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Biomedical subjects

H Sahebjami

Publications and source records attributed to H Sahebjami.

At least 37 records · Page 2Linked to original sources

Changes in fatty acids in phospholipids of the bronchoalveolar fluid in bacterial pneumonia and in adult respiratory distress syndrome.

Fatty acids of the phospholipid fraction of bronchoalveolar lavage fluid from patients with bacterial pneumonia or with the adult respiratory distress syndrome were chromatographed and the patterns compared with those for a control group. In the control group, palmitic acid (16:0) was the predominant fatty acid, accounting for 58.0% (SD 8.25%) of the total fatty acid, a proportion significantly higher (p less than 0.001) than in the distress-syndrome group (42.1%, SD 4.88%) or the acute pneumonia group (32.1%, SD 1.73%). There was a greater proportion of oleic acid (18:1) in the disease groups; thus the ratio of palmitic to oleic acid was useful in distinguishing these three groups. No patient with a palmitic/oleic acid ratio greater than 2.45 had evidence of parenchymal inflammation. Of those with a ratio less than 1.3, 89% had acute bacterial pneumonia.

Adolescent↗

Theophylline: constant-rate infusion predictions.

This study was undertaken to evaluate a method of prospectively estimating appropriate aminophylline infusion rates in acutely ill, hospitalized patients with bronchospasm. Steady-state serum theophylline concentrations (Css), clearances (Cl), and half-lives (t1/2) were estimated by the Chiou method using serum concetrantions obtained 1 and 6 h after the start of a constant-rate intravenous aminophylline infusion in 10 male patients averaging 57 years of age. Using an enzyme-multiplied immunoassay (EMIT) system for theophylline analysis, pharmacokinetic estimations were excellent for Css (r = 0.9103, p less than 0.01) and Cl (r = 0.9750, p less than 0.01). The mean estimation errors were 9.4% (range 0.8-21.5) for Css and 12.3% (range 1.3-28.0) for Cl. There was no correlation between patient age and Cl. This method is useful for rapidly individualizing aminophylline therapy in patients with acute bronchospasm.

Adult↗

Changes in connective tissue composition of the lung in starvation and refeeding.

Adult male rats were starved by allowing them one fifth of their measured daily food consumption until they lost 40% of their initial body weights. Some of these rats were then refed until their initial body weights were reached. We measured the total content of the following in the lung tissue of fed, starved, and refed animals: (1) elastin, (2) hydroxyproline, and (3) protein. Body weight and lung dry and wet weights were significantly reduced in starved and similar in refed rats compared with fed animals. Total contents of crude connective tissue, hydroxyproline, elastin, and protein were significantly lower in starved than in fed rat lungs. After refeeding, hydroxyproline content returned completely to levels found in fed rats, but other components only partially returned to normal values. These results provide a biochemical counterpart for our previous observations on the effects of starvation and refeeding on lung mechanics and morphologic aspects. It appears that the emphysema like changes in the lungs of starved rats are at least partly related to the loss of connective tissue elements.

Animals↗

Effects of starvation and refeeding on lung biochemistry in rats.

Adult rats received one fifth of their measured daily food consumption until they lost 40% body weight. Some of these rats were then refed until they reached their initial body weight. We measured the following in fed, starved, and refed animals: (1) disaturated phosphatidylcholine (DSPC) content of lung tissue and of lavage fluid, (2) protein content of lung tissue and of lavage return, and (3) DNA and RNA content of lung tissue. In starved lungs, tissue and lavage DSPC content, total protein and RNA contents, and RNA/DNA ratios were significantly lower than in fed rats. After refeeding, DSPC values returned completely to normal, whereas protein, DNA, and RNA contents were significantly higher than in fed rats. The RNA/DNA ratio was similar in the fed and refed groups. Changes in lavage DSPC are consistent with the increased surface elastic forces in starvation and their return to normal with refeeding reported by us previously. It appears that starvation leads to a reduction in cell size without changes in cell number and that refeeding is associated with a more significant increase in cell number than in cell size.

Animals↗

Emphysema-like changes in the lungs of starved rats.

We examined the effects of starvation on lung structure in rats allowed only one fifth of their measured daily food consumption until they lost 40% of their initial body weight, and evaluated volume-pressure relationships in saline-filled lungs, lung morphometric and connective tissue morphologic features and lung ultrastructure by scanning electron microscopy. Compared with rats fed full rations, the volume-pressure curve was shifted upward and to the left and the chord compliance was significantly increased. In the starved rats, enlargement of air spaces and alveolar wall destruction was associated with a significant increase in mean linear intercept and a decrease in internal surface area. Elastic fibers appeared short, irregular, and fewer in number in starved lungs. Scanning electron microscopy showed enlarged air spaces, thin, irregular, and effaced alveolar walls, and an increased number and size of interalveolar pores in the starved group. We concluded that starvation results in mechanical and morphologic changes in the lung similar to those seen in emphysema, and that starved lung may be a useful experimental model for the study of emphysema.

Animals↗

Influence of starvation on enzyme-induced emphysema.

Adult rats were exposed to an aerosol of 10% papain for 8 h twice in a 2-wk interval. The control rats were exposed to isotonic saline in the same manner. Three weeks after the final exposure rats were divided into four groups: emphysema-fed, emphysema-starved, control-fed, and control-starved. Starved animals received one-third of their measured daily food consumption and water ad libitum for 6 wk. Final body weight, dry and wet weights of lungs and postfixation lung volume (VL) were significantly lower in starved rats. Dry-to-wet weight ratios were not significantly different among the groups, but VL/body weight was significantly higher in starved animals. Elastic recoil pressure of lung tissue determined in saline-filled lungs decreased and chord compliance over mid- and high-volume ranges increased significantly in starved animals both in control and emphysema groups. Mean linear intercept of air spaces was greater and internal surface area was smaller in starved rats in each group. Therefore, it appears that starvation aggravates the preexisting emphysematous processes in rat lungs.

Animals↗

Static volume-pressure relationship in normal rats at various stages of growth.

Static deflation air volume-pressure (V-P) curves were studied in 136 open-chested normal male rats ranging from 103 to 604 g in weight. The lungs accepted a greater volume of air as rats grew in size, but beyond 8 weeks of age, the volume expressed per g of lung weight progressively decreased. In older rats, V-P curves in precent maximum lung air volume (%MLV) were shifted upward and to the left compared to younger rats. We believe that these differences reflect various phases in the postnatal growth of rat lungs and loss of tiss elasticity due to the aging process, respectively. Lung air volume at 30 cm H2O Ptp (MLV30) showed a significantly higher linear relationship with body weight (r = 0.93) than with lung-heart weight (r = 0.80) as the independent variable. We present V-P nomograms and discuss two techniques of measuring V-P relationships with their specific applications.

Aging↗

Effects of starvation and refeeding on lung mechanics and morphometry.

Rats receiving one fifth of their usual daily food consumption for 10 days showed a significant increase in static recoil pressure of the lung (Pst[L]) due to surface forces at low lung volumes during inflation; their tissue Pst (L) decreased significantly over the entire volume-pressure loop compared to that of control rats. After 1 week of refeeding, the surface Pst (L) returned almost completely to normal, but tissue Pst (L) remained abnormally low. In starved rats, air-space enlargement with minimal loss of interalveolar septa was associated with a significant increase in mean linear intercept and volume fraction of air spaces, and with a significant decrease in corrected internal surface area and surface fraction of air space. These alterations returned partially toward normal in the refed group. We conclude that starvation increases surface elastic forces, decreases tissue elasticity of lung, and leads to air-space enlargement; redeeding leads to restoration of surface forces without the return of tissue elasticity to normal and to less severe air-space enlargement.

Animals↗

Exercise stress and enzyme-induced emphysema.

Rats were exposed to an aerosol of 10% papain for 8 h found in pilot studies to produce marked emphysema. One week after exposure some animals were forced to exercise in a motor-driven activity wheel 2 h daily for 4 wk, while others remained at rest. Another group of rats which served as the control were exposed to saline under the same conditions and divided into exercise and rest groups. Elastic recoil pressure (Pst) of lung was measured from static deflation pressure-volume curves with air and saline. Pst measured in air-filled lungs was not significantly different between the emphysema-rest and emphysema-exercise groups. When inflated with saline the Pst was significantly reduced in the emphysema-exercise compared to the emphysema-rest group at high and mid (100, 80, 60%) lung volumes. Pst in air- and saline-filled lungs was not significantly different between the control-rest and control-exercise groups. We therefore conclude that mechanical stress resulting from physical exercise decreased Pst of lung tissue in emphysematous rats.

Animals↗

The effect of betamethasone on pressure-volume characteristics of nonfetal rat lungs.

Betamethasone was administered to rats for 28 days, and body weight, lung weight, and descending pressure-volume relations were measured in their excised lungs. In rats treated with corticosteroid, lung and body weights increased less rapidly than in control rats, but the ratio of lung wet weight to body weight and the per cent dry weight remained the same in both groups. The absolute lung volume was significantly greater at each pressure in the control rats; but when expressed per lung weight, the lungs of rats treated with corticosteroid held more air. When corrected for lung size, the only difference in the lung pressure-volume curves between groups existed at transpulmonary pressures of 0 and 5 cm H2O, where the lungs of the rats treated with betamethasone contained more volume, whether inflated with air or with saline. We concluded that betamethasone administered to nonfetal rats has little influence on the lung's pressure-volume characteristics, which cannot be ascribed to differences in lung size.

Animals↗