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Biomedical subjects

H Bachofen

Publications and source records attributed to H Bachofen.

At least 19 recordsLinked to original sources
PubMed1992

Surface properties of rat pulmonary surfactant studied with the captive bubble method: adsorption, hysteresis, stability.

Surface tension-area relations from pulmonary surfactant were obtained with a new apparatus that contains a leak free captive bubble of controllable size. Rat pulmonary surfactant was studied at phospholipid concentrations of 50, 200 and 400 micrograms/ml. At the highest concentration, adsorption was rapid, reaching surface tensions below 30 mN/m within 1 s, while at the lowest concentration, approximately 3 min were required. Upon a first quasi static or dynamic compression, stable surface tensions below 1 mN/m could be obtained by a film area reduction of approximately 50%. After three to four cycles the surface tension-area relations became stationary, and the tension fell from 25-30 to approximately 1 mN/m for a film area reduction of less than 20%. Hysteresis became negligible, provided the films were not collapsed by further area reduction. Under these conditions, the films could be cycled for more than 20 min without any noticeable loss in surface activity. After only three to four consecutive cycles, surfactant films exhibited the low surface tensions, collapse rates and compressibilities characteristic of alveolar surfaces in situ. Remarkably, surface tension and area are interrelated in the captive bubble which may promote low and stable surface tensions. If the surface tension of the captive bubble suddenly increases ('click') because of mechanical vibration or unstable surfactant, the bubble shape changes from flat to more spherical. The associated isovolumetric decrease in surface area prevents the surface tension from rising as much as it would have in a constant-area situation. This feedback mechanism may also have a favorable effect in stabilizing alveolar surface tension at low lung volumes.

Adsorption↗
PubMed1992

[New aspects of asthma therapy].

Until recently, optimal bronchodilatation and in particular the inhalation of beta-agonists was considered the mainstay of asthma therapy. Steroids were added only in case of an unsatisfactory treatment effect. Recent epidemiological surveys, revealing an association between asthma mortality and the use of beta-agonists, and well controlled treatment studies suggest a change of concepts. Considering the long-term course of asthma, early suppression of asthmatic airway inflammation appears to be at least as important as an effective bronchodilatation. A prerequisite for a success of an individually taylored pharmacologic treatment is a comprehensive management of the disease, inclusive a continuous patient education.

Anti-Inflammatory Agents↗
PubMed1992

[Chronic asthmatic bronchitis].

Many patients with chronic obstructive pulmonary disease (COPD) episodically or continuously have asthmatic signs with a degree of reversibility in response to bronchodilators. In such cases, the diagnosis 'chronic asthmatic bronchitis' is often used, although the cause-effect relationship between COPD and asthmatic manifestations is not established. Hence, the 'chronic asthmatic bronchitis' is not a pathogenetic diagnosis, but rather a working diagnosis which implies a specific treatment of the reversible component of chronic airway obstruction. Certainly, the most important measure to avoid a rapid progression of COPD is the elimination of damaging agents by inhalation (smoking). In addition, it was a widely accepted belief that these patients require a continuous inhalation therapy with beta-agonists or anticholinergics. However, there is new evidence, indicating that a continuous treatment might accelerate the decline in ventilatory function and that a better long-term outcome might be achieved by on-demand inhalations.

Aged↗
PubMed1991

[Why is the lung dry?].

The extremely thin blood-gas barrier, the high blood perfusion rate and the deformability of the lung required for ventilation call for safety measures in order to keep the peripheral airspaces dry. The protective factors are provided in part by the particular structural organization of the lung, in part by physiological safeguards. Amongst the structural safety factors the extremely low permeability of the alveolar epithelial cell layer, the effective drainage system of interstitial spaces, and the loose connective tissue layers which surround vessels and bronchi, and which can act as transient fluid reservoirs, should be mentioned. The physiologic safety factors include the low hemodynamic pressures in the pulmonary vessels, the high colloid-osmotic pressure of blood, the decrease in perimicrovascular colloid-osmotic pressure on increased transcapillary fluid filtration, the interstitial pressure gradient between peripheral and central parts of the lung, and the minimal mechanical forces acting on the fine lung parenchyma owing to the low surface tensions provided by alveolar surfactant. Whether the active pumping mechanism improving reabsorption of edema fluid is also operative under normal conditions has not yet been clarified.

Blood Pressure↗
PubMed1990

[Respiration physical therapy?].

This review assesses the role of physical modalities - chest physical therapy, breathing exercises, breathing training, and physical exercises - in the treatment of patients with pulmonary diseases. Controlled studies suggest that "routine" exercises yield a disappointing effort-benefit ratio, but that individually adapted programs may improve the well-being and functional ability of selected patients.

Breathing Exercises↗
PubMed1989

A captive bubble method reproduces the in situ behavior of lung surfactant monolayers.

We tested a new captive bubble surface tensiometer with films adsorbed from aqueous suspensions of rabbit lung surfactant and a bovine lung surfactant lipid extract and with films of dipalmitoyl-sn-3-glycerophosphorylcholine (DPPC) spread from solvents. The lack of tubes penetrating the bubble surface eliminated potential leakage pathways for the surface film, which was compressed by increasing external pressure. Surface tensions and areas were calculated directly from bubble shapes without the need of pressure measurements. After only one to two compressions, the rabbit surfactant films exhibited the low surface tension, collapse rates, and compressibilities characteristic of the alveolar surface in situ and approached the behavior of spread DPPC films. The bubble "clicking" phenomenon described earlier by Pattle (Proc. R. Soc. Lond. B Biol. Sci. 148: 217-240, 1958) was also reproduced, but only with the bovine extract, which did not perform as well as the rabbit surfactant in surface tests. These findings suggest that surfactant apoprotein SP-A, which was probably present in the rabbit but not the bovine preparations, enhances both adsorption and stability of pulmonary surfactant monolayers.

Animals↗
PubMed1988

Ultrastructural aspects of pulmonary edema.

The alveolar septa are designed for gas exchange as well as for the exchange of water and solutes. The organization of the tissue elements and the ultrastructural architecture of the alveolar septa minimize the interference between gas and liquid exchange even when excess water begins to accumulate in the septal interstices and the alveoli. Larger amounts of alveolar edema fluid, however, profoundly alter both function and structure of the lung parenchyma. As to the routes of abnormal fluid movement, the ultrastructural findings are not always conclusive, though in some types of permeability edema frank anatomic disruptions of the endothelial and epithelial barriers can be observed. On the other hand, in hemodynamic edema the permeability barriers appear to be intact. However, experiments involving macromolecular tracers and the presence of numerous red blood cells in the interstitial and alveolar spaces indicate that transient separations of cell junctions have taken place.

Acute Disease↗
PubMed1988

Low plasma concentrations of ionized calcium in patients with asthma.

It has been suggested that calcium homeostasis is abnormal in the vascular smooth muscle of hypertensive patients and in the bronchial smooth muscle in asthmatics. We have found the mean baseline concentration of plasma ionized calcium to be significantly lower both in 12 asthmatics with exercise-induced asthma (EIA) [1.16 +/- 0.01 (SE) mmol/l, P less than 0.001] and in 20 asthmatics without EIA (1.16 +/- 0.01; P less than 0.001) compared with 42 healthy subjects (1.24 +/- 0.01). The mean concentrations of plasma ionized calcium were not significantly different in asthmatics with and without EIA when measured either before treadmill exercise, during the last seconds of this exercise, or 10 or 20 min after exercise but were significantly lower than in another seven healthy subjects who undertook the same exercise protocol. Total plasma calcium concentrations in the three exercising groups were not significantly different at any point in time. The results suggest that in bronchial asthma an alteration of calcium metabolism may be important, but they also suggest that there is no simple relationship between the plasma ionized calcium concentration and acute exercise-induced bronchoconstriction.

Asthma↗
PubMed1979

[Follow-up of severe adult respiratory distress syndrome].

The results are presented of the clinical, radiological and pulmonary function follow ups in 6 patients 19 to 35 months after the onset of a most severe adult respiratory distress syndrome (ARDS). The previously healthy young patients required ventilatory support for 16 to 135 days, reflecting the severity of the ARDS. In agreement with earlier studies, lung function improved rapidly in the first year but barely thereafter. Nineteen to 35 months after the ARDS a mild to moderate degree of restrictive ventilatory impairment could be detected in all our patients, associated with a significant arterial hypoxemia on exercise in five. Additionally, three patients showed signs of reversible airway obstruction. If the subacute course rather than the acute phase of the disease is taken as the criterion, there appears to be a relationship between the severity of the ARDS and the residual impairment of lung function. The fact that even most severe lung damage eventually led to a more or less significant loss of the functional reserves of the lung, but hardly ever ended in chronic respiratory failure, justifies all possible intensive care efforts in the treatment of those patients.

Adult↗
PubMed1979

[The rate of isometric inspiratory pressure change as a measure for the CO2 sensitivity of the respiratory center in patients with obstructive lung disease].

In healthy persons with and without loaded breathing, in asthmatics, and in patients with chronic obstructive lung disease (COLD) the rate of isometric inspiratory pressure development ([dp/dt]max) has been measured in order to assess the clinical significance of (dp/dt)max as an index of the motor output of the respiratory center in response to increased levels of carbon dioxide. During unloaded breathing normal subjects showed an excellent correlation between the ventilatory and the (dp/dt)max responses to CO2. Normal persons breathing through an external expiratory flow resistance, the asthmatics, and the patients with COLD had not only a blunted ventilatory response, but also a reduced (dp/dt)max response. The parallel changes observed in both variables indicate that under conditions of mechanical loading the (dp/dt)max does not exclusively reflect the motor output of the respiratory center, but is influenced by other factors such as the work of breathing and the mechanical efficiency of the respiratory pump. Accordingly, measurements of (dp/dt)max are of little help in deciding whether the development of CO2 retention in patients with obstructive airway disease is primarily due to increased mechanical load or to decreased sensitivity of the respiratory center.

Adult↗
PubMed1979

Alterations of mechanical properties and morphology in excised rabbit lungs rinsed with a detergent.

To assess the influence of alterations of lung surfactant on the geometry of peripheral air spaces, the morphology of detergent-rinsed rabbit lungs was studied. In comparison to normal excised rabbit lungs, fixed in the same manner by vascular perfusion at different points on the deflation pressure-volume curve, the most important differences are as follows. 1) With decreasing lung volume there is a progressive collapse of alveoli; at low lung volume (40% of total lung capacity (TLC) (most alveoli are collapsed, and the air is contained in overextended ducts. 2) Accordingly, the alveolar surface area-to-volume ratio is considerably smaller in particular at medium and low lung volumes. 3) There is only a slight change of mean air-space curvature between 80 and 40% TLC. Hence, the results indicate that in detergent-rinsed lungs volume changes are brought about predominantly by recruitment and derecruitment of alveoli. It appears that both a normal surfactant and the mechanical interdependence within the fibrous continuum are required to maintain a normal respiratory surface area within the lung volume range of normal breathing.

Animals↗
PubMed1979

Alveolar volume-surface area relation in air- and saline-filled lungs fixed by vascular perfusion.

The influence of volume changes and interfacial forces on the geometry of peripheral air spaces was studied in excised rabbit lungs inflated with either air or saline and fixed by vascular perfusion at four points of the deflation limb of the pressure-volume curve corresponding to 100, 80, 60, and 40% of the total lung capacity (TLC). In air-filled lungs pleating and folding of alveolar septa were observed, especially in alveolar corners. However, the alveolar surfaces were smooth, except at low lung volumes where some surface crumpling occurred. In saline-filled lungs pleats were absent; the alveolar surface was irregular at all inflation levels due to undulating walls and bulging capillaries. Morphometry indicated that at all alveolar volumes (VA) the surface areas (SA) were larger in saline- than air-filled lungs. No simple mathematical function was found to characterize the relation between SA and VA over the entire volume range studied. Within the range of normal breaths (80 to 40% TLC) the best fit for n in the function SA = k.VnA was 0.58 for saline-filled lungs (r = 0.93) and 0.33 for air-filled lungs (r = 0.68), suggesting different and complex deflation patterns.

Animals↗
PubMed1979

A simple method for computing airway resistance and specific airways conductance from scalar plethysmographic recordings.

An alternative procedure to evaluate plethysmographic tracings is described for the determination of airway resistance (Raw) and specific airway conductance (SGaw). Raw and SGaw obtained with this method reflect the average resistive impedance over one breathing cycle. Although both work and apparative expenditures are minimal, the results are well comparable with those calculated with more involved methods. The technique is particularly well suited for patients with impaired cooperation since SGaw can be determined without measuring the intrathoracic gas volume.

Airway Resistance↗
PubMed1978

Adaptation of the growing lung to increased Vo2: III. The effect of exposure to cold environment in rats.

This study was undertaken to further test the hypothesis that increased Vo2 operates as a stimulus for enhanced lung growth leading to a pulmonary diffusing capacity adapted to the body's O2 requirements. Vo2 was augmented by raising 4-week-old rats for 3 weeks at 11 degrees C ambient temperature, with controls kept at 24 degrees C; this led to an increase in Vo2 averaged over 24 h by 64%. In contrast to previous experiments with waltzing mice this regime did not affect body growth, as the final body weights were identical in both groups. In the cold-exposed rats the lung volume was larger by 24%, due to an increase by 26% in air volume (at about TLC), 13% in capillary blood volume and 19% in tissue volume. The alveolar and capillary surface areas were increased by 18%, and Dm and Dl by 17% and 21% respectively. It is concluded that the hypothesis of adaptation of pulmonary gas exchange capacity to increased Vo2 cannot be rejected. Whilst in previous experiments some doubts had to be retained as to the specificity of the stimulus, because of its rather marked effect on body weight, this reservation does not hold in this case. The structural modifications which lead to increased Dl in the various experimental models are discussed.

Adaptation, Physiological↗