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Biomedical subjects

V Popa

Publications and source records attributed to V Popa.

At least 37 records · Page 2Linked to original sources
PubMed1988

Lymphocytic interstitial pneumonia of common variable immunodeficiency.

We report the beneficial effect of steroids in a 27-year-old woman with lymphocytic interstitial pneumonitis (LIP) and common variable immunodeficiency (CVID). Exertional dyspnea, x-ray infiltrates, and pulmonary physiologic abnormalities decreased or increased during 3 1/2 years of follow-up in parallel with the administered dose of prednisone. This observation rules out concomitant spontaneous remission as the explanation of steroid-induced improvement of LIP in CVID. Steroid treatment was apparently safe: the frequency and severity of recurrent bronchial infections did not change, although IgG replacement therapy was not provided.

Adult↗
PubMed1987

Captopril-related (and -induced?) asthma.

A 51-yr-old nonsmoking male patient without any history of previous allergies, asthma, hay fever, or urticaria developed attacks of asthma when captopril was added to the nadolol and dyazide treatment for his high blood pressure. A double-blind challenge with nadolol and captopril decreased FEV1 by 3 and 12%, respectively. This confirmed the history of captopril-related asthma. As angiotensin-converting enzyme seems to play a role in the genesis and metabolism of bronchomotor mediators, this rare form of drug-induced asthma is important for both clinicians and airways pharmacologists.

Asthma↗
PubMed1986

The relationship between acetylcholine- and histamine-induced constriction of large airways in normal subjects and subjects with asthma: a possible role for postreceptor mechanisms.

Whether in man histamine (H) and acetylcholine (ACH) airway responses are interrelated is controversial. With the use of quantitative nebulization and specific airway conductance (Gaw/VL), we recorded noninvasive pharmacologic tests of H- and ACH-induced bronchoconstriction in 11 normal subjects (N) and nine subjects with asthma (AST) with and without pretreatment of 0.75 mg (A0.75) and 1.50 mg (A1.50) of inhaled atropine. Provocation dose 40 (PD40) for H or ACH were different in N (0.8 X 10(-2) mol/L and 2.9 X 10(-2) mol/L, respectively) and AST (5.0 X 10(-3) mol/L and 7.8 X 10(-3) mol/L) but linearly related. The ratio PD40-ACH/PD40-H was comparable in N and AST and similar to the ratio ACH sensitivity/H sensitivity found in vitro for large airways. The slopes of log dose-response curves (SLDRC) to H and SLDRC to ACH were of similar magnitude both in N and AST and linearly related; however, for either agonist, bronchial sensitivity (PD40) and reactivity (SLDRC) failed to correlate. After A0.75, the dose ratios (DR) of H and ACH were large, with substantial intersubject variability, and similar in N (4.32 and 9.54, respectively) and AST (5.97 and 5.64). Although numerically comparable, DR of H and DR of ACH were unrelated. After A1.50, DR of H remained unchanged (4.53 in N and 5.44 in AST), but DR of ACH further increased (17.37 in N and 8.13 in AST). Pretreatment with A0.75 respected the linear relationship of PD40-H versus PD40-ACH but blurred that of reactivity to these agonists. After A0.75 or A1.50, delta Gaw/VL was similar in N and AST. Except for PD40, none of the tests recorded could distinguish AST from N. In conclusion, H-induced bronchoconstriction is substantially but not exclusively mediated via ACH pathway. We hypothesize that H and ACH responses anastomose within the cholinergic pathway at a sensitivity and a reactivity level; the former level is ostensibly downstream from and unrelated to the latter. In AST, the reactivity to H and ACH, the bronchodilating, anti-histaminic (DR of H) and antimuscarinic (DR of ACH) effects of atropine are normal and so is ostensibly the anastomosis between H and ACH reactivity levels. The level of H and ACH sensitivity distinguishes AST from N. ACH-sensitivity site may be located at the H- greater than ACH anastomosis.

Acetylcholine↗
PubMed1986

Bronchial cholinergic tone and sensitivity in normal and asthmatic subjects.

In nine patients with asthma and 11 normal subjects, by means of specific airway conductance (Gaw/VL) and flow volume loops, we measured: resting airway caliber, bronchodilation after 0.75 and 1.50 mg of quantitatively inhaled atropine (A0.75 and A1.50), provocation dose-40 of acetylcholine (ACH) (PD40-ACH), dose ratio of ACH (DR-ACH) after saline solution, A0.75 and A1.50, and the slope of log-dose response curves to ACH (SLDRC-ACH). Normal and asthmatic subjects showed different PD40-ACH (1.26 +/- 1.37 mg and 0.34 +/- 0.32 mg) but similar resting Gaw/VL, delta Gaw/VL after A0.75 or A1.50, DR-ACH after A0.75, and SLDRC-ACH. There was no correlation between atropine-induced bronchodilatation PD40-ACH or any of the above-mentioned tests. We conclude that in normal subjects and in those with asthma, extramuscarinic or postmuscarinic receptor mechanisms may account for the presence of comparable atropine-induced bronchodilatation and resting Gaw/VL in spite of widely different PD40-ACH. The regulatory site responsible for PD40-ACH, the only test separating asthmatics from normal subjects, seemingly is located downstream from the regulatory site of other nondiscriminative tests.

Acetylcholine↗
PubMed1986

Respiratory pharmacology. Beta-adrenergic drugs.

This article reviews the enormous literature on beta agonists, emphasizing three aspects: the structural, pharmacokinetic, pharmacodynamic, and toxicologic properties that are essential for understanding the clinical application of these drugs; the relative advantages and disadvantages of various routes of administration, including the different ways of prescribing the aerosols; and the pharmacologic factors that may limit the further development of these compounds for therapy.

Administration, Inhalation↗
PubMed1986

The classic antihistamines (H1 blockers) in respiratory medicine.

For almost a quarter of a century, the pharmacology of H1 blockers remained quasi-stagnant, isolated from the rapid evolution of clinical pharmacology. However, exciting new developments concerning the role of histamine in asthma, and special pharmacodynamic features of new H1 blockers, have revived our interest in these drugs.

Animals↗
PubMed1985

The effect of thermal treatment of immunoglobulin E as measured with competitive and noncompetitive assays: is circulating immunoglobulin E serologically heterogeneous?

Using two-double antibody assays (DA) and a noncompetitive assay (PRIST), we measured in 20 atopic and 10 normal sera the total IgE before and after its heating at 56 degrees C for 30-120 min. After heating the sera or radiolabeled IgE, DA detects a reproducible increase in total IgE associated with a large intersubject variability of the inhibition curves. On the contrary, heated total IgE measured with PRIST decreases and there is no intersubject difference in the observed change. In conclusion, DA assays of IgE reveal a heterogeneous response to heating which might be related to interindividual differences in the tertiary/quaternary structure of the D sigma 2 domain of Fc sigma.

Binding, Competitive↗
PubMed1982

Standardization of the double-antibody method for IgE determination: use of different monoclonal IgE as tracer, immunogen or standard.

We wanted to determine whether the competitive radioimmunoassay for IgE is influenced by various combinations of three monoclonal IgE (IgEND, IgEPS, IgESHA) used as tracer or standard, and anti-IgEND and anti-IGEPS as first antibody. When the immunogen for the first antibody was identical with the monoclonal tracer or standard IgE, the latter two bound preferentially to the first antibody. These unusual assays led to inhibition curves that ran in parallel to those produced by usual assays, i.e. assays in which the tracer and the immunogen were different monoclonal IgE and the standard was a polyclonal IgE. When serum samples were analyzed for their IgE content, the unusual assay produced values that were linearly related to those produced by a usual or another, unusual, assay. However, the values of IgE produced by a usual assay were, in general, significantly different from those obtained by unusual assays. We conclude that as suspected, but never demonstrated before, the competitive assay for IgE requires the use of two different monoclonal IgE as tracer and immunogen; application of unusual assays requires their prior calibration against a usual assay.

Animals↗