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Biomedical subjects

J Orehek

Publications and source records attributed to J Orehek.

At least 19 recordsLinked to original sources
PubMed1990

Manufacturer's information insert and subjective theophylline side-effects.

In Western Europe medicine packages contain an insert prepared by the manufacturer which enumerates the drug side-effects. We investigated the influence of this insert on alleged theophylline side-effects. Forty literate adult asthmatics were randomly allocated into two groups (n = 20 each): theophylline packages contained the manufacturer's insert in group A but not in group B. Theophylline was prescribed (10 mg.kg-1 body weight qd) for one week. During this period the patients filled a diary grading 13 different symptoms from 0 to 3; 5 of these symptoms were listed on the insert as theophylline side-effects. On the eighth day the patients were interviewed and theophylline blood levels measured. Theophylline side-effects were significantly more marked in group A than in group B, whereas the other symptoms were of similar magnitude. Eight patients prematurely stopped their treatment in group A vs 3 in group B, because of alleged intolerance. Theophylline blood levels did not differ significantly in the two groups; neither did they in the subgroup which stopped treatment and in the one which complied to prescription. We conclude that side-effects were suggested to the patients by the insert and/or that the insert increased their awareness of side-effects, with a subsequent detrimental influence upon compliance to therapy.

Adult↗
PubMed1988

Attenuation of hyperventilation-induced bronchospasm by terfenadine: a new antihistamine.

The effect of terfenadine, a selective H1-receptor antagonist devoid of central nervous system side effects, was evaluated on hyperventilation-induced bronchospasm in 11 adult subjects with asthma in a double-blind, placebo-controlled, crossover study. Increases in specific airway resistance (SRaw) were induced by isocapnic hyperventilation with dry air on two occasions, 7 days apart. Before the tests, the subjects received oral terfenadine (120 mg, twice daily) or placebo for 3 days with the last dose administered 3 hours before the test. Baseline SRaw and spirometric values (vital capacity and FEV1) were similar for the two tests. Terfenadine yielded a significant (p less than 0.001) parallel shift to the right of the stimulus (hyperventilation)-response (SRaw) curve; 100% increases in SRaw occurred at ventilation rates of 44 L/min after placebo treatment and 64 L/min after terfenadine treatment. These data suggest that histamine release plays a role in hyperventilation-induced bronchospasm despite the fact that increase in plasma histamine has not been found in this situation, in contrast to exercise-induced bronchospasm.

Adolescent↗
PubMed1988

Attenuation of bronchofiberscopy-induced cough by an inhaled beta 2-adrenergic agonist, fenoterol.

We investigated the antitussive effect of fenoterol in 40 patients (34 males) undergoing bronchofiberscopy for diagnostic purposes. The patients were randomly allocated into two groups, one receiving two puffs (400 micrograms) of fenoterol and the other two puffs of placebo, from a metered-dose inhaler in a double-blind fashion. The following procedure was used: premedication with 0.5 mg atropine sulfate and 100 mg hydroxyzine administered intramuscularly; 50 min later, aerosol administration; 10 min after aerosol administration, a standardized topical anesthesia was performed. As soon as the bronchofiberscope had entered the trachea, sounds were recorded for a 5-min period, while the tracheobronchial tree was systematically inspected. Additional lidocaine (2% solution, 2 ml boluses) was injected into the airways if troublesome cough occurred. The two groups did not differ significantly in terms of age, sex ratio, and smoking history. In contrast, both the number of coughs and the volume (ml) of additional lidocaine were significantly smaller in the fenoterol group than in the placebo group: m +/- SEM: 35.0 +/- 5.5 versus 51.6 +/- 6.5, p less than 0.01 and 1.9 +/- 0.5 versus 3.3 +/- 0.4, p less than 0.01, respectively. Thus, fenoterol exhibits antitussive properties and can usefully be administered before bronchofiberscopy.

Administration, Inhalation↗
PubMed1979

Mechanisms of the bronchoconstrictor effects of deep inspiration in asthmatic patients.

A single deep inspiration (DI) is commonly followed by transient airflow obstruction in asthmatic patients. In some patients, however, DI results in a sustained response which suggests that more than one mechanism may be responsible. We have studied the characteristics of the response to repeated DI, and their modificatiion by various pharmacological agents, by measuring specific airway resistance (sRaw) in ten subjects who showed reproducible and consistent increases in sRaw after DI. Two types of reaction were observed: type A (n = 8) had an immediate maximum and usually short persistence; type B (n = 2) had a delayed maximum with a progressive increase. In type A reactions repetition of DI showed different patterns of response--either a reproducible reaction to each DI or a plateau effect. In type B reactions the response spontaneously increased with repeated DI. Type A responses to DI were inhibited completely by a beta-adrenergic stimulant (BAS), largely by an anticholinergic drug (AC, ipratropium bromide), but in no case by disodium cromoglycate (DSCG). Type B responses were inhibited completely by BAS, largely by DSCG, and partially by AC. These findings suggest that the response to DI is due to bronchoconstriction, which in type A reactions is of reflex origin, vagally mediated, and is due in part or wholly to mediator-release in type B reactions.

Adolescent↗
PubMed1979

Bronchodilator effects of antiasthmatic cigarette smoke (Datura stramonium).

In 12 asthmatic patients with mild airway obstruction we have measured the effect on specific airway resistance (sRaw) of inhaling the smoke of one Datura stramonium cigarette. In 11 patients sRaw decreased substantially after the cigarette, the mean maximal decrease being 40% at the 30th minute. In seven patients the subsequent inhalation of 200 micrograms salbutamol caused no further decrease in sRaw. In the remaining four patients salbutamol induced a larger decrease in sRaw than the cigarette smoke. The inhalation, however, of a synthetic anticholinergic agent (SCH 1000, 600 micrograms) proved as effective as salbutamol in these patients. In one patient the cigarette smoke and SCH 1000 produced only a negligible amount of bronchodilatation whereas the bronchial obstruction was reversible with salbutamol. Minor side effects were observed in six patients after the cigarette.

Adult↗
PubMed1977

[Treatment of acute asthma. Comparison of the effectiveness of corticosteroids and of a combination of corticosteroids and an adrenergic beta-stimulant (author's transl)].

Two comparable groups of patients hospitalised for acute asthma received an intravenous infusion for two hours, containing corticosteroids in the first group and corticosteroids combined with an adrenergic beta-stimulant in the second. Course was assessed by the hourly measurement of forced expiratory volumen in one second (FEV1), heart rate and blood pressure. It was found that corticosteroids alone had a modest action (5,1% improvement in FEV1). By contrast, the combination of corticosteroids with an adrenergic beta-stimulant resulted in a rapid and pronounced improvement in FEV1 (19,9%), without producing any undisrable side-effects. No changes in arterial blood gases were noted under the influence of treatment. Injectable adrenergic beta-stimulants are therefore worthy of use in the treatment of an asthma attack, in the absencd of any contraindication.

Adrenal Cortex Hormones↗
PubMed1977

Bronchial response to inhaled prostaglandin F2alpha in patients with common or aspirin-sensitive asthma.

The effect of aerosolized prostaglandin F2alpha (PGF2alpha) on specific airway resistance (SRaw) has been measured in patients with common (n = 10) or aspirin-sensitive asthma (n = 5). In all subjects PGF2alpha caused a dose-related increase in SRaw, but considerable individual differences in sensitivity were observed. The patients with aspirin intolerance did not differ from regular asthmatics in terms of their response to PGF2alpha. Two types of reactions to PGF2alpha could be distinguished from their time-course: immediate and short-lasting (3 cases) or delayed and long-lasting (12 cases). Inhalation of a beta-adrenergic drug rapidly and completely reversed the effect of PGF2alpha, suggesting that the increase in SRaw was due to bronchospasm. In 7 subjects the inhalation of an anticholinergic drug (SCH 1000) prior to PGF2alpha inhibited to a large extent the effect of the latter, suggesting that the cholinergic system played an important role in the bronchial response to PGF2alpha. In 9 subjects no correlation was found between the bronchial sensitivity to carbachol and PGF2alpha.

Aerosols↗
PubMed1977

[Effect of beta-adrenergic stimulation on the closing volume in normal subjects (author's transl].

In 12 normal subjets we studies the effects of beta-adrenergic stimulation (Salbutamol, 500 microgram inhaled) on the closing volume (CV) and the closing capacity and on the ratios of these indexes to the vital capacity (VC) and the total lung capacity, respectively. CV and CV/VC % increased in ten subjects wereas it decreased in two subjects. On an average, the changes were small but significant (p less than 0.01) and could be duplicated in four subjects. Similar studies have yielded variable results. The reasons for those variation could be attributed either to technical or/and individual differences in the resulting effect of beta stimulation on respiratory mechanics.

Adrenergic beta-Agonists↗
PubMed1977

Airway response to carbachol in normal and asthmatic subjects: distinction between bronchial sensitivity and reactivity.

By constructing cumulative dose-response curves to inhaled carbachol in 12 normal and 17 asthmatic subjects with comparable baseline specific airway conductance, we have shown that there were wide variations among subjects in the dose of carbachol needed to cause a 25 per cent decrease in specific airway conductance (bronchial sensitivity) and in the slopes of the curves (bronchial reactivity). Furthermore, there was no significant correlation between these 2 characteristics of the bronchial response to carbachol. The mean dose-response curves of the asthmatic and the normal subjects were widely divergent, indicating that the asthmatic subjects differed from normal subjects more in terms of bronchial reactivity than in bronchial sensitivity. This suggests that different mechanisms determine the sensitivity and reactivity of the bronchial tree, and that hyper-reactivity is the main feature of the asthmatic response. Both should be assessed when the bronchial response to bronchoconstrictor agents is measured.

Asthma↗
PubMed1977

[Ventilatory response to lung inflation after induced bronchospasm in healthy conscious subjects (author's transl)].

In 10 healthy conscious subjects we have studied the effect of a sustained bronchospasm induced by aerosol of carbachol on the pattern of breathing and the ventilatory response to lung inflation which reflects the Breuer Hering reflex. Bronchospasm was assessed by measuring airway resistance and functional residual capacity by plethysmography. After bronchospasm the ventilatory response to inflation was unchanged and the role played by afferents related to such a reflex in controlling pattern of breathing was preserved. Moreover the ration between the threshold volume of the reflex and tidal volume (VT) remained constant. These data suggest that this ration could represent a central set point for VT control. Variable changes in the ventilatory pattern were also observed and are discussed in relation to the previous data.

Adult↗
PubMed1977

[Diagnostic, etiologic and therapeutic problems confronting the anesthesiologist in cases of bronchial spasm. Apropos of 4 cases].

The authors recall the symptoms of peroperative and early postoperative bronchospasm. They emphasise the etiology and the treatment. In fact, bronchospasm may be induced by several causes:--mechanical or chemical vagal stimulation;--direct or allergic-induced histamine liberation, induced by certain drugs (mainly curare);--taking beta-blockaders before operation, favoured by the use of morphine during operation;--finally, any irritation of the bronchi (inhalation of gastric juice, pulmonary embolism, pulmonary oedemal). The treatment is etiological but also symptomatic:--enrich the inspired air with oxygen;--inject I.V. 1/2 to 1mg of atropine;--in case of failure, one should use Salbutamol I.V. which is very effective during contraction of the bronchial muscles;--massive corticosteroid therapy will be effective in mucosal oedema.

Adrenal Cortex Hormones↗
PubMed1977

A new simple spirometric index for use with bronchial provocation tests.

Spirometric indices such as the forced expiratory volume in one second (FEV1), the maximal expiratory flow rate (MEFR) and the maximal midexpiratory flow rate (MMFR) can be criticized for use with bronchial provocation tests since they are either partly effort-dependent or dependent on the forced vital capacity (FVC). These criticisms can be avoided by the use of a new index corresponding to the volume of air expired in one second starting at 75% of the control FVC, called the (FEV1)-25. This study was performed to evaluate the relative sensitivity of the (FEV1)-25 and the classical FEV1 in detecting airway obstruction caused by an inhaled carbachol aerosol in 20 asthmatic subjects. The mean fall in (FEV1)-25 of 46% following carbachol inhalation compared with a mean fall in FEV1 of 35% indicates that, in addition to its theoretical advantages, the (FEV1)-25 is a sensitive index for use with bronchial provocation tests.

Adolescent↗