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J W Shepard

Publications and source records attributed to J W Shepard.

47 records · Page 3Linked to original sources
PubMed1983

Transpleural CO2 diffusion in excised dog lungs.

Previous studies of transpleural gas diffusion have reported both linear and nonlinear relationships between total gas transfer and the transpleural driving gradient estimated as the difference between pleural and end-tidal gas tensions. The present studies were undertaken to explain these conflicting results by examining the role of convective mixing as well as the validity of using measurements of end-tidal gas to estimate subpleural gas tensions and calculate the transpleural partial pressure gradient. Nine excised nonperfused dog lungs were ventilated with room air under varying conditions of frequency (f), tidal volume (VT) and pleural CO2 concentration (FplCO2). The relationship between CO2 elimination (VCO2) and the transpleural CO2 concentration gradient estimated by (FplCO2-FETCO2) was found to be linear for every level of ventilation (constant convective mixing) studied. The slope of this relationship, equal to the pleural CO2 diffusing capacity (DplCO2) was found to decrease as ventilation was decreased whether achieved by reductions in f or VT. Because changes in membrane geometry were insufficient to explain the differences in DplCO2, seven additional excised dog lungs were studied ultrastructurally following 4 h of ventilation with room air at a pleural CO2 concentration of 6%. Previous studies under similar conditions have shown that changes in type II pneumocyte lamellar body volume density Vv(LB/cyto) are related to the alveolar concentration of CO2. The results indicated that the concentration of CO2 in alveoli located within 1 mm of the pleural surface was substantially greater than the value estimated by FETCO2. Consequently, (FplCO2-FETCO2) over-estimates the transpleural concentration gradient and produces erroneously low estimates of the diffusing capacity of the pleural membrane.

Animals↗
PubMed1983

The ultrastructure of rat type II pneumocytes: effects of age, sex, and strain.

The morphology of type II pneumocytes was investigated in Fischer 344 and Sprague-Dawley rats to determine whether differences in age, sex, and/or genetic strain influence type II cell ultrastructure. In Fischer 344 rats the type II pneumocytes increased in size with age due to an increase in the cytoplasmic component of the cell. Although mitochondrial volume density increased with age no significant changes in lamellar body volume density or lamellar body size were detected. No ultrastructural differences were observed between the type II cells in 6-week-old male and female Fischer 344 rats. However, substantial ultrastructural differences were found to exist among type II cells from the Fischer and Sprague-Dawley strains. Lamellar body volume density was 60% greater, P less than 0.001, in the Fischer rats due to the larger size of individual lamellar bodies. While mitochondrial volume density was also 22% greater in the Fischer rats, P less than 0.01, type II cell size was similar in the two strains. These results indicate that the ultrastructure of type II cells can differ within a genetically inbred strain as a function of age as well as between genetically different strains of the same species.

Age Factors↗
PubMed1982

Factors regulating lamellar body volume density of type II pneumocytes in excised dog lungs.

Pulmonary arterial occlusion (PAO) produces multiple alterations in the physiological/biochemical environment of lung cells as well as dysfunction of the lung's surfactant system, which is considered to play a significant role in mediating lung injury. The present studies were performed using 66 excised dog lungs to evaluate the impact of alterations in ventilation, substrate availability, alveolar CO2 tension, hydrogen ion and bicarbonate concentrations, and temperature and neural denervation on the lamellar body (LB) volume density of type II pneumocytes. Ventilating excised nonperfused dog lungs with room air (0% CO2) for 4 h at 38 degrees C resulted in severe reductions (68-77%) in LB volume density. Supplementing inspired gas with 5% CO2 prevented LB depletion, while ventilation with 2.5% CO2 moderated the severity of depletion to 17-27% of control. Ventilation with 10% CO2 tended to increase LB volume density by increasing the number of LBs per cell, whereas reductions in LB volume density predominantly resulted from a decrease in LB size. The level of ventilation had no significant effect on LB volume density independent of inspired CO2 concentration. Reducing temperature to 5 degrees C prevented LB depletion. Lung perfusion with autologous whole blood failed to moderate the severity of LB depletion during room air ventilation despite the increased availability of metabolic substrates for cellular metabolism. Adding hydrochloric acid to maintain physiologically normal hydrogen ion concentrations in the perfusing blood had a small effect in ameliorating the severity of LB depletion. These results indicate that alveolar CO2 tension and bicarbonate concentration are major factors regulating the LB content of type II pneumocytes and suggest an important link between the gas exchange and phospholipid metabolic functions of the lung.

Animals↗
PubMed1981

Gas exchange in nonperfused dog lungs.

Gas exchange was studied under conditions of zero perfusion both in situ and in vitro. Six dogs, anesthetized with pentobarbital sodium, underwent surgical interruption of both pulmonary and bronchial circulations to the left lung. Despite the absence of perfusion, O2 uptake for the left lung ranged from 0.76 to 0.98 ml/min, whereas CO2 elimination greatly exceeded O2 uptake ranging from 1.68 to 4.34 ml/min. In addition, CO2 output was observed to vary directly with the level of minute ventilation (VE) and inversely with end-tidal CO2 concentration. To investigate the mechanisms responsible for these findings we studied 20 excised, ventilated, but nonperfused dog lungs to evaluate the relative roles of tissue metabolism and transpleural diffusion to gas exchange. The results obtained with these excised lungs under conditions of varying VE and extrapleural gas concentrations indicate that the high respiratory exchange ratios observed in situ can be explained by the greater rate with which CO2 diffuses through the pleura, and that reduced ventilation decreases total gas transfer by decreasing the transpleural partial pressure driving gradient. Our data further document that the concentration of CO2 in alveolar gas may differ significantly from that present in inspired gas under conditions of ventilation-perfusion ratio equal to infinity, and that tissue metabolism as well as transpleural diffusion contribute to gas exchange in nonperfused lung.

Animals↗
PubMed1980

Lamellar body depletion in dogs undergoing pulmonary artery occlusion.

We have investigated the relationship between pulmonary artery occlusion (PAO) and the surfactant system of the lung by studying the ultrastructural responses of type II alveolar pneumocytes to PAO of 4-12 h duration in 16 mongrel dogs. In six of these animals, the occluded lung was allowed to reperfuse for 6 h before killing and in four animals subjected to PAO of 4 h duration, the occluded lung was ventilated with 5% CO2 balance air. PAO by itself resulted in a dramatic 80% reduction in the volumetric density of lamellar bodies (LB) in the type II cells. This resulted predominantly from a decrese in volume of the individual LB. Although reperfusion was associated with an increase in LB volume density toward normal, 6 h of reperfusion was insufficient to re-establish normal type II cellular morphology. Ventilation of the occluded lung with 5% CO2 prevented LB depletion indicating that alveolar CO2 tension may affect the release and/or synthesis of LB in type II pneumocytes.

Animals↗
PubMed1979

Effects of isoproterenol on distribution of perfusion in embolized dog lungs.

In 19 mechanically venilated, anesthetized dogs, autologous venous thrombi were formed in the inferior vena cava and subsequently released. Serial perfusion lung scintigrams revealed the postembolic distribution of pulmonary blood flow before, during, and after the infusion of isoproterenol at 2.2 micrograms/min. Isoproterenol failed to restore perfusion to embolically occluded regions. When reperfusion occurred it was attributable to clot resolution. Gas exchange and hemodynamic measurements obtained in seven thromboembolized animals showed no scan evidence of reperfusion during the isoproterenol infusion. After embolization, cardiac output increased from 1.7 to 2.6 liter/min (p less than 0.05), and PvO2 from 38.0 to 45.3 mm Hg (p less than 0.05). Shunt fraction remained unchanged. The postembolic infusion of isoproterenol was associated with a further increase in cardiac output to 3.6 liter/min (p less than 0.01), an elevation in PvO2 to 50.7 mm Hg, along with a decrease in pulmonary vascular resistance from the postembolic mean of 448 to 246 dynes.sec.cm-5 (p less than 0.05). Perfusion defects following acute pulmonary thromboembolization are not altered by the infusion of the potent pulmonary vasodilator, isoproterenol. Infusion of this drug following thromboembolization may have potential therapeutic benefit by reducing pulmonary vascular resistance, increasing cardiac output, and elevating the mixed-venous oxygen tension.

Animals↗
PubMedDate not supplied

Pseudocataplexy.

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Adolescent↗