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J Gil

Publications and source records attributed to J Gil.

At least 307 records · Page 17Linked to original sources

Morphometry of pinocytotic vesicles in the capillary endothelium of rabbit lungs using automated equipment.

Pinocytotic vesicles are one of several anatomic factors relevant to the permeability for macromolecules of capillary endothelia. We quantitified the number and distribution of pinocytotic vesicles present in the endothelium of pulmonary capillaries. Several similar studies have been reported in the past for endothelia of systemic capillaries, but the technical difficulties involved in this difficult application of morphometry never have been discussed. In the present work, an on-line microprocessor was used to assist with the processing of the point-counting data. The average figures from nine rabbit lungs for parameters thought to be relevant to characterize the population of vesicles are: thickness of the endothelium (TAUen) 0.192 microns; number of vesicles per volume unit of cell (NVen), 131 vesicles/microns3; vesicular load of each cell front (N/S)b, 196 vesicle/microns2, and (N/S)i, 181 vesicles/microns2. The number of vesicles per volume unit (NVen) is smaller than that which has been described for systemic capillaries.

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Fusion of pinocytotic vesicles in liquid filled lungs: a mechanism of cellular damage.

Lungs of anesthetized rabbits were filled unilaterally with macromolecule-containing solutions (Dextran 40 and albumin) for 20 min. which generally resulted in fluid resorption from the flooded lung. Electron microscopic examination revealed the following: (1) formation of chains of vesicles, similar or identical to pinocytotic vesicles, which start from depressions or fluid-immersed cellular surfaces in macrophages, or endothelial and squamous epithelial cells; and (2) formation of intracellular blisters as a result of the apparent fusion of numerous pinocytotic vesicles. Both observations seem to be augmented forms of normal phenomena. The hypothesis is advanced that the chains of vesicles are related to the increased amount of undulation of the cell surface and to cellular invaginations that follow relaxation of tensions at the surface of cells immersed in fluid. The blisters could be the result of the increase of bidirectional flow of vesicles across the squamous cells. This brings an increased risk of collision because of the absence of lysosomes in the thin cytoplasmic extensions of endothelial and squamous epithelial cells. It is concluded that, even in very early stages, flooding per se produced some form of cellular alterations with a potential for leading to more overt lung pathology such as cell death and desquamation which would greatly increase tissue permeability.

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Protection and therapy of mice with acute and chronic experimental virus infections with propionibacterium granulosum kp-45.

The protection of mice against experimental infections with three different viruses (herpes simplex, vaccinia and mouse hepatitis) by Propionibacterium granulosum strain KP-45 and isolated cell walls was investigated. Pretreatment of NMRI mice with P. granulosum strain KP-45 3-7 days prior to HSV intranasal infection resulted in lowering of mortality rate (herpes encephalitis) from about 95% in controls to 15-30%. Pretreatment of NMRI mice prior to vaccinia virus infection also caused a significant decrease of the number of specific tail lesions. Infection of BALB/c mice with mouse hepatitis virus type 3 (MHV-3) resulted in development of acute infection with lethality in 4-6 days, while in fairly resistant C3H mice chronic infection manifested by loss of weight, uncoordination followed by paralysis and death in few months was observed. Pretreatment of BALB/c mice 3-7 days prior to MHV-3 infection lowered the mortality rate to about 25-30% while no effect was observed in animals injected with P. granulosum KP-45 on the day of virus inoculation. In chronic MHV-3 infections treatment with P. granulosum KP-45 was started 2 weeks after virus inoculation and was continued every 10 days. This resulted in a significant lowering of the number of paralysed mice and in a decrease of the mortality rate. Titre of MHV-3 recovered from livers of infected mice 4 months after virus inoculation was also significantly lower in animals treated with P. granulosum KP-45 or isolated cell walls.

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Alveolar volume-surface area relation in air- and saline-filled lungs fixed by vascular perfusion.

The influence of volume changes and interfacial forces on the geometry of peripheral air spaces was studied in excised rabbit lungs inflated with either air or saline and fixed by vascular perfusion at four points of the deflation limb of the pressure-volume curve corresponding to 100, 80, 60, and 40% of the total lung capacity (TLC). In air-filled lungs pleating and folding of alveolar septa were observed, especially in alveolar corners. However, the alveolar surfaces were smooth, except at low lung volumes where some surface crumpling occurred. In saline-filled lungs pleats were absent; the alveolar surface was irregular at all inflation levels due to undulating walls and bulging capillaries. Morphometry indicated that at all alveolar volumes (VA) the surface areas (SA) were larger in saline- than air-filled lungs. No simple mathematical function was found to characterize the relation between SA and VA over the entire volume range studied. Within the range of normal breaths (80 to 40% TLC) the best fit for n in the function SA = k.VnA was 0.58 for saline-filled lungs (r = 0.93) and 0.33 for air-filled lungs (r = 0.68), suggesting different and complex deflation patterns.

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Morphologic aspects of alveolar microcirculation.

Direct observations of the flow direction and connections between arteries and veins in the mammal lung are difficult. When we divide the lung into smaller units like acini or segments we can observe a central supply of the unit with arterial blood that has venous drainage at different points of the periphery. Consideration of the situation prevailing at birth strongly suggests a preferential flow direction through paths located in primary septa at the bottom of alveoli. Capillaries of the secondary septa placed between alveoli open to the same duct represent collaterals of the mainstream flow filled only if pressure conditions permit. Another significant feature is the presence of pleated alveolar septa. While capillaries inside the interalveolar wall mostly appear flat or collapsed, the capillaries of the pleated alveolar corners are always wide open. Often they show openings into a small venule placed inside the pleated area, which strongly suggests that the pleated areas contain the venous side of the capillaries.

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Isolation and characterization of lamellar bodies and tubular myelin from rat lung homogenates.

Three surface-active fractions which differ in their morphology have been isolated from rat lung homogenates by ultracentrifugation in a discontinuous sucrose density gradient. In order of increasing density, the fractions consisted, as shown by electron microscopy, primarily of common myelin figures, lamellar bodies, and tubular myelin figures. The lipid of all three fractions contained approximately 94% polar lipids and 2% cholesterol. In the case of the common myelin figures and the lamellar bodies, the polar lipids consisted of 73% phosphatidylcholines, 9% phosphatidylserines and inositols, and 8% phosphatidylethanolamines. In the case of the tubular myelin figures, the respective percentages were 58, 19, and 5. Over 90% of the fatty acids of the lecithins of all three fractions were saturated. Electrophoresis of the proteins of the fractions in sodium dodecyl sulfate or Triton X-100 revealed that the lamellar bodies and the tubular myelin figures differed in the mobilities of their proteins. The common myelin figures, however, contained proteins from both of the other fractions. These data indicate that, whereas the lipids of the extracellular, alveolar surfactant(s) originate in the lamellar bodies, the proteins arise from another source. It is further postulated that the tubular myelin figures represent a liquid crystalline state of the alveolar surface-active lipoproteins.

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