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Biomedical subjects

J D Crapo

Publications and source records attributed to J D Crapo.

At least 181 records · Page 10Linked to original sources
PubMed1979

Disaturated phosphatidylcholine in rat lungs with altered numbers of type II alveolar epithelial cells.

Rats exposed to 85 per cent oxygen for 9 days demonstrated an increase in lung deoxyribonucleic acid (DNA) specific acitvity for [3H]-thymidine and a significant increase in the volume of interstitial and alveolar epithelial cells. This included a 63 per cent increase in the number of Type II alveolar epithelial cells. Lamellar body volume per lung significantly increased in animals exposed to oxygen and was related to the increased number of Type II cells, because lamellar body volume expressed per Type II cell remained relatively constant and was comparable to control values. The concentration of whole lung disaturated phosphatidylcholine also increased significantly, but the concentration of unsaturated phosphatidylcholine did not increase. Concomitantly, there was a significant decrease in [32P]-orthophosphate and [14C]-palmitate disaturated phosphatidylcholine specific activity that was proportional to the increased number of alveolar epithelial Type II cells present.

Animals↗
PubMed1979

Pulmonary morphology in a multihospital collaborative extracorporeal membrane oxygenation project. I. Light microscopy.

This report presents the light microscopic morphology found at autopsy in 59 patients who participated in an organized controlled trial of extracorporeal oxygenation as therapy for acute respiratory failure. Observations were recorded as objectively as possible and were analyzed by computer. The experimental therapy produced no specific alteration in the observed pulmonary lesions. Many of the lesions tabulated had significant correlation coefficients with time, all of which were higher when correlated with the duration of respiratory failure than with the duration of the entire acute illness. The rapid progression of the lesions to fibrosis is emphasized as is the predilection of both early and late lesions to involve alveolar ducts to a far greater degree than the distal alveolar spaces. A unifying mechanistic hypothesis consistent with these observations, as well as others, is that the lesions may result as much from oxygen damage as from the original acute illness.

Adult↗
PubMed1978

Estimation of the mean caliper diameter of cell nuclei. I. Serial section reconstriction method and endothelial nuclei from human lung.

In morphometric studies of lung tissue, accurate determination of the total number of any specific type of cell, such as the endothelial cell, requires knowledge of the shape of the cell nucleus. This knowledge of shape is necessary to calculate the mean caliper diameter, which, in turn, is an indispensible element of the equation for the number of nuclei (therefore cells) per unit volume (NV). Nine human hung endothelial cell nuclei were therfore reconstructed in dental wax from serial sections and were found to be pleomorphic triaxial ellipsoids. Five of these approached an oblate shape. The axes of these nine nuclear models were directly measured and a computer program using numerical integration was written to determine the mean caliper diameters of these ellipsoids. The estimated mean semi-axes of the nine nuclei were (+/-SD) 5.98+/-1.61, 3.61+/-0.70, 1.36+/-0.34; and the estimated overall mean caliper diameter for the total population of human lung endothelial nuclei was 7.97+/-1.27 micrometers.

Cell Nucleus↗
PubMed1978

Estimation of the mean caliper diameter of cell nuclei. II. Various cell types in rat lung.

Morphometric studies of lung tissue in which the number of cell nuclei (therefore cells) are determined require the determination of the mean caliper diameter for each type of cell nucleus studied. We determined the mean caliper diameter for the five most common classes of cells found in the gas exchange portion of rat lung. This was done by serially sectioning through ten nuclei from each class of cells and then constructing wax models of the nuclei. Most of the nuclei were found to be triaxial ellipsoids and direct measurements taken from the models were used to calculate the following estimated overall mean caliper diameters (+/-SE): alveolar type I nuclei, 7.97+/-0.2 micrometers, alveolar type II nuceli, 6.77 +/-0.19 micrometers, interstitial cell nuclei, 7.64+/-0.35 micrometers, endothelial cell nuclei, 7.22+/-0.19 micrometers, and alveolar macrophage nuclei, 7.65+/-0.17 micrometers.

Animals↗
PubMed1978

Pathologic changes in the lungs of oxygen-adapted rats: a morphometric analysis.

Animals exposed to 85 per cent O2 for 5 or more days acquire the ability to survive for prolonged periods in 100 per cent O2. The basis of this acquired "tolerance" is poorly understood, but it has been proposed to be related to biochemical changes occurring in the lung cells. In order to quantify the structural changes that occur in the lungs of oxygen-adapted rats, rats were exposed to 85 per cent O2 for 7 days and then studied using morphometric techniques. The oxygen-adapted rats had a normal number of alveolar type I epithelial cells and a moderate increase in the number of alveolar type II cells. The alveolar type I epithelium was intact over the entire alveolar surface and appeared to have a normal ultrastructure, whereas alveolar type II cells demonstrated occasional changes in mitochondrial structure. In the interstitial compartment, there was a large increase in the number of interstitial cells and a significant increase in the noncellular components of the interstitium. The major area of pulmonary damage occurred in the vascular compartment, where entire segments of the capillary bed were lost and the total number of endothelial cells decreased by 45 per cent. A significant change in pulmonary vascular hemodynamics was suggested by a 49 per cent decrease in total capillary lumen volume and a decrease in the hematocrit of blood in the pulmonary capillary lumen to 57 per cent of the value found in aortic blood.

Adaptation, Physiological↗
PubMed1977

The failure of aerosolized superoxide dismutase to modify pulmonary oxygen toxicity.

Superoxide (O2-.) is a highly toxic free radical that may be an important component of pulmonary O2 toxicity. The primary defense against this free radical is superoxide dismutase. Rats were exposed to aerosolized superoxide dismutase, and it failed to modify either the time course or the cumulative toxicity of 100 per cent O2. Because the aerosolized enzyme can be expected to be delivered only to the extracellular space of the lung, it is suggested that the primary site of production and of damage due to O2-induced free radicals must be within the intracellular space.

Aerosols↗
PubMed1976

Oxygen-induced changes in pulmonary superoxide dismutase assayed by antibody titrations.

Previous studies have demonstrated a 50% increase in pulmonary superoxide dismutase (SOD) activity in oxygen-adapted rats and have suggested that SOD plays a significant role in the development of "tolerance". To further study these events, the cuprozinc SOD was purified from rat liver and found to be similar to previously purified cuprozinc superoxide dismutases. A rabbit antisera to rat cuprozinc SOD was produced and used to perform antibody titrations of SOD in the lungs of rats exposed to 85% O2 for 5 days. The absolute amount of cuprozinc SOD increased 41% by antibody titration which accounted for most, if not all, of the 48% increase demonstrated in total SOD activity. Spectrophotometric assays at pH 7.8 and 10.0 of pure rat cuprozinc SOD and crude lung homogenates suggest that there is also a manganese SOD present, but the role of that SOD in the development of oxygen tolerance has not been established.

Adaptation, Physiological↗
PubMedDate not supplied

Quantitative aspects of immunogold labeling in embedded and in nonembedded sections.

We tried to control immunolabeling conditions so that information about antigen concentration could be achieved by quantifying labeling patterns. Working with immunogold labeling procedures in ultrathin cryosections, we observed that differential penetration of immunoreagents causes considerable differences in labeling efficiency between various cell structures. Therefore, in these nonembedded sections, labeling densities can only be used to measure variations in antigen concentration within one cell structure. After embedding the tissue in 30% polyacrylamide (PAA), differences in penetration were negated. The equalizing effect of PAA on the labeling efficiency enabled us to design a simple immunocytochemical method by which concentrations of a protein can be measured in situ at subcellular levels, provided that no variations in the protein's structural conformation occur that would affect its immunoreactivity. In spite of a higher sensitivity observed for Ig-gold, we preferred to use protein A-gold in our system because of the low nonspecific labeling and the more precise antigen detection by the latter immunomarker.

Amylases↗
PubMedDate not supplied

Extracellular superoxide dismutase localization and activity within the human placenta.

Maintenance of low vascular tone within the placenta is mediated by nitric oxide (NO). The half-life of NO is very short, as superoxide anion (O2-) rapidly inactivates NO to form peroxynitrite. Superoxide dismutases compete with NO for O2-. By scavenging O2-, superoxide dismutase promotes the vasodilatory action of NO. Extracellular superoxide dismutase (EC-SOD) is present in high concentrations within the extracellular matrix of systemic arteries and has been proposed to mediate vascular smooth muscle tone by increasing NO bioavailability. The localization and activity of EC-SOD within the human placenta has not been determined. Placental EC-SOD may be involved in placental vascular tone, and abnormal activity may lead to pre-eclampsia secondary to increased O2--mediated inactivation of NO. To investigate this possibility, the activity and localization of human placental EC-SOD was determined in normal women, and then compared to pre-eclamptic women. Placental EC-SOD localized within the villous extracellular matrix around arterioles, and there were no differences in distribution between normal and pre-eclamptic women. There were no differences in placental EC-SOD activity between normal and pre-eclamptic subjects in either center (33.7+/-4.1 versus 33.1+/-2.5, P=0.6), or peripheral (34.3+/-5.6 versus 34.0+/-3.5, P=0.9) samples. EC-SOD localization around villous vessels suggests that EC-SOD serves potentially to protect the fetal vasculature from O2-, in both normal and pre-eclamptic pregnancies. Placental EC-SOD distribution and activity is not different between pre-eclamptic and normal women, suggesting that EC-SOD is not involved in the vascular changes seen in pre-eclampsia.

Adult↗