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Biomedical subjects

J Orehek

Publications and source records attributed to J Orehek.

At least 73 records · Page 4Linked to original sources
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↗
PubMed1976

[Paradoxical effect of forced inspiration: a new characteristic of asthmatic disease?].

In normal subjects, forced inspiration may dilate the bronchi and be considered as a defence or compensatory reaction in certain cases. In asthma, forced inspiration has the opposite effect. Bronchospasm occurs or becomes worse, usually moderately and transiently, but sometimes to a marked and lasting degree. These reactions may be prevented by anticholinergic and sympathomimetic drugs. They should be avoided and one should thus prohibit the manoeuvres which trigger them off. One should take them into consideration during respiratory function tests. This paradoxical effect of forced inspiration seems to exist to various degrees in most asthmatic patients, it may be considered as a diagnostic sign of asthma.

Asthma↗
PubMed1976

Effect of short-term, low-level nitrogen dioxide exposure on bronchial sensitivity of asthmatic patients.

Our purpose was to determine whether exposure to a realistic concentration of nitrogen dioxide (NO2) could increase the bronchial sensitivity of asthmatic patients to bronchoconstrictor agents. We established dose-response curves for changes in specific airway resistance (SRaw) in response to aerosolized carbachol in 20 asthmatics after each had spent 1 h in an exposure chamber breathing on one occasion unpolluted air and on a separate occasion 0.1 ppm NO2: sequence of exposures to unpolluted air and to low levels of NO2 were randomized in a single-blind fashion. NO2 induced a slight but significant increase in initial SRaw and enhanced the bronchoconstrictor effect of carbachol in 13 subjects: curves were shifted to the left and the mean dose of carbachol producing a twofold increase in initial SRaw was decreased from 0.66 mg to 0.36 mg (P less than 0.001). In contrast, NO2 neither modified the initial SRaw nor the bronchoconstrictor effect of carbachol in seven subjects. In 4 out of the 20 subjects, exposure to a higher concentration of NO2 (0.2 ppm) yielded variable results. Potentiation of the carbachol bronchoconstrictor response by NO2 could not be related to any physical or clinical characteristics of the subjects tested. Although the mechanisms underlying the NO2 effect remain controversial, the present results demonstrate that very low levels of NO2 can adversely affect some asthmatics.

Adolescent↗
PubMed1975

[Study of clinical pharmacology of acebutolol in 5 asthmatic patients].

Respiratory function (V.E.M.S.-C.V.) and cardiovascular function (pulse and blood pressure) were studied in 5 asthmatic patients who were given isoprenaline aerosols after I.V. injection of normal saline solution (in the first step) and acebutolol (in the second step). The respiratory function is not disturbed by acebutolol. On the other hand, the cardio-accelerating effect of isoprenaline was not neutralized by acebutolol during these two assays, but significantly reduced.

Acebutolol↗
PubMed1975

[Exercise test in the asthmatic patient. Study of 75 patients].

Frequency of exercise-induced asthma has been studied in 75 unselected asthmatic patients (adults and children) by measuring the forced expiratory volume at one second (FEV1) and the vital capacity (VC) before and after a treadmill exercise, continued until heart rate was at least equal to 80 p.cent-85 p.cent of maximum heart rate. In 19 subjects (25 p.cent), a more than 20 p.cent decrease from control value of FEV1 was recorded ten minutes after exercise ended. Exercise-induced bronchial obstruction was relieved by a beta adrenergic bronchodilator aerosol inhalation. In the group of 19 subjects having exercise-induced asthma, a significant positive correlation was found between pre-exercise FEV1 values and post-exercise FEV1 decreases. In the whole group of 75 subjects exercise-induced asthma was related to the severity of asthma and not to other clinical or physical characteristics of the subjects. From the data of other authors it appears that frequency of exercise-induced asthma is variable. The reasons of those differences are discussed.

Adolescent↗
PubMed1975

Effect of maximal respiratory manoeuvres on bronchial sensitivity of asthmatic patients as compared to normal people.

Cumulative dose-response curves to carbachol given by aerosol were established using plethysmographic measurements of specific airways resistance (SRaw) in 10 patients with asthma and five healthy subjects. Two experiments were performed--a control test and one in which maximal respiratory manoeuvres (MRM) (two maximal inspirations and two maximal expirations) were made before each carbachol inhalation. MRM did not modify the dose-response curves in the normal subjects. In the patients these manoeuvres enhanced the bronchoconstrictor effect of carbachol: curves were shifted to the left and the mean dose of carbachol producing a twofold increase in initial SRaw was decreased from 0.373 mg to 0.189 mg (P less than 0.001). Bronchial provocation tests using methods which require MRM--for example, forced expiratory volume at one second--could overestimate the bronchial sensitivity of patients with asthma.

Adolescent↗
PubMed1975

Effect of beta adrenergic blockage on bronchial sensitivity to inhaled acetylcholine in normal subjects.

Dose-responses curves were established in 10 normal subjects by measuring, with a body plethysmograph, the changes of specific airway conductance (SGaw) produced by aerosolized acetylcholine. Doses of acetylcholine producing a 50 per cent decrease of control SGaw (ED50) were found to be largely variable among individuals. Beta-adrenergic blockade with intravenous propranolol (0.2 mg per kilogram) resulted in a mean potentiation of the acetycholine effect (mean ED50 after propranolol was significantly lower than mean ED50 before). This potentiating effect of propranolol, however, was also subjected to individual variations, suggesting individual variability of the sympathetic system. The range of variation in acetylcholine sensitivity was not narrowed by propranolol treatment and no correlation was found between initial acetylcholine sensitivity and propranolol potentiation. This suggests that variability of the sympathetic system is not the main factor in determining individual variation in acetylcholine sensitivity. Even when propranolol was very effective in increasing airway sensitivity, this sensitivity was still less marked than usually encountered in asthmatic patients. This suggests that beta-adrenergic blockade cannot create, if alone, the bronchial hypersensitivity characteristic of asthma.

Acetylcholine↗
PubMed1975

Beta-adrenergic function in airways of healthy and asthmatic subjects.

We measured the short-term effects of beta-adrenergic blockade with propranolol (0.2 mg/kg iv), followed by stimulation with salbutamol (200 mug inhaled), on specific airway conductance (SGaw) heart rate, and systemic blood pressure (BP) in 11 healthy subjects, and 11 symptom-free asthmatics with normal lung function values. Propranolol induced a significant bronchoconstrictor effect in both groups, stronger in asthmatics than in normals: mean SGaw decreased 34.6 +/- 25% against 9.4 +/- 9% (p less than 0.01). Six of the 11 asthmatics exhibited a more pronounced bronchoconstriction than the most responsive healthy subject. Large individual variations were seen in both groups although they were greater in the asthmatics. A similar rise in SGaw was produced by salbutamol in both groups. The decrease of heart rate provoked by propranolol was similar in the two groups, averaging 18.6%, with no further change after salbutamol. The blood pressure was slightly decreased by propranolol in both groups. The results indicate that normal subjects have a weak and variable bronchodilator beta-adrenergic activity. In most asthmatics beta-adrenergic tone appeared more pronounced. The individual differences in response to propranolol observed in both groups suggest that asthmatic patients differ quantitatively rather than qualitatively from healthy subjects with respect to beta-adrenergic receptor function. There was no association between clinical findings and the degree of bronchomotor effect of propranolol in the patients with asthma. This study does not support the view that airways of asthmatic patients have a decreased beta-adrengeric receptor function.

Adult↗
PubMed1975

[Induced beta-adrenergic stimulation and blockade in asthma bronchomotor effects (author's transl)].

Patients with asthma, exhibiting spontaneous bronchial obstruction, from mild to medium severity, were examined by body plethysmography. Results were expressed as specific airway resistance (SRaw) in preference to specific conductance, the latter leading to errors, in particular in cases with dissimilar baseline values. After the inhalation of a beta-stimulating drug (salbutamol), the decreases in SRaw was directly related to initial SRaw, either in a group (n equal 30) or in individual cases. After the injection of a beta-blocking drug (propranolol), the increase in SRaw, found abnormal in 60% of the subjects, could be related to initial SRaw neither in a group (n equal 40) nor in individual cases. These findings indicate that submaximal bronchial obstruction in patients with asthma is mainly due to a bronchoconstriction, whatever the degree of the obstruction may be. On the opposite, there is an increased bronchodilator adrenergic influence in a majority of patients, not predictable after the degree of initial airway obstruction.

Adrenergic beta-Agonists↗
PubMed1975

Bronchoconstrictor effects of a deep inspiration in patients with asthma.

A deep inspiration from functional residual capacity to total lung capacity, performed at a low flow rate by a group of 40 unselected adult patients with asthma, yielded an immediate and transient increase (71 per cent, P smaller than 0.001) in specific airway resistance. In 2 of the 40, deep inspiration provoked an attack of asthma. The effect of deep inspiration can be attributed to a vagal bronchoconstrictor reflex, because it was prevented or decreased in most of the cases by inhalation of an anticholinergic drug. Beta-adrenergic blockade by propranolol potentiated in a minority of subjects the bronchoconstrictor response to deep inspiration. Deep expiration also induced a bronchoconstrictor effect, which was weaker than that of deep inspiration. It follows that functional studies of asthmatics may be biased if the technique requires maximal respiratory maneuvers.

Adolescent↗
PubMed1975

Contractile responses of the guinea-pig trachea in vitro: modification by prostaglandin synthesis-inhibiting drugs.

Prostaglandins (PG) E2 and F2alpha, characterized by thin-layer chromatography and bioassay, were released from guinea-pig trachea contracted with acetylcholine or histamine. Inhibition of contraction with atropine or mepyramine, or by the removal of calcium, abolished the prostaglandin release. PGE2 and PGF2alpha were also released after gentle mechanical irritation of the mucosal surface, but not the adventitial surface, of the trachea. This release of prostaglandins occurred in the absence of calcium and was prevented by treatment of the trachea with indomethacin. Incubation (20 minutes) of tracheal spirals with indomethacin (0.6 mug/ml) 1) reduced the basal tension of the spiral; 2) reduced responses to low doses of histamine, serotonin, acetylcholine, barium or potassium; and 3) increased responses to high doses of these agonists. These effects lasted despite washout but were reversed by the addition of arachidonic acid. Subthresholdquantities of PGF2alpha after indomethacin treatment restored responses to minimally effective doses of the agonists. Aspirin (50 mug/ml), 5,8,11,14-eicosatetrayonic acid (2 mug/ml) and sodium salicylate (100 mug/ml) had effects similar to indomethacin (0.6 mug/ml). Alterations produced with 5,8,11,14-eicosatetrayonic acid and sodium salicylate were reversed with washing. Restoration of resting tension after indomethacin did not qualitatively change the results. Indomethacin at higher doses (greater than 30 mug/ml) inhibited responses to all histamine doses but this effect was reversible with washing. The results suggest that basal tension of the guinea-pig trachea may be due to an intramural production of PGF2alpha and that during the development of active tension, prostaglandins E2 and F2alpha are released which modulate the intensity of the contraction.

5,8,11,14-Eicosatetraynoic Acid↗