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Biomedical subjects

I Zimmermann

Publications and source records attributed to I Zimmermann.

At least 91 records · Page 5Linked to original sources
PubMed1980

[The place of attack of beta-2 receptor stimulating bronchodilators. Fenoterol (Berotec) in allergic airway obstruction in dogs, hypersensitive to Ascaris suum].

On dogs sensitive against Ascaris suum extract an increase of the airway resistance can be caused by challenge alone on the upper part or the lower part of the airways by Ascaris suum extract. Fenoterol as beta 2-receptor stimulator is capable to decrease this reaction by deposition of this drug on the upper part as on the lower part of the airways. The effect of Fenoterol on the upper part of the airways is much stronger and lasts much longer than on the lower part of the airways or by intravenous route. A direct effect of the beta 2-receptor stimulator Fenoterol on the sensoric part of the reflex way of the reflex bronchoconstriction must be considered. It will be also discussed that the local application of Fenoterol on the upper part of the airways may influence also the reaction of the bronchial muscles in the lower part of the airways without a direct resorptive-systemic effect. The relationship of these findings for the clinical situation on man has to be investigated.

Airway Obstruction↗
PubMed1980

[Effects of acetylcholine- and histamine inhalations also of hypoxia on the arterial plasma-histamine concentration (experiments on dogs). III. Communication (author's transl)].

Inhalation of acetylcholine causes increased histamine concentration in the arterial plasma. This increase is smaller than that following allergen inhalation. The increase in Edyn following ACH inhalation may be related to the histamine released to only a very limited extent. Comparison of the effects of histamine inhalation and allergen inhalation on Edyn and plasma histamine concentration leads to the assumption that sensory receptors are located nearer to the surface of the mucosa than that of the mast cells. Hypoxemia is followed by a slight increase in the arterial plasma histamine concentration. The increase in Edyn corresponds to that caused by allergen inhalation although the increase in Edyn and that in the plasma histamine are much smaller.

Acetylcholine↗
PubMed1980

[Arterial plasma histamine concentration for airway obstruction due to different areas of the bronchial system. IV. Communication (author's transl)].

The separate inhalation of A.E. aerosol in the upper and the peripheral parts of the airways in allergic dogs is followed by an increase of the histamine concentration in the arterial plasma. The correlation between the plasma histamine concentration and dynamic elastance and the correlation between dynamic elastance and arterial oxygen pressure is very similar following the challenge of the upper and the peripheral parts of the airways. The results argue for reflex bronchoconstriction also by challenge of the more peripheral airways. The results are in accord with the idea that the answer of Edyn depends on a product of local histamine concentration and the area in which the histamine is released. The number of sensory receptors per surface area which is suspected to be greater in the upper part of the airways may also be important.

Airway Obstruction↗
PubMed1980

[Allergen-induced airway obstruction and histamine concentration in arterial and venous plasma. First communication (author's transl)].

In 19 dogs sensitized against Ascaris suum extract we measured dynamic elastance, arterial plasma histamine concentration, pressure in the A. femoralis, and arterial blood gases. In six dogs the venous plasma histamine concentration was also analyzed. Ascaris extract (A.E.) inhalation increased both the arterial and the venous plasma histamine concentration significantly. The venous concentration was 61% of that detected in the arterial blood. At the same arterial plasma histamine level a large variety of dynamic elastance was measured which shows great individual differences in the sensitivity of the bronchoconstrictive system. This histamine released by the bronchopulmonary system works mostly via reflex bronchoconstriction. There was significant correlation between dynamic elastance and arterial oxygen pressure as well as between arterial plasma histamine concentration and systemic blood pressure.

Aerosols↗
PubMed1980

[Histamine concentration in arterial plasma in the course of repeated antigen challenges of the bronchopulmonary system. Second communication (author's transl)].

Repeated ascaris extract (A.E.) exposure on dogs sensitized against this allergen at intervals of 90, 180, and 360 min is followed by different increases in the histamine concentration in the arterial plasma. At 90 min, a significantly smaller amount of histamine becomes measurable in the arterial plasma. Edyn increases unproportionally strong. One hundred eighty minutes after the first exposure A.E. inhalation is again followed by a clearly increased histamine concentration in the arterial plasma. Edyn still increases unproportionally strong. Three hundred sixty minutes after the first A.E. exposure another exposure revealed a stronger increase in the histamine concentration in the arterial plasma, the Edyn increase being smaller than at the first exposure. These results are of importance with regard to the sensitivity of the airways and the investigation of antiallergic and bronchospasmolytic drugs.

Aerosols↗
PubMed1980

[Arterial plasma histamine concentration during inhalation of allergen and acetylcholine before and after vagotomy. V. Communication (author's transl)].

In allergic dogs ascaris extract (A.E.) inhalation and, to a less extent, acetylcholine inhalation cause a significant increase in the histamine concentration in the arterial plasma. A.E. and acetylcholine cause a similarly strong increase in Edyn. After bilateral vagotomy A.E. and acetylcholine inhalation entail only a minimal increase in Edyn. The increase in the arterial plasma histamine concentration is as strong as before vagotomy. The results support the assumption that both A.E. and acetylcholine act on the sensory receptors of the reflexway via a reflex mechanism. PO2a decreases as Edyn increases. However, after vagotomy PO2a still decreases significantly although Edyn changes hardly. A.E. and acetylcholine are assumed to have a direct effect on the non-vagus controlled peripheral airways. The peripheral airways are mainly responsible for changes in the arterial blood gases but show no effect on Edyn or airway resistance measurements.

Acetylcholine↗
PubMed1980

Pulmonary haemodynamics in coal workers' pneumoconiosis and non-pneumoconiotic patients with chronic obstructive airways disease.

The pulmonary haemodynamics of 22 patients with advanced forms of coal workers' pneumoconiosis (CWP) and chronic obstructive airways disease (COAD), and 24 patients with advanced forms of COAD without pneumoconiosis were studied. The results obtained permitted a haemodynamic distinction between these two groups of patients. The differences, at rest and during 25 W exercise, are discussed.

Aged↗
PubMed1980

Experimental induced bronchial hyperreactivity.

Bronchial hyperreactivity can be influenced by antigen inhalation as well as by infections which affect the bronchial tree. Bronchial hyperreactivity characterizes the obstructive airway diseases. In order to study this problem, we have performed in our laboratory a series of experiments concerning this problem. The influence of proteolytical enzymes on acetylcholine-induced bronchoconstriction was tested in a series of animals. After enzymes inhalation, an extreme enlarged answer to acetylcholine exposure was observed. Bronchial hyperreactivity induced after histamine and also after antigen administration and the influence of antihistamine was also tested in a series of experiments. The hyperreactivity of bronchial system observed after experimental pulmonary embolism was finally studied on a series of animals. The influence of vagus blockade on this induced bronchial hyperreactivity was also tested. After vagus blockade no bronchoconstrictoric answer was observed. The relation of bronchial hyperreactivity to localization of sensoric receptors can be assumed.

Acetylcholine↗
PubMed1980

[Ganglion in the ulnar nerve sulcus as a cause of ulnar nerve irritation].

A ganglion at the cubital tunnel is a rare cause of ulnar nerve compression. Wrong or late diagnosis may be common. In one of the two described cases the diagnosis was made promptly, so that the early operation was followed by full restitution. In the other patient, at first the site of compression was supposed to be at the wrist. Only at the second operation was the ganglion in the cubital tunnel detected and removed. The result was unsatisfactory because motor loss was permanent.

Adult↗
PubMed1979

The role of upper airways and of sensoric receptors on reflex bronchoconstriction.

The influence of bilateral transection of the nervi laryngici cranialis, laryngici caudalis and glossopharyngici on ACH and allergen-induced bronchoconstriction was tested in 15 dogs. In three dogs the free preparation of bilateral nervi laryngici cranialis was performed for control measurements. Partial transection of pulmonary left nervus vagus was performed in three dogs and compared to radical transection of the same nerve in three animals. Transection of the nervi laryngici cranialis as well as of the nervi glossopharyngici was followed by the inhibition of the allergen-induced bronchoconstriction. The bronchoconstriction following ACH challenge was not influenced by transection. Bronchoconstriction induced by allergen returned to the same values within three weeks after surgical intervention. Partial unilateral dissection of the vagus nerve on lung hilus shows a small decrease in bronchial constriction induced by allergen and by ACH. Complete unilateral dissection of the vagus nerve on the lung hilus reduced the bronchial constrictoric response to both substances significantly.

Acetylcholine↗
PubMed1979

The role of upper airways in antigen-induced bronchoconstriction.

The bronchoconstrictor effect of antigen was tested in 15 dogs. The upper and the lower airways were sequently exposed through a specially confected endotracheal tube. The antigen was also generally administered through a mouth mask. Bronchoconstriction was induced after each kind of exposure. The results argue for reflex bronchoconstriction. The sensory receptors localized in the upper part of the airways are responsible for about 50% of antigen-induced bronchoconstriction. The decrease of PO2a was less marked following Ascaris suum extract aerosol administration to the upper part of the airways. Control measurements demonstrated the reproducibility of antigen-induced bronchoconstriction.

Aerosols↗
PubMed1979

The location of sensoric bronchoconstricting receptors in the upper airways.

The bronchoconstrictoric influence of allergen and acetylcholine aerosol was tested in 16 boxer dogs. The animals were exposed to these substances through a mask. The aerosol was also administered directly to three restricted areas of the trachea. Both substances induced a strong bronchoconstriction when administered through the mouth. Only the allergen showed a similar strong bronchoconstriction when administered to a restricted area in the upper third of the trachea.

Acetylcholine↗
PubMed1979

The side of action of bronchodilating drugs (beta 2-stimulators) on antigen-induced bronchoconstriction.

The prophylactic effect of a sympathicomimetic drug (Fenoterol) was tested separately for the upper and the lower respiratory tract on 14 boxer dogs exposed to antigen challenge. In the lower airways, a restricted short-lasting diminution of bronchoconstriction was observed when both antigen and Fenoterol were administered to these airways. Administration of Fenoterol to the upper respiratory tract showed a long-lasting strong local effect in prevention of antigen-induced bronchoconstriction. There is a strong long-lasting effect of sympathicomimetic bronchodilators on the sensoric part of the reflex way into the airways. There is, with similar dosages, a weak short-lasting direct effect of these drugs on bronchial muscles.

Aerosols↗