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Biomedical subjects

L Srivastava

Publications and source records attributed to L Srivastava.

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

Hormonal effects of smoking--I: Effects on plasma renin activity.

It is generally recognized that smoking is associated with an increased risk for the development of coronary artery disease. Since it has been suggested that increased plasma renin activity (PRA) may be a risk factor for cardiovascular disease, PRA was measured in a group of smokers and nonsmokers. PRA was measured under basal conditions, following intravenous (IV) furosemide administration and after a short burst of smoking. In addition, the effect of nicotine on renin secretion was evaluated in vitro. Smoking was associated with a significant increase in pulse rate and systolic blood pressure, but no significant change in diastolic blood pressure in both groups. Basal PRA was similar among smokers and was not significantly influenced by smoking in either group. PRA increased significantly following IV administration of furosemide, but there was no significant difference between the two groups. Incubation of rat kidney slices with nicotine also did not result in increased renin secretion. These findings confirm that smoking affects the cardiovascular system, but no significant effect of smoking on PRA was observed both in vivo and in vitro experiments. These findings suggest that the increased risk for the development of coronary artery disease associated with smoking is not mediated by increased PRA.

Adult↗
PubMed1986

Hormonal effects of smoking--II: Effects on plasma cortisol, growth hormone, and prolactin.

Effect of smoking on the plasma levels of cortisol, growth hormone, and prolactin was evaluated in a group of smokers and nonsmokers. Plasma levels of these hormones were measured under basal conditions and following a short burst of smoking. In addition, to determine the mechanism of action of nicotine on the release of these hormones, rat renal cortical slices were incubated with nicotine and the generation of cyclic AMP was measured in vitro. Increasing concentrations of nicotine in the incubation medium resulted in increased generation of cyclic AMP. Basal levels of plasma cortisol were similar for both smokers and nonsmokers. After smoking, the cortisol levels increased significantly among smokers only and the levels achieved were significantly higher compared with nonsmokers. Mean prolactin curves were higher among nonsmokers compared with smokers, whereas growth hormone levels were similar in the two groups. These data suggest that the effects of smoking on pituitary/adrenal hormones differ among smokers and nonsmokers and that these effects may be mediated through increased generation of cyclic AMP induced by nicotine.

Adult↗
PubMed1986

Enzyme-linked immunoabsorbant assay of apolipoprotein AII in plasma, with use of a monoclonal antibody.

We produced a monoclonal antibody (C2-22) to human apolipoprotein (Apo) AII and describe its use in an enzyme-linked immunoabsorbant assay (ELISA) for Apo AII in human plasma and lipoprotein subfractions. No cross reactivity of the antibody with Apo CI, CII, CIII, E, or ablumin was detected. Apo AI and low- and very-low-density lipoprotein cross reacted by 0.25%, less than 0.2%, and less than 0.3%, respectively. Whole plasma high-density lipoprotein (HDL) and HDL subfractions (HDL2 and HDL3) produced parallel displacement curves. This quantitative ELISA is based on competition between solid-phase-bound Apo AII and free Apo AII. Bound C2-22 is detected by alkaline-phosphatase-labeled second antibody. The standard curve for the assay is linear for plasma diluted 500-fold originally containing 140 to 1140 mg of Apo AII per liter. Delipidation of plasma samples exposed no additional antigenic sites. Within- and between-run CVs were respectively 8.4% and 8.7% at 327 mg/L of Apo AII, and 6.8% and 7.4% at 587 mg/L. Results correlated well with those by a polyvalent-antisera-based RIA procedure: r = 0.916, p less than 0.01, RIA = 0.896 ELISA -19.1 mg/L.

Animals↗
PubMed1985

Chelation in metal intoxication XVII: Antidotal efficacy of polyaminocarboxylic acids on acute chromate toxicity.

Some polyaminocarboxylic acids containing amino and carboxyl groups as metal binding sites in different structural arrangements were evaluated for their relative efficacy in protecting against acute chromate intoxication in mice. Nitrilotriacetic acid (NTA) and 1,2 cyclohexylenediamine tetraacetic acid (CDTA) were most effective in preventing mortality (50-70%) due to a lethal dose of potassium chromate at one-tenth of their respective LD50.

Amino Acids↗
PubMed1985

Impairment of granulomatous inflammatory response to Histoplasma capsulatum by inhibitors of angiotensin-converting enzyme.

Systemic infection with Histoplasma capsulatum induced a granulomatous inflammatory response in the lymphoreticular organs of C57BL/6 mice that was associated with elevated levels of angiotensin-converting enzyme (ACE) in the spleens. To determine the influence of ACE on the granulomatous response, either captopril or MK 421, two inhibitors of ACE, were administered intraperitoneally to mice 6 h after intravenous injection of H. capsulatum and then daily for 1 week. Each ACE inhibitor sharply reduced ACE activity in the spleens of infected mice. Both drugs worsened the clinical severity of infection and significantly increased the growth of H. capsulatum in livers and spleens of mice infected for 1 week. The histopathological changes in mice given captopril were more severe, with massive infiltrates of macrophages in proximity to large aggregates of yeasts. Conversely, the administration of captopril for 2 weeks during the resolving phases of infection did not slow the healing of the granulomatous lesions, nor did it provoke a relapse of infection. Captopril did not promote the growth of H. capsulatum in artificial medium. This drug was not cytotoxic to peripheral blood leukocytes or to splenic leukocytes from normal and infected mice. Administration of captopril to normal mice for 1 week did not depress the response of splenocytes of concanavalin A or to phytohemagglutinin, nor did it diminish delayed-type hypersensitivity responses in vivo. Finally, captopril did not augment the growth of H. capsulatum within macrophages. Our results suggest that ACE may participate in the regulation of the granulomatous inflammatory response to H. capsulatum and that ACE inhibition impairs the protective effects of granulomatous inflammation during acute H. capsulatum infection.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Investigation of possible zoonotic reservoirs of Indian kala-azar.

Possible animal reservoirs of Indian kala-azar were investigated during a recent outbreak of the disease; dogs, Rattus rattus and Bandicoota bengalensis were examined. Microscopical and serological examinations were carried out and antileishmanial antibodies found in five out of 226 B. bengalensis.

Animals↗
PubMed1983

Effects of sarcoid and steroids on angiotensin-converting enzyme.

Serum angiotensin-converting enzyme (ACE) has been claimed to be a useful guide in the treatment of pulmonary sarcoidosis. We reviewed the clinical course of 36 patients with sarcoidosis who had ACE levels determined on 2 or more occasions during the course of treatment with prednisone for a total of 55 paired observations. There was a clinical deterioration in 13 instances. Of these 13, there was a rise in ACE level in only 7. There was a clinical improvement in 19 instances. Of these 19, only 12 had a fall in ACE level. There was a negative correlation (r = -0.80) between changes in steroid dose and serum ACE level. Of 23 instances where steroids were increased, there was a fall in ACE level. Thus, ACE levels were not useful for following disease activity in patients during a change in medication.

Adrenal Cortex Hormones↗
PubMed1982

Pleural plaques in asbestosis: effect of Candida albicans.

Effect of chrysotile dust alone or together with Candida albicans administered intratracheally in guinea pigs was studied in the genesis of pleural plaques over a period of 12 months. A significant increase of mucopolysaccharides, phosphorus, calcium and -SH content was detected in pleural fluid of animals treated with chrysotile and Candida albicans together than in those treated with chrysotile or Candida albicans alone. The results suggest that an infection of Candida albicans accentuates the effect of chrysotile by altering the biochemical parameters preceding to the formation of pleural plaques.

Animals↗