PubMed Health⌕ Search

Biomedical subjects

A L Bell

Publications and source records attributed to A L Bell.

At least 91 records · Page 5Linked to original sources

Correlation of lung compliance and quantities of surfactant phospholipids after acute alveolar injury from N-nitroso-N-methylurethane in the dog.

Acute alveolar injury was induced in dogs by subcutaneous injection of 8 mg of N-nitroso-N-methylurethane per kg of body weight. Two to seven days after the injections, the change in respiratory compliance was measured, alveolar and lung tissue disaturated phosphatidyl choline (DSPC) were quantified, and fatty acid patterns of alveolar phosphatidyl choline were determined. Progressive decreases occurred in respiratory compliance and in alveolar and tissue DSPC. Mean alveolar DSPC decreases occurred in respiratory compliance and in alveolar and tissue DSPC. Mean alveolar DSPC decreased to 22% (p less than 0.001) of that of the control study and significant linear correlation (p = 0.02) between respiratory compliance and alveolar DSPC quantity was found. Mean tissue DSPC decreased to 60% of that of the control study (p less than 0.001) and reductions in alveolar and in type II cell DSPC were estimated to be nearly equivalent. The proportion of palmitate in lavage phosphatidyl choline was increased by a mean of 9%. These studies demonstrated a decrease in surfactant lipids correlated with decreased compliances in acute alveolar injury and suggested that qualitative and quantitative changes in surfactant result from injury to alveolar type II cells.

Animals↗

Effect of positive end-expiratory pressure on lung compliance in dogs after acute alveolar injury.

We studied the effect of positive end-expiratory pressure (PEEP) on lung compliance (CL) in 17 dogs during the early phase of acute alveolar injury induced by the subcutaneous administration of N-nitroso-N-methylurethane (NNNMU). The acute phase of this injury is characterized by necrosis of the alveolar epithelium and by decreased CL, which is caused by abnormal surface forces and which correlates with decreased alveolar surfactant lipids. During the control period and after NNNMU both CL decreased significantly with increments of PEEP (p less than 0.001) and plots of FRC versus PEEP had a rising curve with a decreasing slope. Static volume-pressure curves obtained in vivo in 6 dogs showed a rightward shift of the curve without increase of hysteresis after NNNMU. these data suggest that in the surfactant-deficient lung, PEEP predominantly causes overdistention of patent alveoli rather than recruitment of closed air spaces. The physiologic response of the NNNMU-injured lung to PEEP differs from that of severely edematous lungs but is similar to that of surfactant-deficient lungs of premature lambs.

Animals↗

Quantification of surfactant phospholipids in the dog lung.

We quantified total phospholipid (PL), total and disaturated phosphatidylcholine (PC and DSPC), phosphatidylglycerol (PG), and total protein in alveolar washings and lung tissue in 22 dog lungs. Quantitative recovery of alveolar material and assessment of its possible contamination by blood lipids were important determinants of methodology. To remove blood, the vessels of half the lungs were perfused with a fluorocarbon emulsion before lavage. The volume of blood removed by perfusion and the quantity and fatty acid patterns of its whole blood and plasma PL and PC were determined. Washings of unperfused lungs contained means of 21% more PL and 24% more PC than those of perfused lungs. Although this excess could be accounted for by the PL and PC in pulmonary blood, the hemoglobin and total protein content of washings and their PC fatty acid patterns indicated that blood lipids were not a major source of the excess lipid in washings of unperfused lungs. Using more recent morphometric estimates rather than the indirect ones previously used by others, the quantity of alveolar DSPC (1 mg/g lung) is calculated to be 1.8 times the amount necessary to form a packed monolayer on the internal surface of the lung at functional residual capacity.

Animals↗

Alveolar epithelial injury causing respiratory distress in dogs: physiologic and electron-microscopic correlations.

Structural and mechanical changes were correlated in 29 dogs with acute alveolar injury induced by the subcutaneous administration of N-nitroso-N-methylurethane (NNNMU). The injury was characterized by necrosis and repair of alveolar epithelium while the vascular endothelium remained essentially intact. Compliance of the lung (CL) decreased and elastic recoil increased as epithelial necrosis occurred. During recovery, improved elastic recoil coincided with epithelial regeneration, although CL remained abnormal. The late phase was characterized histologically by widespread closure of clusters of alveoli alternating with dilated small air spaces. The process resulted in distortion of lung architecture and resembled interstitial fibrosis. Reduced lung volume and decreased distensibility of dilated small air spaces may have accounted for the persistently abnormal CL. Because of the specific site of anatomic involvement, the predictable evolution of deranged lung mechanics, and the similarity to human lung injury (adult respiratory distress syndrome), the lung injured by administration of N-nitroso-N-methylurethane is a suitable model to study pathophysiology and types of therapy in a controlled setting.

Animals↗

Volume-pressure and morphometric observations after acute alveolar injury in the dog from N-nitroso-N-methylurethane.

Volume-pressure diagrams during inflation with air and saline were made with the lungs of 6 control dogs and 24 dogs with acute alveolar injury induced by subcutaneous injection of 6 mg of N-nitroso-N-methylurethane per kg of body weight 3 to 14 days before study. The extent of alveolar closure was estimated by measuring the mean linear intercept of the remaining open air spaces after inflation of the lung with liquid formalin at a pressure of 40 cm H2O. This alveolar closure was defined as irreversible. The volume-pressure diagrams and compliance data derived from them during the 3 to 4, 5 to 7, and 9 to 14 day periods after injection were analyzed and compared with the morphometric data. The diagrams with air inflation showed a progressive downward shift beginning with the 3 to 4 day period. This shift was at least partly independent of volume loss. The diagrams with saline inflation were unchanged during the 3 to 4 day period, but showed a downward shift, largely due to volume loss thereafter. Irreversible alveolar closure, reflected by an increased mean linear intercept, was present in the 3 to 4 day period, and its extent increased with time, correlating inversely with total lung capacity and saline compliance. The data indicate that decreased lung compliance and volume during the first 7 days of injury induced by injection of N-nitroso-N-methylurethane were due largely to increased surface tension and that tissue forces became a significant factor later. They suggest that the altered tissue forces were due principally to irreversible alveolar closure.

Animals↗

Experimental acute alveolar injury in the dog. Morphologic--mechanical correlations.

In 26 dogs, a single subcutaneous injection of N-nitroso-N-methylurethane produced acute lung injury characterized by tachypnea cyanosis, increased static lung recoil, and decreased lung compliance. During the first few days, light microscopic examination revealed widespread interstitial and perivascular edema and alveolar collapse. At the same time, electron microscopy showed the major alteration to be widespread necrosis of both types of alveolar epithelial cells without significant injury to the vascular endothelium. During recovery, new epithelial cells appeared which probably were derived from granular pneumocytes. These cells developed into mature granular pneumocytes through a phase in which they resembled fetal granular pneumocytes. The late stage was characterized by a picture resembling diffuse interstitial fibrosis but which was due to irreversible closure of clusters of small airspaces with no apparent increase in collagen. Elastic recoil of the lungs, as reflected by peak inspiratory airway pressure, increased during the acute phase and showed a return toward normal that was coincident with the appearance of mature granular pneumocytes in the regenerating epithelium. Lung compliance decreased during the acute phase and in most animals returned toward normal during the recovery phase. These observations strongly suggest that the alteration in lung mechanics is related to epithelial necrosis and that recovery is related to epithelial regeneration.

Acute Disease↗

Photoreceptor spike responses in the hardshell clam, Mercenaria mercenaria.

Spikes were recorded from single axons in the siphonal nerve of the hardshell clam Mercenaria mercenaria which respond to dimming of light. No axons were found to respond to the onset, or increase, of illumination. In a dark-adapted state there is little or no ongoing spike activity. The responsive area of a single axon is a circle of approximately 85 microm diameter on the inner siphon wall. The number of spikes elicited at the off of constant-duration flashes grows as approximately the 0.4 power of flash intensity. For constant intensity and constant light-time fraction, the off-response increases with increasing duration at least up to 500 s duration. For long durations, the response grows as the logarithm of stimulus duration. Subthreshold light can suppress the off-response from preceding illumination. In a light-adapted state, the off-response is greater and its latency shorter than in the dark-adapted state. The fine structure of groups of cell processes thought to comprise the photoreceptor in Mercenaria is described. On the basis of morphological and physiological findings it is suggested that phototransduction occurs in the fine distal processes of the axons from which we have recorded. Axonal processes were found to contain well organized pentalaminar whorls which may be the site of photo-pigment concentration. The action spectrum obtained from the integrated responses of nerve bundles appears to be that of a single Dartnall pigment having maximal absorption at about 510 nm.

Animals↗

Changes in fine structure during silk protein production in the ampullate gland of the spider Araneus sericatus.

The ampullate silk gland of the spider, Araneus sericatus, produces the silk fiber for the scaffolding of the web. The fine structure of the various parts of the gland is described. The distal portion of the duct consist of a tube of epithelial cells which appear to secrete a substance which forms the tunica intima of the duct wall. At the proximal end of the duct there is a region of secretory cells. The epithelium of the sac portion contains five morphologically distinct types of granules. The bulk of the synthesis of silk occurs in the tail of the gland, and in this region only a single type of secretory droplet is seen in the epithelium. Protein synthesis can be stimulated by the injection of 1 mg/kg acetylcholine into the body fluids. 10 min after injection, much of the protein stored in the cytoplasm of the epithelial cells has been secreted into the lumen. 20 min after stimulation, the ergastoplasmic sacs form large whorls in the cytoplasm. Protein, similar in electron-opacity to protein found in the lumen, begins to form in that portion of the cytoplasm which is enclosed by the whorls. The limiting membrane of these droplets is formed by ergastoplasmic membranes which lose their ribosomes. No Golgi material has been found in these cells. Protein appears to be manufactured in the cytoplasm of the tail cells in a form which is ready for secretion.

Acetylcholine↗

Synthetic myosin filaments.

A stable preparation of myosin filaments was formed in a medium at pH 8.0. The filament length varied from 0.2 to 0.5 micron. Most of the material sedimented at 21S, but there was a minor peak (due to monomer) at 6.8S. The filaments did not taper and had large bulbous irregularities at the ends.

Animals↗