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Biomedical subjects

H J White

Publications and source records attributed to H J White.

At least 37 records · Page 2Linked to original sources
PubMed1986

Pulmonary functional and morphological changes induced by a 4-week exposure to 0.7 ppm ozone followed by a 9-week recovery period.

Male Fischer-344 rats (control, C = 12; experimental, E = 11) were subjected to pulmonary-function testing procedures. The experimental group was then exposed to 0.7 ppm ozone for 28 d, 20 h/d, and both groups were tested at the termination of the exposure and after 4 and 9 wk of recovery in clean filtered air. Another group of animals (C = 6, E = 12) was similarly treated, but at each test point one-third were sacrificed for microscopic evaluation. When percent changes from preexposure values were compared to controls at each time point, the ozone exposure produced obstructive changes in the lung, including significant decreases (p less than 0.05) in forced expiratory flows (MEF25 40.3%, MEF10 70.7%), lung volumes (IC 22.5%, FVC 21.8%), and DLCO (20.7%); and a significant increase in functional residual capacity (FRC 61.1%). The total lung capacity (IC + FRC) was not significantly changed by the ozone. Microscopic examination revealed characteristic lesions in the region of terminal bronchioles and central acinar alveoli marked by peribronchiolar edema, bronchiolization of alveolar duct epithelium, and type II cell proliferation in involved alveoli with increased numbers of macrophages and a few leucocytes. Clearly discernable was a focal interalveolar-alveolar duct reaction made up of fibroblasts, a few inflammatory cells, and conspicuous mast cells, all embedded in a loose metachromatic matrix. After 4 wk of recovery, all measurements of lung volume and DLCO had returned to the values of the control group; however, even after 9 wk some of the measurements of lung flow (MEF25, MEF10) remained significantly although less depressed (27.9 and 40.1%, respectively). Histologically, after 4 wk recovery, there remained only a slight unevenly disturbed inflammatory reaction. In these foci there was often a residual, narrower, more condensed band of eosinophilic material, presumably collagen, that sometimes contained interspersed mast cells. After 9 wk, this collagen accumulation within the thickened wall of the alveolar duct could occasionally still be noted. These data suggest that the florid response seen at the end of exposure was related to the obstructive changes measured and that, with recovery, the residual central acinar-alveolar duct thickening may be responsible for the persistently diminished air flows.

Animals↗
PubMed1984

Functional and morphologic changes in the lungs after a single intratracheal instillation of silica.

The functional and morphologic consequences in the lungs of a single intratracheal instillation of silica dust were evaluated over 6 months. Male Fischer-344 rats were subjected to pulmonary function tests that measured lung volumes, forced expiratory flows, and carbon monoxide diffusing capacity (DLCO). Then saline (0.7 ml, n = 10) or saline containing either 10 mg (n = 9) or 40 mg (n = 14) of silica dust was instilled in the trachea, and each animal was tested 3, 12, and 24 wk later. Morphologic studies were performed on 27 rats similarly treated (3/group/time). By 3 wk after instillation, the inspiratory capacity, forced vital capacity, and DLCO diminished significantly (p less than 0.01) in the high-dose group. After 3 wk, the response tended to level off. Forced expiratory flows were not significantly affected. By contrast, biochemical analysis of lung collagen content indicated a linear accumulation throughout the experimental period. Microscopic evaluation revealed intra-alveolar accumulation of lipoproteinaceous material (alveolar proteinosis) by 3 wk in both dose groups, which persisted through the 24-wk experimental period. A few fibrotic nodules were seen as early as 3 wk in the 40-mg silica group, and their numbers increased with time, whereas they were relatively sparse in the 10-mg silica group throughout the experimental period, despite the diminished functional measurements. These data suggest a closer temporal correlation of the functional decrements observed to the evolution of the alveolar changes than they do to the development of fibrosis. We conclude that the development of nodular fibrosis was not the major contributing factor to the observed functional changes.

Animals↗
PubMed1983

Hepatic and splenic injury in dogs caused by direct impact to the heart.

The purpose of this study was to explore the possibility that nonpenetrating cardiac impact can directly result in hepatic and splenic injury through hemodynamic effects. Impact upon the anterior surface of the heart was produced in 34 open-chest anesthetized dogs. In 15 dogs the velocity of impact was 12 m/sec and in 19 dogs it was 18 m/sec. Pressure in the inferior vena cava transiently reached 194 +/- 25 mm Hg in the dogs impacted at 12 m/sec and 377 +/- 44 mm Hg in dogs impacted in 18 m/sec. Aortic pressure transiently reached 449 +/- 32 mm Hg in dogs impacted at 12 m/sec and 682 +/- 33 mm Hg in dogs impacted at 18 m/sec. Gross capsular lacerations of the liver occurred in six dogs (18%) following cardiac impact. All dogs showed hepatic congestion and most showed microscopic injury of liver cords, central veins, and portal tracts. Dogs that survived cardiac impact for the duration of observation (90 minutes) showed focal acute inflammation of liver triads and hepatic sinusoids, indicating a more subtle degree of injury. The spleens of eight dogs showed areas of grossly visible subcapsular hemorrhage. Subcapsular congestion of the spleen occurred in almost all dogs. This study shows therefore that nonpenetrating cardiac impact may result in hepatic and splenic injury. A likely mechanism may be the extraordinarily high venous pressure that develops at the instant of impact, although transient striking elevations of arterial pressure may also contribute.

Acute Disease↗
PubMed1982

Effect of estradiol on chlamydial genital infection of female guinea pigs.

Female guinea pigs were treated daily with 1 mg of beta-estradiol-3-benzoate intramuscularly beginning 14 days before intravaginal inoculation with the chlamydial agent of guinea pig inclusion conjunctivitis and continuing during the course of the infection. Treatment with estradiol was found to markedly influence the course of genital infection with the chlamydial agent of guinea pig inclusion conjunctivitis, producing infections of greater intensity and longer duration than those in control animals. Moreover, pathogenesis was altered in that ascending infection was observed, resulting in endometritis, cystic salpingitis, and cystitis. Infection in the controls was limited to the cervix and vagina. Estradiol treatment increased the apparent number of infected cells in the cervix and vagina as detected by histopathology and immunofluorescent staining. Humoral and cell-mediated immune responses to the chlamydial agent of guinea pig inclusion conjunctivitis were comparable in estradiol-treated and untreated animals. These data indicate that hormonal manipulation may have profound effects on the course of chlamydial genital infections.

Animals↗
PubMed1981

Early pulmonary response of the rat lung to inhalation of high concentration of diesel particles.

Light microscopy was used to study the pathologic alterations in the rat lung after timed diesel exposures to 6000 micrograms m-3 of diesel particulates ranging from 6 h to 9 weeks. As a general reaction, an increase in alveolar macrophages containing diesel particles, an increase in type II pneumocytes, and an accumulation of inflammatory cells within the alveoli and septal walls was observed. Histochemical differentiation between type II cells and alveolar macrophages was clearly delineated by the use of the PAS (periodic acid Schiff) stain in which macrophages stained positive and type II cells negative for this reaction. After the 9-week exposure, the accumulation of macrophages and accompanying type II cell reaction resulted in the formation of alveolar complexes that seemed to be preferentially localized near the terminal bronchioles. The similarity of the lesion to that of 'macrophage alveolitis' produced in animals repeatedly exposed to coal dust is emphasized, although the ultimate clinical significance of the complex formation cannot be assessed within the time limits of the experimental observation.

Aerosols↗
PubMed1981

A new animal model for the study of Chlamydia trachomatis genital infections: infection of mice with the agent of mouse pneumonitis.

A new animal model for the study of genital infections caused by Chlamydia trachomatis has been developed. Female mice were successfully infected after intravaginal inoculation with the C. trachomatis agent of mouse pneumonitis. Evidence for infection was obtained by detection of chlamydial inclusions in smears of cervical scrapings treated with Giemsa stain. Chlamydiae were observed in sections of cervical tissues examined by light and electron microscopy as well as by immunofluorescence microscopy. An antibody response to the agent of mouse pneumonitis was also demonstrated in sera after infection. The mouse model of genital infection with the agent of mouse pneumonitis offers an opportunity to investigate many questions related to pathogenesis and immunity associated with C. trachomatis genital infections.

Animals↗
PubMed1979

Microorganisms seen by scanning and transmission electron microscopy in Legionnaires' disease from human lung.

In addition to several anomalous structures, other general forms of definitely rod-shaped microorganisms have been found by scanning and transmission electron microscopy in the lung tissue taken at autopsy from a patient who succumbed to confirmed Legionnaires' disease with extensive necrotizing lobar pneumonia. The microorganisms were greatly varied in size and shape. They were micrographed in the act of fission. These forms have been found to some extent throughout the tissue. No nickel was demonstrated, either in the lung tissue or in the microorganisms.

Humans↗
PubMed1979

Identification of heparin resistance during cardiac and vascular surgery.

An investigation of the response of the activated clotting time to systemic heparinization during cardiopulmonary bypass and peripheral vascular surgery was prompted by the death from clotting of a patient with endocarditis while undergoing valve replacement. The activated clotting time during cardiopulmonary bypass was thereafter maintained at 300 to 400 seconds. Consumption of heparin sodium, derived from an individual dose-response curve, was 0.01 to 3.86 units/kg/min. There was no correlation between initial heparin resistance and the subsequent rate of consumption. Some patients undergoing peripheral vascular surgery required additional heparin after an initial standard dose of 8,000 units so as to maintain their activated clotting time at twice the control values. These data are discussed in relation to previous articles, and recommendations are made for adequate intraoperative heparinization.

Adolescent↗
PubMed1979

Annulate lamellae in human tumor cells.

Annulate lamellae have been found in a primitive neuroectodermal tumor, a metastatic cerebellar tumor, a testicular seminoma, a retinoblastoma and three melanomas. These annulate lamellae are arranged in stacked parallel arrays in the cytoplasm of tumor cells. The number of annulate lamellae observed to comprise a single stack varies from 2--4 in the seminoma tumor to 5--18 in the cerebellar tumor. Although the functional significance of annulate lamallae is still unknown, in many instances they have been found to be continuous with rough-surfaced cisternae of the endoplasmic reticulum and ribosomes have been demonstrated on the surface of annulate lamellae. This may suggest that annulate lamellae participate in protein synthesis.

Cerebellar Neoplasms↗
PubMed1979

An ultrastructural demonstration of the agent of Legionnaires' disease in the human lung.

The authors have provided ultrastructural demonstration from human material of a small rod shaped organism that represents the causative agent of Legionnaires' disease. The organisms are found mainly in intracytoplasmic vacuoles of alveolar cells. They have a thin outer cell wall and a more delicate plasma membrane. On the basis of morphology, arguments are presented to classify these unusual organisms as rickettsia-like.

Bacteria↗
PubMed1979

Target tissues associated with genital infection of female guinea pigs by the chlamydial agent of guinea pig inclusion conjunctivitis.

Female guinea pigs were experimentally infected in the genital tract with the strain of Chlamydia psittaci that causes guinea pig inclusion conjunctivitis. Chlamydiae were found frequently in superficial squamous epithelial cells of the exocervix, along with heavy involvement at the squamocolumnar junction. In this zone chlamydiae were observed in columnar cells, but inflammation and chlamydial inclusions were not observed in true endocervical epithelium. These observations were supported by results of immunofluorescence microscopy. Electron micrographs revealed typical chlamydiae within surface epithelial cells at the squamocolumnar junction; various stages of the growth cycle (elementary, reticulate, and intermediate bodies) were also present. Cytopathologic features were not remarkable, but peripheral distribution of organelles, rarefaction of the cytoplasm, and loss of microvilli were observed.

Animals↗