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V Popa

Publications and source records attributed to V Popa.

At least 19 recordsLinked to original sources
PubMed1990

The relationship between conductance and functional residual capacity during drug-induced bronchoconstriction.

UNLABELLED: We wondered if the inverse changes in airway conductance (Gaw) and functional residual capacity (FRC) during histamine (H) and acetylcholine (ACH) challenge are interrelated or occur at random. In 14 normal and 14 asthmatic subjects, we determined FRC and Gaw changes corresponding to changes in specific airway conductance (SGaw) around -40 percent produced by an aerosol of H or ACH inhaled quantitatively and with measured lung deposition. We also assessed the elastic recoil following H inhalation (5A). We found that in 11 normal and nine asthmatic subjects, after H or nine normal and 11 asthmatic subjects after ACH, Gaw and 1/FRC were linearly and directly related (p less than 0.05). The steepness of this slope was directly related to the resting Gaw values. A similar relation was uncovered in the literature for asthmatic patients at rest or during recovery from natural asthma. As the elastic recoil was normal and did not change after H, it could not explain delta FRC at delta SGaw of -40 percent. IN CONCLUSION: (1) during H or ACH challenge, Gaw-FRC relationship in normal or asthmatic subjects tends to be hyperbolic and dependent on resting Gaw; (2) such a relationship is seemingly present in other bronchoconstrictor responses with a different pathogenesis; and (3) during bronchoconstriction, as Gaw vs FRC is no longer linear, SGaw becomes volume dependent.

Acetylcholine↗
PubMed1989

The effect of inhaled naloxone on resting bronchial tone and exercise-induced asthma.

UNLABELLED: We wanted to determine whether 10 mg naloxone inhaled quantitatively could modulate the resting bronchial tone and respiratory response in exercise-induced asthma (EIA). In 11 asthmatic subjects, we measured specific airway conductance (SGaw) and forced expiratory flow (FEF) before and after the inhalation of naloxone or saline. In another 10 asthmatic subjects, we measured SGaw, FEF, and the ventilatory gas exchange, heart rate, and blood pressure responses produced by a treadmill exercise during 3 separate days: without any pretreatment (Day 1) or preceded by the inhalation of either 10 mg naloxone (Day 2) or saline (Day 3). We found that after 10 mg inhaled naloxone only one of 11 subjects bronchodilated, displaying an isolated, reproducible delta SGaw greater than 40% at 30 and 60 min. In the EIA protocol, the cardiopulmonary responses during exercise remained similar on all experimental days, but in seven of 10 subjects (all with %FEV1/FVC greater than or equal to 70% delta SGaw was -60 +/- 11%, + 1 +/- 40%, and -52 +/- 7% during no treatment, naloxone, and saline days, respectively (p less than 0.05). FEF changes were comparable on all days (p greater than 0.05). IN CONCLUSION: (1) consistent with the general role of endogenous opioids, these neurotransmitter/neuromodulators can modulate a stress-related bronchoconstrictor response (EIA), but only very seldom the resting bronchial tone. (2) Naloxone does not blunt EIA through a decrease in the asthmogenic stimulus (i.e., ventilation) or airway caliber change, but presumably through competition with the endogenous opioids released during exercise.

Administration, Inhalation↗
PubMed1988

Domiciliary metaproterenol nebulization: a bacteriologic survey.

We wanted to determine whether domiciliary jet nebulization (DJN) leads to contamination of the equipment with fungi or aerobic bacteria and, eventually, to respiratory colonization or pneumonia in daily users of the equipment. We surveyed from this standpoint 23 veterans 65 +/- 10.1 years of age, present or former smokers, treated with steroids more than 7 months in the year preceding the survey, and with FEV1/FVC of 42 +/- 11%; they all were daily users of the equipment, diluting the metaproterenol solution with nonbacteriostatic saline dispensed in multiple-dose bottles of 500 to 1000 ml (protocol 1 [P1]). After this protocol was completed, the large saline bottles were replaced by 20 cc vials; 11/23 completed 1 year of this treatment (protocol 2 [P2]). Equipment contamination was checked in all initial 23 patients after one-time nebulization in the laboratory with fresh material (protocol 3 [P3]). We found that DJN leads to equipment contamination in 20/23 subjects of P1 and 3/11 subjects of p2; saline bottles and the nebulizer were the most frequently contaminated items (32/41 equipment items in P1 and 10/55 in P2). The contamination was predominantly bacterial with oropharyngeal saprophytes (19 in p1, O in P2) or gram-negative bacilli (47 in P1, 8 in P2). Bacterial growth was heavier in P1 than in P2. During P3, three equipment items became contaminated in 3/23 subjects; the flora was oropharyngeal. No patient developed respiratory colonization or developed pneumonia during 9000 patient days of DJN.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Pharmacodynamic aspects of chlorpheniramine-induced bronchodilatation.

In 12 asthmatic (A) and ten normal (N) subjects, we measured the effect of inhaled saline solution, acetylcholine, histamine (H), and chlorpheniramine (CP) on specific airway conductance and forced exploratory flows. We found that CP dilated the bronchi in six asthmatic patients and one normal subject by acting on bronchial H1 receptor. This action is also modulated by the abnormal functions of this receptor-transducer, explaining why CO exerts a tonic effect only in subjects with H hyperresponsiveness. Furthermore, as shown by CO and CP + H responses, bronchial histamine seems to be present primarily in large airways and in relatively small amounts. We also found that bronchial H, the abnormal H1 receptor-transducer, and the bronchial caliber are regulated independently of each other. Consequently, this limits the therapy with H1 blockers in asthma.

Acetylcholine↗
PubMed1988

Provocation dose and discriminant analysis in histamine bronchoprovocation. Are the current predictive data satisfactory?

In 20 normal subjects (N) and 20 asthmatic patients (A) using bronchodilators as needed, the PD40, PD10, PD15, PD20, PD10T, and PD20C were measured (PD being provocation dose, subscript being -% delta in Gaw/VL for PD40, lowest FEV1 for PD20C, and best FEV1 for the remaining PDs; 10T means delta FEV1 greater than -10 percent). For discriminant analysis we used an ad hoc graphic (best case) method, a ceiling method based on highest PD in A and two methods (logistic and linear) which considered PDs in both N and A (PDN and PDA, respectively). The distribution of PDN and PDA had substantial overlap and appeared log normal. The PD15, PD20, and PD20C displayed the smallest mean misclassification error followed by PD10T, PD40, and PD10. The linear and logistic methods produced balanced sensitivity and specificity but, predictably, a misclassification error higher than that of the graphic method. The ceiling method proved unsatisfactory with 100 percent sensitivity but approximately equal to 60 percent specificity. Using linear and logistic methods, the posttest likelihood of asthma could be expressed as a function of its pretest likelihood and level of PD recorded. We concluded that: (1) the most discriminant PDs are PD20, PD15 and PD20c; and (2) new normative data for diagnostic bronchoprovocation are needed, because: (a) when PDA and PDN overlap, the currently used ceiling method leads to a high misclassification rate, while the linear and logistic method based on mathematical model have a better discriminant ability; (b) to separate PDA from PDN and allow the application of the ceiling method, "as-needed bronchodilators" is not a reproducible criterion.

Adolescent↗
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↗