elastin bronchi and pulmonary arteries. Mean linear intercepts are greater and alveolar internal surface areas are less than those in control animals, fulfilling the generally accepted definition of emphysema. Physiologic confirmation is provided by a leftward shift of the saline volume-pressure curves when compared with those in control animals. Ultrastructurally, the alveolar walls are effaced and pores of Kohn are enlarged. There are areas in which elastin is absent leaving remnant microfibrils, and there are other changes consistent with active elastin synthesis. Biochemical data demonstrate no difference in elastin content as micrograms/ml of fat-free dry weight but do demonstrate increased collagen content in experimental animal lungs compared with that in control lungs. Ultrastructural similarities to enzyme-induced models of emphysema suggest the presence of elastin degradation in our model. We speculate that although the copper-deficient, zinc-supplemented state may stimulate protein synthesis in general, elastin is being degraded by endogenous means, but collagen is not.

Air Pressure↗
PubMed1982

Cell number and cell characteristics of the normal human lung.

Eight normal human lungs obtained from patients dying from causes not related to the lung were subjected to morphometric analysis to determine the number of cells in the alveolar region and their mean volume and surface characteristics. The age range was 19 to 40 yr, average body weight was 74 kg, and the average fixed lung volume was 4,300 ml. The overall mean nuclear diameters of the nuclei of 5 major cell types in the lung parenchyma were found to have little variation, with means ranging from 7.54 to 8.77 micrometers. Alveolar type I epithelial cells were found to comprise 8% of the cells and to be one of the largest cells, having a mean volume of 1,764 micrometers 3 and covering an average of 5,098 micrometers 2 of alveolar surface. Seven percent of the alveolar surface was covered by alveolar type II cells, which make up 16% of the total alveolar cells and have a mean volume that is half that of the type I pneumocyte. Capillary endothelial cells make up 30% of the lung cells and were significantly smaller in both size and average surface area than the alveolar type I cells. Cells in the interstitial space comprised 37% of the total cells. The number of alveolar macrophages showed great variability, ranging from 19% of alveolar cells in 1 person to 3 to 5% in the nonsmoking females. The alveolar cell population characteristics found in resected lobes from 2 nonsmoking females were found to be similar to 2 nonsmoking females studied after autopsy. An interspecies comparison of characteristics of cells from the alveolar regions of normal lungs from humans, baboons, and rats showed that proportions of cells in the alveolar region and their average thickness, size, and surface areas were relatively constant.

Adult↗
PubMed1982

Biology of disease: free radicals and tissue injury.

A free radical is any molecule that has an odd number of electrons. Free radicals, which can occur in both organic (i.e., quinones) and inorganic molecules (i.e., O(2)), are highly reactive and, therefore, transient. Free radicals are generated in vivo as by products of normal metabolism. They are also produced when an organism is exposed to ionizing radiation, to drugs capable of redox cycling, or to xenobiotics that can form free radical metabolites in situ. Cellular targets at risk from free radical damage depend on the nature of the radical and its site of generation. In this review we survey cellular sources of free radicals and the reactions they can undergo and discuss cellular defenses and adaptive mechanisms.

Animals↗
PubMed1981

Rat lung surfactant kinetics biochemical and morphometric correlation.

Biochemical and morphometric techniques were combined to estimate the distribution and flux or rat lung disaturated phosphatidylcholine (DSPC) in surfactant pathways. We found 126 +/- 8 X 10(6) alveolar epithelial type II (AEP II) cells per lung, each containing 150 +/- 30 lamellar bodies (LB). High yields of LB were isolated by centrifugation of lung homogenates with a discontinuous sucrose density gradient. Measurement of DSPC in LB and alveolar lavage (LV) material demonstrated that only 30% (LB 14%, LV 16%) of lung DSPC was present in these surfactant compartments. Radiolabeling of lung DSPC with [14C]palmitate demonstrated a product-precursor-relationship between LB and LV and a surfactant-associated DSPC flux of 90 microgram-lung-1 X h-1. We conclude that, although only 16% of lung DSPC is in an intracellular surfactant pathway at any time, all this DSPC is ultimately secreted onto the alveolar surface.

Animals↗
PubMed1981

Pulmonary injury in rats following continuous exposure to 60% O2 for 7 days.

Morphological, biochemical, and physiological studies were done on rats exposed to 60% O2 for 7 days. This exposure did not induce O2 tolerance but instead caused a significant decrease in survival time of animals subsequently exposed to pure O2. The activity of lung superoxide dismutases and glucose-6-phosphate dehydrogenase were unchanged after exposure to 60% O2. A decrease in lung compliance was suggested by changes in the total lung capacity and in the pressure-volume curves of excised lungs. Ventilation of these animals with large tidal excursion resulted in pulmonary edema. Morphometric analyses revealed a significant decrease in alveolar air volume and an increase in the number of alveolar macrophages. The most significant lesions involved the pulmonary vascular bed. The volume and thickness of the capillary endothelium was decreased. There were focal areas of pericapillary fluid accumulations, and a number of the smaller vessels had perivascular edema. These findings suggest that significant pulmonary injury occurs in rats exposed to 60% O2 and that the primary site of injury is the pulmonary capillary endothelium.

Animals↗
PubMed1981

A quantitative histologic study of avian osteopetrotic bone demonstrating normal osteoclast numbers and increased osteoblastic activity.

Hyperostotic diseases caused by increased osteoblastic activity are poorly understood partially because a suitable animal model is not available for their study. In contrast, a hyperostotic disorder caused by defective osteoclasts (mammalian osteopetrosis) is better understood, largely because of advances made with a murine model of the disease. The avian form of osteopetrosis is caused by RNA tumor viruses, but the role of osteoblasts and osteoclasts is not clear. We have performed a morphometric analysis of osteopetrotic avian bone to provide basic information about changes in the cells of bones from animals developing the disease. Chick embryos were injected at 12 days of incubation with a virus (MAV-2(0)) that induces osteopetrosis at a high frequency. Changes in bone volume were detected 14 days after virus injection. By 3 weeks of age, the bone volumes of osteopetrotic chicks were 4.7-fold larger than controls. The mean caliper diameter of an osteoclast was the same in osteopetrotic and normal bone. The number of osteoclasts per tibia increased in osteopetrotic animals, but the density of osteoclasts decreased. The presence of an increased number of osteoclasts of a normal size rules out the possibility that the virus causes osteopetrosis by selectively killing osteoclasts. The total bone-nonbone interface increased in osteopetrosis, and greater than 90 per cent of interface surface was devoted to bone deposition. These results indicate that avian osteopetrosis is an osteoblastic, proliferative disorder of bone and may serve as an excellent animal model for human diseases in which osteoblasts increase in number.

Animals↗
PubMed1980

Determination of the mean caliper diameter of lung nuclei by a method which is independent of shape assumptions.

When determining the number of nuclei (therefore cells) present in a known volume of tissue it is necessary to determine the overall mean caliper diameter of nuclei for each cell type studied. Most previous methods for determining the mean caliper diameters (D) of of cell nuclei were strongly dependetn upon assumptions of the shape of the particles in question (Greeley et al., 1978). A computer program has now been designed to calculate D from three-dimensional reconstructions of nuclei in a manner that is independent of all shape assumptions. The Ds of ten capillary endothelial cell nuclei from normal rat lungs have been determined by this shape-independent method. The resulting overall mean caliper diameter for this group of ten nuclei varied only slightly from that previously estimated for them by a method which assumes them to be triaxial ellipsoids. In a similar comparison, the Ds for ten normal human lung endothelial cell nuclei were determined by both methods. The overall mean caliper diameter determined by the shape-independent method was 10% larger than that estimated by the shape-dependent method. This suggests that human lung endothelial nuclei vary significantly from the shape assumption (triaxial ellipsoid) employed in the shape-dependent method, and the shape-independent method was considered to yield a more accurate measurement of D.

Animals↗
PubMed1980

Factors determining degree of inflation in intratracheally fixed rat lungs.

The total lung capacity (TLC) of rats was measured in vivo and was compared to the displacement volume of the lungs following intratracheal fixation with glutaraldehyde or formaldehyde solution. When glutaraldehyde was used the speed of infusion of the fixative was an important factor in the final degree of lung inflation achieved. With a low rate of fixative infusion and a final pressure of 20 cm of fixative the glutaraldehyde-fixed lungs inflated to 55% TLC. With a high initial flow of glutaraldehyde and a final pressure of 20 cm of fixative the lungs inflated to 84% TLC. Fixation of lungs inside the intact chest wall was found to result in a higher degree of inflation. With a reservoir height of 20 cm and a low rate of fixative infusion lungs fixed in situ reached 74% TLC, whereas lungs fixed in situ, but from animals that have been exsanguinated prior to fixation, inflated to only 58% TLC. This suggests that the volume of the blood in the lungs prior to infusion of glutaraldehyde influences the degree of inflation achieved. Formaldehyde-fixed lungs required 72 h to be completely fixed and they were inflated to 90% TLC when a reservoir height of 20 cm was used. Because of the slow rate of fixation using with formaldehyde solution the rate of infusion was found not to limit the degree of inflation that could be achieved.

Animals↗
PubMed1980

Pulmonary tissue volume in isolated perfused dog lungs.

Lung tissue volume (Vt) and pulmonary capillary blood flow (Qc) were measured with an acetylene rebreathing technique in intact and isolated perfused dog lungs. Qc (1.73 +/- 0.17 l/min) was consistently greater than pump flow (0.87 +/- 0.10 l/min) in isolated perfused lungs because acetylene disappearance from the lung was increased by diffusion across the pleura into the room. In spite of the increased acetylene loss, Vt can be measured in isolated lungs with reproducibility similar to that in intact animals (Vt intact = 207 +/- 63 ml, Vt isolated perfused = 208 +/- 61 ml).

Animals↗
PubMed1980

Structural and biochemical changes in rat lungs occurring during exposures to lethal and adaptive doses of oxygen.

The lungs of rats exposed to 100% O2 until death and to 85% O2 for as long as 14 days were studied using morphometric and biochemical techniques. The primary injury leading to death in rats exposed to 100% O2 was injury to the pulmonary capillary endothelium, where 44% of the endothelial cells were destroyed; there was a corresponding decrease in capillary surface area and in capillary lumen volume. Animals exposed to 85% O2 had proliferation and hypertrophy of alveolar Type II epithelial cells. In addition, 41% of the capillary endothelial cells were destroyed, but the endothelial cells that survived 7 days in 85% O2 were hypertrophied, and after this point no further destruction of the pulmonary capillary bed took place. Exposures to 85% O2 led to enhanced activity of the copper-zinc and manganese superoxide dismutases, which might be related to the apparently adaptive structural changes that occurred in the alveolar Type II epithelium and in the capillary endothelial cells.

Adaptation, Physiological↗
PubMed1980

Morphological, morphometric and x-ray microanalytical studies on lung tissue of rats exposed to chrysotile asbestos in inhalation chambres.

Rats were exposed to NIEHS short-range and to NIEHS intermediate-range chrysotile fibres for periods varying from one hour to one year. Following the exposures, the lungs from each animal were fixed by intratracheal instillation of 2% glutaraldehyde. Studies of fibre location following short exposure periods suggest that inhaled asbestos reaches the connective tissue compartment of the lung by passing through epithelial cells. X-ray energy microanalytical techniques were used to determine the magnesium to silicon ratios in fibres in situ. Inhaled particles were found to have decreased Mg:Si ratios if they were located in the interstitium, and many of the particles located within the alveolar airspaces had an even more marked decrease in the Mg:Si ratio. Morphometric techniques were used to quantitate structural changes occurring in the asbestos-treated animals. After three months of exposure, both types of chrysotile asbestos fibres caused similar increases in the volume of the alveolar epithelium, the interstitium and in alveolar macrophages. After twelve months of exposure, greater lung injury, involving both the alveolar epithelium and the interstitium, was found in animals exposed to the intermediate-range fibres. Physiological studies done after one year of asbestos exposure demonstrated a fall in total lung capacity and in vital capacity, which was most marked in the animals exposed to the intermediate-range fibres. These studies suggest that both classes of chrysotile fibres cause lung injury but that long fibres have the greater toxicity.

Animals↗