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Biomedical subjects

B N Gupta

Publications and source records attributed to B N Gupta.

At least 73 records · Page 4Linked to original sources
PubMed1989

Respiratory health effects from occupational exposure to wood dust in sawmills.

Spirometric lung functions were recorded for 109 workers (mean age 26.4 +/- 8.2 yr) occupationally exposed (mean exposure 8.9 +/- 7.7 yr) to soft wood dust in local sawmills along with 88 unexposed controls (mean age 28.7 +/- 9.9 yr) belonging to the same socioeconomic status to assess the prevalence of respiratory impairment in the exposed population. The results of the study showed a significantly higher prevalence of overall respiratory impairment in the exposed group even after standardizing for smoking habits (p less than 0.001). The adjusted rate for respiratory impairment in the exposed group was 29.4% as compared to 2.2% observed in the unexposed controls. The pattern of respiratory abnormality observed in the sawmill workers was predominantly the restrictive type (28.4%), indicating lower levels of forced vital capacity (FVC) in the exposed group; while in the control group, there were none with lung restriction The prevalence of airflow limitation, however, was similar in the exposed workers (1.8%) and controls (2.2%), thereby, indicating that bronchial obstruction was independent of wood dust exposure. It is concluded that the dust exposure in sawmills is associated mainly with restrictive type of pulmonary impairment in the exposed workers.

Adolescent↗
PubMed1988

Behavioral studies in petrol pump workers.

Behavioral studies were conducted on 90 petrol pump workers to study the effect of petrol on the central and peripheral nervous systems. Sixty-four control subjects of similar age and socio-economic status were also taken for purposes of comparison. Maudsley Personality Inventory (MPI), Benton Visual Retention Test, Digit Span Test, Progressive Matrices, Digit Symbol Test and Mirror Drawing Test were used for behavioral studies. Immediate and delayed memory were found to be significantly affected in exposed workers. Intellectual capacity and psychomotor ability were also significantly affected (P less than 0.01). Psychomotor ability and visuomotor learning ability were more affected (P less than 0.05) among the exposed subjects than among the controls. However, stability and extroversion-introversion ability remained unaffected.

Humans↗
PubMed1988

Effect of sodium lauryl sulphate and nickel alone and in combination on the skin of guinea pigs.

Guinea pig skin was treated with 50 mg/kg sodium lauryl sulphate (SLS) and nickel (Ni) alone and in combination (50 mg/kg SLS and 50 mg/kg Ni) for 7 and 14 days. Release of acid phosphatase, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, beta-glucuronidase, lactic dehydrogenase and malic dehydrogenase was observed, following treatment with SLS and Ni alone or in combination. Similarly, the skin contents of amino nitrogen and sulphydryl groups also increased significantly. These alterations were slightly more marked when the skin was treated simultaneously with the combination of SLS and Ni. The present study suggests that industrial workers or populations exposed simultaneously to SLS and Ni are more prone to dermal irritation or inflammation.

Acid Phosphatase↗
PubMed1987

Pathologic changes following acute methyl isocyanate inhalation and recovery in B6C3F1 mice.

Male and female mice were exposed by inhalation to 0, 3, 10, and 30 ppm methyl isocyanate for 2 hr followed by a 91-day recovery period. Sixteen of 80 (20%) male mice in the 30-ppm group died following exposure with seven deaths occurring in the first 24 hr. Two female mice died, one each in the 30- and 10-ppm concentration groups. Five mice/sex/group were examined at 2 hr and at 1, 3, 7, 14, 28, 49, and 91 days following exposure. Treatment-related changes were restricted to the respiratory system. At 30 ppm there was extensive necrosis and erosion of the respiratory and olfactory epithelia in the nasal cavity. Severe necrosis and epithelial erosion were also found in the trachea and main bronchi. Epithelialization occurred rapidly and most of the denuded turbinates were covered by flattened epithelium by Day 3. On the turbinates, recovery was essentially complete with the exception of small areas in the olfactory epithelia where lesions were present in the male mice through Day 91. In the trachea and major bronchi, fibrin and cellular debris were present in the airways, which in some cases had organized and formed intraluminal fibrotic projections. These projections became covered by respiratory epithelium. The intraluminal projections and bronchial fibrosis persisted to Day 91. In the males, where the fibrosis was more severe, chronic alveolitis and atelectasis were found. In mice exposed to 3 or 10 ppm, there appeared to be complete recovery. These inhalation studies indicate that methyl isocyanate exposure of mice at or near lethal concentrations causes reversible lesions in the nose and persistent intraluminal and mural fibrosis of the major bronchi.

Administration, Inhalation↗
PubMed1987

Four-day repeated inhalation and recovery study of methyl isocyanate in F344 rats and B6C3F1 mice.

F344 rats and B6C3F1 mice of both sexes were exposed by inhalation to 0, 1, and 3 ppm methyl isocyanate (MIC) for 4 consecutive days (6 hr/day) followed by a recovery period of 91 days. Five mice and rats/sex/group except the 3 ppm group (5 rats/sex on Day 7 and 2 males on Day 28) were killed on Days 7, 28, 49, and 91 after the exposure and examined histopathologically. Forty-nine of 56 male rats, 51 of 56 female rats, and 1 of 56 male mice in the 3 ppm group died by 28 days; early death animals were also examined histologically. Exposure-related changes occurred in rats and mice of both sexes in the 3 ppm group only. Lesions of the nasal cavity in rats and mice were characterized by regeneration of the olfactory and respiratory epithelia secondary to epithelial erosion. By Day 28 the olfactory and respiratory epithelia in mice appeared normal, while in rats incomplete regeneration of the olfactory epithelium was still present. Regeneration of the respiratory epithelium in the trachea of rats occurred in the 3 ppm group and the epithelium appeared to return to normal by Day 28. Lung lesions in rats consisted of mural and/or intraluminal fibrosis secondary to extensive erosion of the respiratory epithelium in the major bronchi to the terminal bronchioles. Acute inflammation of the small airways, occasional hyaline membranes of alveolar walls, and pulmonary atelectasis were also seen. Alveolar fibrosis was observed in rats found dead from Day 14 on and in male rats killed on Day 28. Atrophy of the thymus and spleen, atrial thrombosis of the heart, and hepatocellular necrosis were frequently seen in rats dying following MIC exposure. The lung lesions in mice were qualitatively similar to those in rats, but were restricted to the major bronchi. Minimal intraluminal or mural fibrosis was still present in mice on Day 91. In a separate study, a single 6-hr exposure of five male rats to 3 ppm MIC was followed by a recovery period of 7 days. The lesions of the respiratory system were essentially the same as those in the 3 ppm group killed on Day 7 after the 4-day repeated exposure of MIC, but the alveolar lesions were more severe.

Administration, Inhalation↗
PubMed1987

Safety evaluation of a barrier cream.

A barrier cream containing propylene glycol, silica, xylene, dioctyl adipate and amyl acetate was applied topically for 3 months in 3 species of animal. Patch tests were carried out in human volunteers up to 72 h. The cream produced slight erythema in rats, guinea pigs and rabbits, but the irritation indices remained within safe limits. Histologically, mild focal thickening and moderate thickening of stratum corneum were observed in rats and guinea pigs, respectively, after 3 months of daily application. Patch testing in human volunteers indicated that the barrier cream is reasonably safe for human use.

Adipates↗
PubMed1987

Modulation of cardiovascular reflexes by arginine vasopressin.

Arginine vasopressin (AVP), a potent vasoconstrictor, does not raise arterial pressure in normal humans or neurally intact animals, even during infusions that achieve pathophysiological plasma concentrations. It has been proposed that this is because AVP facilitates the baroreflex control of the circulation. We performed a series of investigations to test this hypothesis, and to determine sites at which AVP might act to augment the baroreflex. In anesthetized rabbits, vasopressin (36 pmol.kg-1.min-1) increased discharge from both medullated and nonmedullated single fibres from aortic baroreceptor nerves during elevations in aortic arch pressure. Similarly, vasopressin (36 pmol.kg-1.min-1) increased the response of left ventricular mechanoreceptor single fibre discharge to elevations of left ventricular end-diastolic pressure. These observations suggest that sensitization of high and low pressure baroreceptors is one mechanism by which vasopressin may facilitate baroreflexes. In a further series of experiments in sinoaortic denervated anesthetized rabbits, vasopressin (18 pmol.kg-1.min-1) facilitated vagally mediated reflex inhibition of renal sympathetic nerve activity during volume expansion. In humans, AVP (0.37 pmol.kg-1.min-1) raised plasma AVP to an antidiuretic level (22 +/- 4 fmol/mL), but did not change blood pressure or the baroreflex control of heart rate or forearm vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Vasopressin facilitates inhibition of renal nerve activity mediated through vagal afferents.

We measured the effect of vasopressin (8 mU X kg-1 X min-1) on reflex inhibition of renal sympathetic nerve activity induced by volume expansion in 13 sinoaortic-denervated anesthetized rabbits. Volume expansion increased left ventricular end-diastolic pressure (LVEDP) from 5.1 +/- 0.7 to 14.1 +/- 1.4 mmHg and decreased renal nerve activity (RNA) from 57.4 +/- 6.9 to 30.2 +/- 5.6 impulses/s. Infusion of vasopressin elevated LVEDP from 6.0 +/- 1.0 to 7.3 +/- 1.1 mmHg and decreased RNA from 61.8 +/- 7.2 to 47.1 +/- 6.3 impulses/s. Heart rate fell from 243 +/- 7 to 231 +/- 9 beats/min; no other significant hemodynamic changes were seen. During the infusion of vasopressin, volume expansion increased LVEDP to 13.7 +/- 1.2 mmHg and decreased RNA to 17.0 +/- 4.2 impulses/s. The slopes relating the percent decrease in RNA to the rise in LVEDP were calculated from values of RNA recorded at several levels of LVEDP. The slope averaged -6.2 +/- 1.1%/mmHg before vasopressin and nearly doubled (-11.9 +/- 1.8%/mmHg) during vasopressin. Infusion of placebo (saline) instead of vasopressin did not alter the reflex inhibition of nerve activity. Bilateral vagotomy abolished the decrease in resting nerve activity that occurred during infusion of vasopressin as well as the reflex inhibition of RNA. These data demonstrate that vasopressin facilitates the reflex inhibition of renal sympathetic nerve activity associated with increases in LVEDP and mediated through vagal afferents.

Animals↗
PubMed1987

Effect of methyl isocyanate (MIC) gas on the eyes of Fischer 344 rats.

The accidental release of methyl isocyanate gas in Bhopal, India, was reported to cause temporary blindness and other eye injuries in many of the exposed people. Methyl isocyanate (MIC) is known to be corrosive and to irritate intact skin and mucous membranes, but little is known about the extent of ocular damage incurred during exposure to its vapors. The eyes of male and female Fischer 344 rats were evaluated immediately after a 2-hr exposure to 0, 3, 10, or 30 ppm of MIC, and periodically thereafter during a 91-day recovery period. During exposure to 10 ppm and higher concentrations, rats kept their eyes partially closed. Copious lacrimation and occasional frothy nasal discharge were evident. Eyes were examined under ultraviolet light after topical application of sodium fluorescein, and histopathologic examination included lids, cornea, lens, retina, optic nerve, and Harderian gland. There was no significant gross or microscopic evidence of epithelial erosion or ulceration of the cornea, or of adjacent tissues immediately after, or at any time following exposures. No skin irritation was noted. It would appear that the natural protective mechanisms of the eye of rats were adequate to prevent ocular damage at these exposure levels.

Animals↗
PubMed1987

The toxicity of inhaled methyl isocyanate in F344/N rats and B6C3F1 mice. II. Repeated exposure and recovery studies.

F344/N rats and B6C3F1 mice were exposed to 0, 1, 3, or 6 ppm methyl isocyanate by inhalation for 6 hr on 4 consecutive days. Deaths of rats were observed following 3 ppm exposures, and mice died after exposures to 6 ppm. Deaths appeared to be related to severe respiratory distress. Survivors in high dose groups lost weight initially, then gained weight at rates equal to controls throughout a 91-day recovery period. Lung weights increased significantly in male and female rats exposed to 3 ppm, but no persistent changes in brain, kidney, thymus, spleen, liver, or testis weights were seen in either mice or rats. Blood and serum from male and female rats were taken for clinical pathology and hematology assessments on day 7 of postexposure, the day prior to the first observed deaths of these animals. No changes or only slight changes were seen in measures of serum alanine aminotransferase, sorbitol dehydrogenase, alkaline phosphatase, or in blood and brain cholinesterase activities. However, serum creatine kinase increased with dose in both males and females. Blood urea nitrogen, creatinine, and methemoglobin were unchanged. No changes were seen in counts of red blood cells or platelets, or in red cell indices. Hemoglobin concentrations and hematocrits were slightly elevated. No changes were noted in absolute leukocyte counts, but counts of segmented neutrophils increased and lymphocytes decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗