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Biomedical subjects

O S Atwal

Publications and source records attributed to O S Atwal.

At least 37 records · Page 2Linked to original sources
PubMed1985

Impairment of sympathetic pulmonary vasoconstriction by 3-methylindole in cattle.

Sixteen Holstein cattle allotted into 4 groups (4 cattle/group) were each given a single oral dosage of 0.2 g of 3-methylindole (3MI)/kg of body weight. The groups were killed at 12, 24, 48, and 72 hours, respectively, after 3MI administration. Comparison of clinical signs, pathologic pulmonary lesions, and in vitro pulmonary artery responses to pharmacologic stimuli was made between the 4 treated groups and 8 control Holstein cattle of similar age. Clinical signs of pulmonary distress first appeared 8 to 12 hours after 3MI administration. After 20 hours, clinical signs included dyspnea, moderate depression, and a marked expiratory grunt. A partial remission of these clinical signs was seen between 30 and 45 hours after 3MI administration. After remission, the cattle had clinical signs of severe dyspnea and depression and expiratory grunts were more pronounced. Pathologic pulmonary lesions, including heavy rubbery lungs, dilated interlobular septae, and subplural air bullae characteristic of pulmonary edema and interstitial emphysema were observed. The lungs of treated cattle did not collapse when the thorax was incised at necropsy. In vitro pulmonary artery strips contracted dose dependently to norepinephrine (NE). Group I tissues (12 hours after 3MI administration) responded similarly to control samples. Group II tissues (24 hours after 3MI administration) had a significant inhibition (P less than 0.05) in response to NE stimulation as compared with controls.

Animals↗
PubMed1984

Ultrastructural pathology of intrapulmonary arteries in 3-methylindole-induced pneumotoxicity in cattle: II. Glycogen accumulation in the smooth muscle cells and intimal changes.

3-Methylindole (3MI) was orally administered as a single dose of 0.1-0.2 g/kg which then produced acute pulmonary oedema in cattle 72 h post-treatment. Electron microscopic examination of intrapulmonary arteries ranging between 35-120 microns in the control animals, revealed microsequestration of rough endoplasmic reticulum (RER) and the storage of proteinaceous material in the dilated cisternae of RER of the endothelial cells. Lung tissue samples collected after 72 h of 3MI administration, showed denudation and hyperplasia of the endothelial cells. Massive storage of glycogen particles and the lamellar bodies in association with glycogen, were observed in the smooth muscle cells of the media. The importance of glycogen accumulation in vascular smooth muscle cells of the pulmonary arteries is discussed in terms of energy utilization and vascular energetics to meet the metabolic requirement of haemodynamic stress arising from alveolar hypoxia and possible vasoconstriction. Furthermore, the suggestion is made, that the alterations may signify the early changes of pulmonary hypertension induced by the toxic effect of 3MI in cattle.

Animals↗
PubMed1984

Occurrence of Mallory body-like inclusions in parathyroid chief cells of ozone-treated dogs.

Ultrastructural characteristics of chief cells of the parathyroid glands of ozone-treated dogs were examined 3 days, 10-13 days and 28 days after treatment. Dilated Golgi cisternae and vacuoles contained low electron dense fibrillar material. These changes in the Golgi were accompanied by massive accumulation of filaments in the perinuclear area where most of the cell organelles were disrupted to the peripheral zone of the filamentous inclusions. These inclusions were not enclosed by a membrane and corresponded with PAS-positive and diastase-resistant material in the chief cells at light microscopic level. Therefore these inclusions were arbitrarily designated as Mallory body-like inclusions.

Animals↗
PubMed1984

Ultrastructural changes in intraacinar pulmonary veins. Relationship to 3-methylindole-induced acute pulmonary edema and pulmonary arterial changes in cattle.

In 3-methylindole (3MI)-treated cattle electron-microscopic examination of intrapulmonary arteries showed changes of an arteritis which could be related to pulmonary hypertension. To further elaborate on this concept, the present study describes the ultrastructural pathology of intraacinar pulmonary veins in cattle 72 hours after oral administration of 3MI. The changes include significant thickening of the muscular pads of the media, massive glycogen accumulation in the venous smooth muscle cells, proliferation of the myointimal cells, focal protrusion of cytoplasmic portion of a smooth muscle cell into an adjacent cell body suggestive of vasoconstriction and emigration of lymphocytes and platelets through the vascular wall. The experimental data are discussed in relation to the ultrastructural pathology of intraacinar pulmonary arteries and acute pulmonary edema. The authors further present evidence that 3MI acute pneumotoxicosis is also associated with drastic vascular changes which may signify sudden elevation in arterial and venous pressures in the pulmonary system of cattle.

Animals↗
PubMed1983

Occurrence of APUD-type cells in the ciliated cyst of the parathyroid gland of ozone-exposed dogs.

Presence of APUD-type cells in the ciliated cysts of the parathyroid glands of ozonized dog is described in this report. These cells were present on the abluminal side of the cyst wall and contained secretory granules with dense core, homogeneous matrix and coated vesicles throughout the cytoplasm. Intermixed with the granules were sheaves of microfilaments which were mostly seen in the perinuclear area. The APUD cells formed hemidesmosomes with the basal lamina.

APUD Cells↗
PubMed1983

Ultrastructural pathology of 3-methylindole-induced pneumotoxicity in cattle. I. Glycogen accumulation in the alveolar type II cells and tubular myelin accumulation in the alveoli.

3-Methylindole (3MI) was orally administered as a single dose of 0.1-0.2 gm/kgm which then produced acute pulmonary edema in cattle. Electronmicroscopic examination of lung tissue collected after 72 hours revealed vesiculation and desquamation of alveolar type I cells as well as hyperplasia of the alveolar type II cells. Hyaline membrane formation, along with massive accumulation of tubular myelin in the alveolar spaces, was observed. Pulmonary capillaries were occluded with microthrombi and leukocytes infiltrated the interstitium as well as the alveoli. Accumulation of large aggregates of glycogen in the alveolar type II cells were the most unusual changes seen in the experimental animals. It is suggested that accumulation of tubular myelin is a structural manifestation of surfactant inactivation by the plasma proteins. Furthermore, the disease process may be complicated by a compositional or quantitative defect in the surfactant produced by the alveolar type II cells, which are pathologically loaded with glycogen.

Animals↗
PubMed1981

Myelinated nerve fibers in the parathyroid gland of the dog: a light and electron-microscopic study.

The distribution of myelinated and non-myelinated nerve fibers in the parathyroid glands of the dog was studied by light and electron microscopy. The mixed fasciculi with myelinated nerve fibers (average diameter 7.0 micron) and unmyelinated fibers were present independent of the adventitia of the arterioles. The mixed fasciculi were accompanied by large amounts of collagen fibrils running in the direction of the nerve fibers. The fasciculi were surrounded by a complete sleeve composed of a perineural epithelial sheath which a basal lamina on both sides. The possibility that these fibers might represent an afferent pathway is discussed.

Animals↗
PubMed1981

Glycogen accumulation in alveolar type II cells in 3-methylindole--induced pulmonary edema in goats.

The present study shows that intravenous infusion of 3-methylindole (3MI) induced acute pulmonary edema in goats. Edematous changes were seen in the alveoli and the interalveolar interstitium. At 72 hours after treatment, an accumulation of glycogen that had a pathognomonic appearance of alpha particles was observed in the alveolar Type II cells. A rich accumulation of glycogen particles and defective lamellar bodies containing triglycerides were the significant morphologic changes in the alveolar Type II cells. These findings suggest that massive glycogen deposition in the alveolar Type II cells is a defect that might interfere with surfactant production, further complicating the disease process.

Animals↗
PubMed1981

Morphology of microvascular changes and endothelial regeneration in experimental ozone-induced parathyroiditis. III. Some pathologic considerations.

Proliferation of the vascular endothelium of the parathyroid glands of dogs exposed to ozone inhalation was studied. Direct observation of mitoses in the endothelial cells were made. Focal hemorrhages in the form of the presence of erythrocytes, clotting, and fibrin deposition in the extravascular spaces were seen. Ultrastructural analysis of transverse section of blood vessels showed intravascular platelet aggregation. Lymphoid cells were observed in the lumen of the blood vessels as well as in the perivascular areas as infiltrates. The possibility is discussed that present vascular reactions signify the morphologic equivalent of an immunologic response.

Animals↗
PubMed1980

Membrane-bound glycoprotein in the alveolar cells of the caprine lung.

An ultramicroscopic analysis of caprine lung glycoproteins, designed to detect plasmalemma-associated sulfoglycoprotein of alveolar type I and alveolar type II cells, was performed. High-iron diamine staining demonstrated a layer containing sulfated glycoproteins at the atypical plasmamembrane of alveolar type I cells and microvilli of alveolar type II cells. The cytoplasmic vesicles of the alveolar type I cell contained the reaction product on the inner leaflet of the vesicular unit membrane. The vesicles showed a variety of interactions with the apical plasma membrane. High-iron diamine staining also demonstrated sulfoglycoproteins in the cytoplasmic granules of the mast cells in the alveolar septum. The present study gives evidence that plasmalemma of the alveolar cells of the goat lung possesses exposed hyaluronic acid groups.

Animals↗
PubMed1979

PAS-positive inclusions in the alveolar type II cells of the caprine lung.

Histochemical analysis of inclusions in the alveolar type II cells was done with the alcian blue-PAS technique. PAS-positive inclusions, which were absent in the sheep and buffalo, were detected in the alveolar type II cells of the goat lung. Mixed diamine-sodium chloride did not stain these inclusions which also showed orthochromatic blue reaction with toluidine blue. The high percentage of alveolar type II cells showing these inclusions suggested that this difference could be explained by the environmental habitat of the goat.

Animals↗
PubMed1979

Ultrastructural pathology of ozone-induced experimental parathyroiditis. IV. Biphasic activity in the chief cells of regenerating parathyroid glands.

Sequential development of electron miscrosopic changes in the rabbit parathyroid gland was monitered during induction of parathyroiditis by 48 hours of ozone 0.75 ppm dosage regimen. By 4 to 7 days, electron microscopy revealed prominence of polyribosomes, rough endoplasmic reticulum, Golgi complex, secretory granules, microtubules, and frequent infoldings of the plasma membrane. Presumable this was the stage of parathyroid hormone synthesis. Between 14 to 18 days, ultrastructural observations showed dilatation of rough endoplasmic reticulum with continuity with annulate lamellae, disaggregation of polyribosome attached to the rough endoplasmic reticulum, and accumulation of numerous solitary free ribosomes in the cytoplasm. The dilated portion of endoplasmic reticulum contained medium electron-dense granular material, which also appeared between the intercellular spaces. The medium electron-dense material assumed to condensed appearance of basal lamina bordering the intercellular matrix. On the basis of the present observation it was concluded that the second set of ultrastructural changes signify the stage of basal lamina reconstruction. The significance of these changes as reparative responses to the inflammatory stimuli was discussed.

Animals↗
PubMed1975

A possible autoimmune parathyroiditis following ozone inhalation. II. A histopathologic, ultrastructural, and immunofluorescent study.

Histologic, ultrastructural, and immunofluorescent changes in the parathyroid glands of rabbits have been studied after 48 hours of ozone inhalation at a dosage of 0.75 ppm. The frequent changes observed included hyperplastic parathyroiditis followed by capillary proliferation and leukocytic infiltration. The progressive cytologic events consisted of the presence of eosinophilic leukocytes, reticuloendothelial and lymphocytic infiltration, disaggregation of the parenchyma, and interstitial edema. The ultrastructural changes consisted of degeneration of nuclei, atrophy of the mitochondria, dilatation and atrophy of the endoplasmic reticulum of the chief cells of the parathyroid gland, proliferation of the venous limb of the capillary network, and the prominent interstitial elements. The immunofluorescent techniques revealed positive immunologic response. These data suggest that ozone inhalation perhaps triggers an immune reaction which causes inflammatory injury to the parathyroid gland. The possibility that the modified functional chemical groups of the parathyroid gland act as autoantigen is discussed.

Aerosols↗