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V T Popa

Publications and source records attributed to V T Popa.

10 recordsLinked to original sources
PubMed1984

The effect of inhaled verapamil on resting bronchial tone and airway contractions induced by histamine and acetylcholine in normal and asthmatic subjects.

In man, the influence of calcium entry blockers (CEB) on nonspecific bronchial sensitivity and resting bronchial tone is controversial. In 10 asthmatic and 8 normal subjects we recorded specific airway conductance (Gaw/VL) and flow volume loops before, 30, 60, and 90 min after the inhalation of saline, 10 (V10) and 20 mg (V20) of verapamil. The dose of inhaled histamine and acetylcholine producing Gaw/VL of -40% (PD40H and PD40ACH, respectively) with and without pretreatment with saline, V10, and, in 15 subjects, V20 was also determined. We measured plasma verapamil concentrations immediately after the end of nebulization of V10 and V20, and 30 and 60 min later. In normal subjects, V10 and V20 produced a maximal % delta Gaw/VL of 22.30 (+/- 19.50) and 33.00 (+/- 15.82), respectively (p less than 0.05). In asthmatics, V10 and V20 produced comparable % delta Gaw/VL of 22.00 (+/- 22.50) and 38.60 (+/- 38.60), respectively. This bronchodilating effect involved predominantly the large airways, persisted for 60 to 90 min, was reproducible, affected only some subjects (11 of 18), and was independent of the resting Gaw/VL, degree of bronchial sensitivity to H and ACH, and the time course of plasma verapamil concentration. The latter reached a maximum of 24.3 +/- 7.1 ng/ml after V20. In both normal and asthmatic subjects, saline or V10 did not significantly alter PD40H and PD40ACH. In normal subjects, pretreatment with V20 increased PD40H 5.3 times and PD40ACH 3.22 times (p less than 0.05). Except in 2 asthmatics, in whom V20 decreased PD40 and PD40ACH, it increased significantly PD40ACH (dose ratio: 3.15, p less than 0.05) but not PD40H.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1984

Biphasic systemic anaphylactic reaction: three illustrative cases.

We report on three patients with early mild systemic reactions triggered by administration of rabies vaccine, immunotherapy with rye grass extract, or yellow jacket sting. After appropriate treatment, these early cutaneous and respiratory symptoms improved considerably, but then flared up three and one half to four hours later. All three patients had specific IgE antibodies against their offending allergen.

Adult↗
PubMed1980

Effect of an H1 blocker, chlorpheniramine, on inhalation tests with histamine and allergen in allergic asthma.

In 15 asthmatic subjects, flow volume loops were recorded before and after quantitative nebulization of increasing concentration of histamine and allergen, until a threshold response (-delta FEV1 > 10%) was obtained. Nine subjects with reproducible threshold doses to these two agents were included in the study. After pretreatment with 10 mg of intravenously administered chlorpheniramine, the threshold dose of histamine increased fourfold in eight subjects and eightfold in one subject, whereas the threshold doses to allergen doubled in seven and remained unaffected in two. One of these two subjects required 15 mg chlorpheniramine intravenously for comparable protection. In three subjects, the threshold dose to inhaled acetylcholine was determined with a similar procedure and found reproducible. Pretreatment with 10 to 15 mg chlorpheniramine increased this threshold dose two to four times, similarly to the effect produced by 0.4 mg of subcutaneously administered atropine. However, 0.4 mg atropine sc. did not alter the airway responses to allergen. The results suggest that intravenously administered chlorpheniramine provided it has a dose ratio of at least four against inhaled histamine, can prevent attacks of allergen-induced asthma. The effect is probably mediated through the H1 rather than the acetylcholine receptor.

Adult↗
PubMed1977

Bronchodilating activity of an H1 blocker, chlorpheniramine.

The purpose of this study was to test the hypothesis that chlorpheniramine (CP), and H1 blocker, can cause bronchodilatation if administered intravenously (iv) and in higher doses than those currently prescribed. In 10 subjects with allergic asthma, forced expiratory flows (FEF) were recorded on different days, at comparable baseline values, before and up to 5 hr after administration of 8 mg per os (po) chlorpheniramine, 10 mg iv CP (repeated twice), 5.5 mg/kg iv aminophylline, and 30 mg po butabarbital as well as during a day without drug. Chlorpheniramine administered intravenously produced reproducible increases (+ delta) in FEF, starting at 15 min, peaking at 120 min, and still persisting at 5 hr; the peak + delta averaged 15% for FEV1 and 27% to 53% for flows at low lung volume. FEF showed a comparable + delta after aminophylline, a smaller + delta after orally administered chlorpheniramine and no significant + delta during butabarbital or control sessions. The ratio change over time/variability was higher for FEV1, FEF50%, and FEF25%-75% than for the remaining parameters. In six subjects a double-blind study (chlorpheniramine vs. saline solution) confirmed the effectiveness of the doses administered in the open study. In three subjects, 10 mg iv chlorpheniramine was given at four different baseline values; the highest + delta occurred when the basal FEV1 was approximately 50% of the predicted value and the basal FEF at low lung volume 30% to 40% of the predicted value. In two subjects, log dose-response curves to 2.5, 5.0, and 10.0 mg iv chlorpheniramine were obtained by using FEV1, FEF50%, and FEF25%-75%. Thus chlorpheniramine in high iv doses can dilate the bronchi, the + delta FEF depending on the dose, the percent of the predicted basal FEF value, and "individual" responsiveness. Withing the dose range used, bronchodilatation to chlorpheniramine and aminophylline administered intravenously was best detected by FEV1, FEF50%, and FEF25%-75%.

Aminophylline↗
PubMed1976

Dose-related dilatation of airways after inhalation of metaproterenol sulfate.

Studies concerning the ability of an inhaled beta2-agonist to produce dose-related bronchodilatation are conflicting. In five asthmatic, five bronchitic, and five normal subjects, specific airway conductance (Gaw/VL), flow-volume curves, and single-breath nitrogen washout were recorded after noncummulative inhalation of 0.65 mg, 1.30 mg, 1.95 mg, and, in some subjects, 2.60 mg of metaproterenol sulfate. Bronchodilatation appeared to be dose-related and was best assessed by using Gaw/VL; in all but one subject with chronic bronchitis, there was a significant linear relationship between log dose and precent change in Gaw/VL. Measurements of flow rate could demonstrate significant log dose-responses in eight subjects, maximum midexpiratory flow being the most sensitive measurement of flow rate, followed in order by forced expiratory volume in one second, flow at 50 percent of forced vital capacity, peak expiratory flow rate, and flow at 75 percent of forced vital capacity. No log dose-respone curve could be observed by using the single-breath nitrogen-washout technique. This demonstration of significant log dose-responses to inhaled metaproterenol is consistent with the response to drugs acting upon receptors and suggests that patients may benefit from increasing doses of bronchodilators.

Asthma↗