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Biomedical subjects

L H Hill

Publications and source records attributed to L H Hill.

At least 19 recordsLinked to original sources
PubMed1995

Comparative study between acute intraoperative arterial elongation and the use of the interpositional vein graft for arterial reconstruction.

This study compares the acute intraoperative arterial elongation technique with the interposition vein-graft method for the closure of small arterial gaps that cannot be repaired by undermining alone. Ten conditioned female mongrel dogs were divided into two groups: a vein graft interposition group and an acute expansion-elongation group. In ten cases, a 25-mm segment of the superficial femoral artery was excised. The resultant defect, measuring 45 to 60 mm, was repaired by an interpositional graft of a comparable size segment of the superficial femoral vein. In ten other cases, a same-size defect was repaired by a tension-free end-to-end anastomosis, following acute intraoperative arterial elongation. The animals were explored at various intervals. Overall results revealed a 100 percent patency rate with the acute expansion-elongation group vs. 80 percent with the vein-graft interposition group. The versatility, time saving, and ease of technique, plus previous clinical experience, is encouraging enough to recommend this method for the sound repair of small arterial defects in clinical cases.

Anastomosis, Surgical↗
PubMed1986

Time course of chemotactic factor generation and the corresponding macrophage response to asbestos inhalation.

Inhalation of asbestos fibers causes a progressive fibrotic lung disease in humans and animals. Pulmonary macrophages are associated with asbestos exposure and have been implicated as significant mediators of the pathogenic process. In previous studies, we showed that macrophages are attracted to sites of asbestos fiber deposition, i.e., alveolar duct bifurcations. We also showed that macrophages accumulated at these sites as the result of asbestos-induced activation of complement proteins on alveolar surfaces, consequently producing C5a, a chemotactic factor for macrophages. In the present study, we have demonstrated the time course of chemotactic factor generation and the corresponding macrophage response in vivo. A complement-dependent chemotactic factor for macrophages was activated during a 3-h exposure to asbestos and reached maximal activity by 3 h postexposure. Macrophage accumulation followed and reached a maximal amount by 24 h postexposure. Rats decomplemented with cobra venom factor exhibited a significant reduction in macrophage accumulation, but the macrophage response ensued when serum complement returned to normal. Approximately 30% of the macrophages lavaged from complement-normal, asbestos-exposed animals contained fibers, whereas only half as many macrophages from decomplemented rats contained asbestos. A small but significant increase in lavaged lung protein was measured in asbestos-exposed animals. Evidence supports the concept that complement proteins on alveolar surfaces are derived from normal transudation of serum components from the pulmonary vasculature. Increased serum transudation could provide a source of alveolar complement that sustains the generation of a chemotactic factor for macrophages.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Induction of early alveolar injury by inhaled asbestos and silica.

Inhaled asbestos fibers and silica crystals are known to cause interstitial fibrotic lung disease in animals and humans. The initial cellular events and biochemical mechanisms that lead to development of disease are poorly understood. In ongoing studies reviewed here it has been shown that inhaled particulates small enough to pass through the conducting airways are deposited initially at the bifurcations of alveolar ducts. Within hours after brief exposure, alveolar epithelial cells phagocytose inhaled particles that subsequently are translocated to interstitial matrix and fibroblasts. Within 48 h after exposure, inhaled asbestos on alveolar surfaces activates a complement-dependent chemotactic factor for macrophages that accumulate at duct bifurcations. Epithelial cells, macrophages, fibroblasts, and the interstitial matrix are significantly altered by brief (1- 5-h) exposure to chrysotile asbestos. The basic mechanisms that mediate these initial events remain to be defined.

Animals↗
PubMed1985

Inhaled asbestos activates a complement-dependent chemoattractant for macrophages.

Pulmonary macrophages migrate to the sites where inhaled chrysotile asbestos fibers initially are deposited (i.e., surfaces of alveolar duct bifurcations). These macrophages have been shown to form a major component of an early asbestos-induced interstitial lesion in rats. In this report, we describe a potential mechanism by which macrophages are attached to these sites of fiber deposition. Chrysotile asbestos fibers used in vitro activate complement proteins in peripheral blood serum and in lavaged cell-free lung proteins. After brief inhalation of chrysotile asbestos, fluids lavaged from the lungs of exposed rats contain substantial chemotactic activity for macrophages compared to fluids from sham-exposed animals (p less than 0.01). We hypothesize that this chemotactic activity is derived from complement activated by inhaled asbestos on alveolar surfaces. This contention is supported by the following observations. Production of chemotactic activity by asbestos in vitro in serum or in lavaged lung fluids was blocked by complement inhibitors. Fractionation, by molecular sieve chromatography, of serum proteins and concentrated proteins lavaged from the lungs of asbestos-exposed rats showed that chemotactic activity was detected in the 14,000- to 18,000-dalton range. This fractionation profile is similar to C5a, the chemotactic product of complement activation. Rats treated with cobra venom factor to deplete circulating complement as well as complement-deficient mice demonstrated significantly depressed macrophage accumulation at sites of asbestos deposition. Pulmonary macrophages are the cells that form the initial inflammatory response to asbestos inhalation. Our findings support the hypothesis that asbestos fibers, and possibly other inhaled particulates, activate complement-derived chemotactic activity on alveolar surfaces. Consequently, macrophages are attracted to the alveolar duct bifurcations where inhaled asbestos fibers are deposited, and this is where the initial lesion of asbestosis is manifested.

Animals↗
PubMed1984

Surface morphology and correlated phagocytic capacity of pulmonary macrophages lavaged from the lungs of rats.

The morphology and phagocytic capacities of pulmonary macrophages recovered by lavage from normal rats were studied in vitro after incubation under various culture conditions. Most adherent macrophages (73 +/- 6%) were flat and exhibited ruffled surfaces. Phagocytosis of carbonyl iron beads by pulmonary macrophages was quantitated using secondary and backscattered electron microscopic techniques. Our results show that macrophage surface features correlate with the phagocytic capacity of the cells, that is, macrophages with ruffled membranes phagocytose a significantly greater number of iron beads than do smooth, unruffled cells (P less than or equal to 0.001). Moreover, an enhanced percentage of smooth cells (48%) was found in populations of tracheobronchial macrophages; this finding correlated with a reduced phagocytic potential. When the percentages of smooth cells were increased experimentally by incubating cells with silica or varying pH conditions, the number of macrophages devoid of carbonyl iron beads was enhanced. The results show that smooth macrophages are functionally impaired compared with ruffled cells. These studies form the basis for assessing functional alterations of macrophages exposed in vivo to inhaled toxic particulates such as chrysotile asbestos and silica.

Animals↗
PubMed1984

In vitro effects of crocidolite asbestos and wollastonite on pulmonary macrophages and serum complement.

Chronic inhalation of asbestos has been associated with interstitial fibrotic lung disease. Wollastonite fibers are currently being used as industrial substitutes for asbestiform materials. Since the pulmonary macrophage has been implicated as a modulator of fibrotic lung disease, we have investigated in vitro effects of crocidolite asbestos and wollastonite on the viability, morphology, and functional capacities of pulmonary macrophages. In addition, we have measured the capacity of these dusts to activate complement in serum, using pulmonary macrophage chemotaxis as a bioassay for activation. Preliminary evidence suggests that complement activation by inhaled dusts promotes inflammation. Acute exposures to wollastonite and crocidolite fibers in vitro had little effect upon pulmonary macrophage viability but affected changes in morphology and phagocytic capacity. Incubation of the dusts with rat serum produced complement activation. The results of these studies suggest that crocidolite and wollastonite exposures in vitro have effects on pulmonary macrophages which may simulate events occurring in the lung following dust exposures.

Animals↗
PubMed1984

Pulmonary macrophage accumulation and asbestos-induced lesions at sites of fiber deposition.

Inhaled chrysotile asbestos fibers are deposited at alveolar duct bifurcations and subsequently are phagocytized there by pulmonary macrophages. The characteristics of the rapid macrophage response at alveolar duct bifurcations following asbestos inhalation has been further evaluated. Significant numbers of pulmonary macrophages accumulated at sites of asbestos deposition within 48 h after a 1-h exposure, whereas duct surfaces of sham-exposed animals were essentially devoid of macrophages. The influx of macrophages was associated with a significantly increased bifurcation tissue area (p less than 0.025), and this alteration persisted for at least 1 month. Two thirds of the accumulated macrophages from alveolar duct bifurcations could be removed by bronchoalveolar lavage. Macrophages recovered by lavage had significant changes (p less than 0.01) in their morphology and in their phagocytic and chemotactic capacities. These cellular alterations could play a role in the pathogenesis of asbestos-related lung disease.

Animals↗
PubMed1983

Interactions of chrysotile asbestos with erythrocyte membranes.

Chrysotile asbestos causes lysis of red blood cells. It has been proposed that the mechanism of hemolysis is mediated through interactions between asbestos and cell membrane glycoproteins. Our studies support this concept and the following results are reported. Electron microscopy shows that asbestos fibers distort red blood cells and bind to cell membranes which may become wrapped around the fibers. This reaction is prevented by pretreatment of the cells with neuraminidase. The distribution of lectins which bind to membrane glycoproteins is altered by treating the cells with asbestos. Cell distortion and membrane deformation consequent to asbestos treatment correlate with a clear increase in the ratio of intracellular Na+:K+ ions.

Animals↗
PubMed1983

Interactions of chrysotile and crocidolite asbestos with red blood cell membranes. Chrysotile binds to sialic acid.

Chrysotile and crocidolite are commonly used forms of asbestos. Hemolysis has been widely used as a test of membrane injury, and it has been shown previously that chrysotile causes rapid breakdown of red blood cells (RBCs), whereas crocidolite is only weakly hemolytic. A reasonable hypothesis set forth to explain the cytotoxic effects of chrysotile maintains that positively charged chrysotile fibers bind to negatively charged sialic acid residues on RBC membranes causing clustering of membrane proteins and increased cell permeability to Na and K ions. Our studies presented here provide two lines of evidence in direct support of this hypothesis. (a) Morphologic--Ultrastructural techniques showed that both chrysotile and crocidolite asbestos bind to and distort more than 85% of RBCs treated for 15 minutes. The distorting effects of chrysotile, but not crocidolite, were almost totally ablated by pretreating the cells with neuraminidase. In addition, gold-conjugated wheat germ agglutinin was used to label the distribution of sialic acid groups on RBC membranes. Pretreatment of the RBCs with chrysotile, but not crocidolite, reduced the number of gold-conjugated wheat germ agglutinin-labeled sites to less than 30% of the control level. (b) Biochemical--The thiobarbituric acid assay was used to determine the percentage of sialic acid that remained with the cell pellet after neuraminidase and/or asbestos treatment. Asbestos treatment alone caused no release of sialic acid from the cells. Neuraminidase treatment for 3.5 hours removed more than 80% of the sialic acid from cell surfaces. Chrysotile, but not crocidolite, asbestos prevented neuraminidase-mediated removal of sialic acid from RBCs. In addition, x-ray energy spectrometry of freeze-dried cells showed that RBCs distorted by chrysotile, but not by crocidolite, exhibited significant alterations in intracellular Na:K ratios. The morphologic and biochemical data strongly support the hypothesis that chrysotile asbestos binds to sialic acid groups on RBC membranes. Consequently, the sialic acid residues are redistributed on the surfaces of distorted cells which then are unable to maintain a normal Na:K balance with the surrounding medium.

Animals↗
PubMed1983

Pulmonary macrophage phagocytosis: quantification by secondary and backscattered electron imaging.

A systematic method for quantifying phagocytosis of carbonyl iron beads by pulmonary macrophages is described. These techniques utilize secondary and backscattered electron imaging. The carbonyl iron composition has a high atomic contrast number which makes it ideal for visualization in the backscatter electron image of the scanning electron microscope. As a result, interiorized iron beads can easily be distinguished from beads attached to the surface of the cell. The morphology and phagocytic capacities of individual macrophages were compared. The results showed that functional heterogeneity exists within the normal pulmonary macrophage population. Ruffled macrophages avidly phagocytized carbonyl iron beads, while smooth cells were functionally impaired. In addition, macrophages which were altered morphologically by exposures to acidic culture conditions or to asbestos demonstrated a decreased capacity to phagocytize carbonyl iron beads. Accordingly, the surface morphology of pulmonary macrophages correlated with their phagocytic capacities. We propose that results obtained from the analyses of individual cells can be used to study the phagocytic capacity of macrophage populations.

Animals↗
PubMed1982

Interstitial accumulation of inhaled chrysotile asbestos fibers and consequent formation of microcalcifications.

Previous studies have shown that inhaled chrysotile asbestos impacts initially at the bifurcations of alveolar ducts in the lungs of rats. Asbestos fibers are transported through alveolar epithelial cells at these bifurcation regions to the interstitium during the 24-hour period after a 1-hour exposure. To further these studies, white rats were exposed to an aerosol of chrysotile asbestos for 1 hour. Animals were sacrificed, and the lungs were fixed by vascular perfusion immediately after and 1 month after exposure. Blocks of tissue were prepared for light and electron microscopy. We report here, at 1 month after exposure, that numerous asbestos fibers had accumulated within the lung interstitium at alveolar duct bifurcations. Many of these interstitial fibers were found in te center of intracellular microcalcifications. The presence of calcifications was proven by X-ray energy spectrometric analysis of the inclusions in situ. Clear X-ray peaks for calcium and phosphorus were demonstrated. The authors propose that 1 month after a 1-hour exposure to chrysotile asbestos, fiber-induced membrane injury in cells of the lung interstitium leads to formation of microcalcifications. This may represent the presence of early cell injury in the initial pathogenetic sequence of asbestosis.

Aerosols↗
PubMed1981

Chrysotile asbestos inhalation in rats: deposition pattern and reaction of alveolar epithelium and pulmonary macrophages.

The initial deposition and subsequent translocation of chrysotile asbestos were studied in the lungs of rats exposed for 1 h in inhalation chambers. Using scanning and transmission electron microscopy of tissue fixed by vascular perfusion, we determined that the majority of fibers that pass through the conducting airways deposits at the bifurcations of alveolar ducts. The farther an alveolar duct bifurcation was from its terminal bronchiole, the less asbestos were observed. The amount of asbestos present on the alveolar duct surfaces was significantly decreased 5 h after cessation of the 1-h exposure. Some fibers were taken up by Type I epithelial cells during the first hour of dusting, and this process continued through the 8-day period in which the animals were studied. As early as 24 h after exposure, there was an accumulation of macrophages at the sites of initial asbestos deposition. This may be a significant cellular response in the early pathogenesis of asbestosis.

Animals↗
PubMed1980

Ultrastructure of the nonciliated bronchiolar epithelial (Clara) cell of mammalian lung: I. A comparison of rabbit, guinea pig, rat, hamster, and mouse.

The morphologic characteristics have been used to define the nonciliated bronchiolar epithelial: (1) abundance of agranular endoplasmic reticulum (AER) and (2) numerous membrane-bound ovoid granules. To quantitatively and qualitatively assess the ultrastructural homogeneity of this lung cell type among laboratory mammals used in lung research, we examined tissue from adult male rabbits, guinea pigs, rats, hamsters and mice. Following fixation by airway infusion at constant pressure (30 cm H2O), lungs were processed by a selective embedding technique and bronchioles of known anatomic location were examined by electron microscopy. Nonciliated bronchiolar epithelium of all five species contained avoid granules and abundant AER. Granules were most abundant in the rat (11.1 +/- 8.8 per cell) and least in the hamster (4.4 +/- 5.2 per cell). Granules were largest in hamster (0.72 +/- 0.25 micrometer) versus 0.44 micrometer or less in the other species. Granules were of uniform electron density except in the guinea pig. AER spherical mitochondria with few cristae were present only in mice, rabbit, and guinea pig. We concluded that there was considerable interspecies variation in abundance, size, and morphology of the granules, in abundance and distribution of AER; and in mitochondrial morphology.

Animals↗
PubMed1980

Ultrastructure of the nonciliated bronchiolar epithelial (Clara) cell of mammalian lung: II. A comparison of horse, steer, sheep, dog, and cat.

Two morphologic characteristics have been used to define the nonciliated bronchiolar epithelial cell: abundant agranular endoplasmic reticulum (AER) and membrane-bound avoid granules. To assess the ultrastructural homogeneity of this cell type in the lungs of large domestic mammals used as experimental models in pulmonary research, we evaluated lungs of horse, steer, sheep, dog, and cat. Bronchioles of known anatomic location were examined by electron microscopy following fixation by airway infusion at standard pressure and processing by selective embedding techniques. Nonciliated bronchiolar epithelium of the horse and sheep had numerous avoid granules (averaging above 15 per cell) and abundant AER. Granules were scarce (averaging less than 2 per cell) in steer and dog and absent in cat. AER was minimal in these species compared to horse and sheep. Glycogen was the dominant cytoplasmic feature in steer, dog, and cat, variable in sheep and rare in horse. Large mitochondria with few cristae and densely staining matrix were present only in cat. We concluded that nonciliated bronchiolar cells of horse and sheep were similar in essential features to this cell type in laboratory mammals, having granules and AER in abundance, while those of steer, dog, and cat were not.

Animals↗
PubMed1980

Ultrastructure of the nonciliated bronchiolar epithelial (Clara) cell of mammalian lung. III. A study of man with comparison of 15 mammalian species.

Two morphologic characteristics have been used to define the nonciliated bronchiolar epithelial cell: (1) abundance of agranular endoplasmic reticulum (AER) and (2) numerous membrane-bound ovoid granules. In this study, we examined lobectomy specimens from three nonsmoking humans: one male (9.5 yr) and two females (62 and 43 yr) for comparison with lung specimens from mammalian species used as experimental models in lung research. Following fixation by airway infusion at constant pressure (20 cm), lung tissue was processed by a selective embedding technique and bronchioles of known anatomic location were studied by electron microscopy. Nonciliated bronchiolar epithelial cells of man contained numerous membrane-bound granules (averaging 6 per cell) in the apical cytoplasm and abundant granular endoplasmic reticulum (GER), AER was not observed. Granules averaged 0.3 micrometer in diameter and contained a fine granular matrix and parallel tubular arrays. After comparing these features in man with those of fifteen other species, we concluded that there is a great deal of interspecies variability in the cellular morphology of the nonciliated epithelial cell of distal conducting airways in mammalian lung. Three categories of this cell were observed: (1) with abundant granules and AER, characteristic of rabbit, guinea pig, rat, hamster, mouse, horse, sheep, and pig; (2) with abundant granules of GER, but no AER, characteristic of man and other primates; and (3) with few granules, little AER, and abundant glycogen, characteristic of steer, dog, cat, and ferret.

Adult↗