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Biomedical subjects

K Morgenroth

Publications and source records attributed to K Morgenroth.

At least 55 records · Page 3Linked to original sources

[Leukotriene synthesis by gastrointestinal tissue and its pharmacologic modification].

Tissues of the gastrointestinal tract synthesize leukotriene (LT) B4 and the sulfidopeptide-leukotrienes LTC4, LTD4 and LTE4 from endogenous substrate. Formation of leukotrienes was demonstrated using radioimmunoassay, high pressure liquid chromatography (HPLC) and bioassay. Under basal conditions the gastrointestinal tissues released minor amounts of leukotrienes only. Formation of lipoxygenase-derived products of arachidonic acid metabolism was, however, significantly increased in the presence of various stimuli. Thus, significant amounts of LTB4 and of sulfidopeptide-leukotrienes were released from colonic and gastric mucosa of guinea-pigs sensitized against ovalbumin when incubations were carried out in the presence of antigen. Antigen-induced leukotriene formation was not found in the muscularis propria and subserosal of ovalbumin-sensitized guinea-pigs. Release of cyclooxygenase-derived metabolites of arachidonic acid, on the other hand, was most abundant in the subserosal layer of the guinea-pig colon and was not influenced by the immunological reaction. Inhibitors of cyclooxygenase, such as indomethacin, reduced gastrointestinal formation of prostaglandins, but not of leukotrienes. Inhibitors of 5-lipoxygenase, however, significantly decreased leukotriene formation. Synthesis of LTB4 and of sulfidopeptide-leukotrienes was also found in human colonic mucosal tissue, using the divalent cation-ionophore A23187 as stimulating agent. HPLC analysis demonstrated that the sulfidopeptide-leukotrienes released were composed of a mixture of LTC4, LTD4 and LTE4. In addition, human colonic mucosal tissue contained high activities of enzymes that rapidly convert LTC4 to LTE4. As in most biological systems LTE4 is less active than LTC4 and LTD4 degrading enzymes might represent a local inactivating mechanism. Mucosal tissue of patients with Crohn's disease synthesized considerably more LTB4 and sulfidopeptide-leukotrienes than non-inflamed mucosa.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Morphology and pathogenesis of pneumoconiosis in dental technicians.

The morphology of pneumoconiosis occurring in dental technicians could be studied by systematic light and electron microscopical investigation of 30 lung preparations from such cases. Diffuse streaky fibrosis and, in some cases, nodular fibrosis was observed together with occasional formation of silicotic nodules that may lead to extensive transformation of the alveolar structure. The etiological relationship between occupational dust exposure and pulmonary changes could be documented by element analysis of dust deposits on histologic sections, and of dusts from grinding and polishing instruments collected in the laboratory. The energy-dispersive X-ray microanalysis used in this study helps to differentiate and delimit this form of pneumoconiosis. The pathogenesis is discussed on the basis of light and electron microscopic results and physicochemical analyses.

Adult↗

Morphological features of the interaction between mucus and surfactant on the bronchial mucosa.

The secretion layer over the bronchial epithelium was investigated on human biopsy material. In the sol phase of the secretion, phospholipid membranes stretched out or arranged in vesicular structures could regularly be demonstrated. They displayed the same structure as the surfactant material in the alveolar space. It can be inferred therefrom that the surfactant is excreted via the bronchial system. It probably contributes to the stabilization of the sol phase of the mucus and thus influences the sliding capacity of the gel phase. So the surfactant has an important function in maintaining mucociliary clearance at the bronchial mucosa.

Adolescent↗

Functional morphology of phagocytosing alveolar macrophages. Long-term electron microscopic and X-ray microanalytical investigations on the rat model.

A single instillation of 1 ml iron dextran (containing 191.3 mg iron(III)hydroxide and 200 mg dextran) was administered under anaesthesia by a polyvinyl catheter into the lower lobe of the right lung in one hundred 4-week-old wistar rats. The animals were killed at intervals ranging between 1 min and 4 weeks. The lower lobe of the right lung was examined by light and electron (transmission and scanning) microscopy. In addition, X-ray microanalyses were performed on tissue sections in the transmission and scanning electron microscopes. The process of phagocytosis of iron dextran by alveolar macrophages can be subdivided into three stages, which we have termed the "phase of attachment" (from 1 to 5 min), followed by the "phase of phagocytosis" (from 5 to 20 min) and finally the "resident macrophage stage" (from 1 to 24 h). X-ray microanalysis shows a high phosphorus content even if iron dextran is concentrated on the surface of macrophages. Phagocytosis of particles between 15 and 40 A in size occurs within minutes, the particles being engulfed in phagosomes, which form as double-layered invaginations of the cell membrane into the interior of the cell. The fusion of phagosomes with lysosomes produces phagolysosomes (type 2 lysosomes) in which iron dextran is broken down into lamellar residual bodies. In these lamellar bodies X-ray microanalysis shows that in addition to abundant iron, there is a high phosphorus content, which may indicate the involvement of surfactant. Only 1 h after instillation, free particles of iron dextran can no longer be demonstrated in the alveoli, although a proportion of the iron dextran remains in resident macrophages (pulmonary tissue macrophages) and some is also found in splenic macrophages.

Animals↗

Morphology of the bronchial lining layer and its alteration in IRDS, ARDS and COLD.

Both light and electronmicroscopic examinations of the collocation of surfactant secreted by the alveoli into the bronchi were performed on material obtained from biopsies and autopsies. In the sol phase and especially along the border between the sol and gel phases of the bronchial mucus layers regularly arranged, partially stretched and partially reticulated osmiophilic membranes could be demonstrated. Their detailed structure corresponds with the structure of the phospholipid membranes of the surfactant in the alveoli. The functional significance of this surfactant portion for bronchial clearance is discussed in relation to the changes in structure of these membranous bodies, and their collocation in the mucus layers in chronic bronchitis, ARDS and IRDS.

Adolescent↗

[The morphology of bronchial clearance].

The secretion of bronchiolar and bronchial epithelium was investigated in human biopsy material by electron microscopy. The secretion of Clara cells in the bronchioli of the goblet cells of bronchial epithelium and the secretion of peribronchial glands produce the gel phase of mucus above the bronchial mucosa. This gel phase is transported on the periciliary sol phase through the cilia beat, which consists of intercellular fluid. Foam-like, regularly arranged surfactant structures are detectable in this sol phase. Due to its surface-active qualities this surfactant, which is formed in the pneumocytes II of the alveolar system, has an anti-adhesive effect on the border between the sol and gel phase of the mucus. Furthermore, it contributes to the stabilisation of the water content in the sol phase, which is of decisive importance for the ciliary mucus transport. The morphological results agree with the results from the physiological and biochemical investigations, indicating that the surfactant has an important function in bronchiolar and bronchial clearance.

Bronchi↗

The dyskinetic cilia syndrome in childhood. Modifications of ultrastructural patterns.

The syndrome of cilia dyskinesia is known as a heterogenous ciliary dysfunction caused by morphological defects of the dynein arms, the nexin links, the radial spokes and by the transposition of microtubules. Supernumerary tubules have been regarded as acquired morphological defects on the background of other bronchopathies. The report of a 9-year-old girl with the clinical signs of ciliary dyskinesis is considered to be an attribution to the clinical and pathological features of this syndrome. The girl's history of chronic bronchopulmonary infections and nasal polyposis resistant to therapy made her suspected to be ill of Kartagener's syndrome. The results of ultrastructural investigations of the mucosa from ciliated epithelium revealed a ciliary structural defect in the bronchi as well as in the nose and the sinuses with supernumerary microtubular doublets and singles, a decentration of the central tubules and shortened dynein arms. The regularity of the electron optical abnormalities implicates a systemic disorder of ciliated epithelium, which is to be summarized to the syndrome of cilia dyskinesis.

Bronchi↗

[Pulmonary dysplasia in infancy. Pathogenesis, pneumologic course studies and therapy possibilities].

Some premature and mature newborns who require intermittent positive airway pressure (IPPV) and high oxygen concentrations for respiratory distress syndrome develop characteristic damage of bronchi and bronchioles termed broncho-pulmonary dysplasia (BPD). According to the radiographic findings the changes are categorized into four progressive stages. Stage 1 describes a radiographic feature with a pattern of fine, faint granularity as it is characteristic for the hyaline-membrane-syndrome. Stages 2 to 4 represent diffuse interstitial emphysema, a bubbly appearance of the lung, atelectasis and a progressive fibrosis. Electronmicroscopic investigations of bronchial imprints could demonstrate a rarefication of the cilia and a ciliary damage which took the form of compound cilia. In addition, a marked increase of goblet cells in the bronchial mucosa as well as a metaplasia of the epithelial cells was present. These findings may be a prerequisite for chronic infections, and perpetuate a cycle which may result in chronic obstructive airway disease. The significance of bronchial and bronchiolar injury in children with BPD is said to be due to IPPV, high inspiratory oxygen concentrations, high fluid intake, vitamin E deficiency or an increased intrapulmonary pressure secondary to a patent ductus arteriosus. When pulmonary mechanics were measured in a baby-body-plethysmograph a high pulmonary resistance and a low dynamic compliance occurred at the first investigation after IPPV or oxygen administration. On re-examination there was a strong tendency to normalisation of x-ray findings and pulmonary mechanics, depending upon the time which elapsed between ventilation and re-examination. Current therapy has to be symptomatic and may include secretolytics, glucocorticoids and bronchodilators. The preventive interventions have to take into consideration ventilation techniques, restrictions in O2 and fluid intake.

Bronchi↗

Release of slow-reacting substance of anaphylaxis and leukotriene C4-like immunoreactivity from guinea pig colonic tissue.

Colonic mucosa, muscularis propria and subserosa from ovalbumin-sensitized guinea pigs were incubated and challenged with antigen in vitro. Slow-reacting substance of anaphylaxis (SRS-A) was determined biologically as well as radioimmunologically in terms of leukotriene (LT) C4-like immunoreactivity. Before antigenic challenge release of immunoreactive LTC4 by all tissues was below or close to the detection limit of the radioimmunoassay. After addition of antigen colonic mucosa released considerable amounts of LTC4-like immunoreactivity, while muscularis propria and subserosa were less active. The biological activity of the SRS-A formed after challenge was antagonized by FPL 55712. Contrary to LTC4-like immunoreactivity release of 6-keto-prostaglandin (PG) F1 alpha was predominant in the subserosa and smaller amounts were released from the smooth muscular and mucosal layers. Synthesis of SRS-A and LTC4-like immunoreactivity, respectively, as well as synthesis of 6-keto-PGF1 alpha was inhibited by the dual inhibitor of lipoxygenase and cyclooxygenase BW755c. The results suggest a role for LTs as local mediators of inflammatory reactions in colonic disease states, particularly those with possible involvement of immunological processes.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗

Electron microscopic investigations on dust penetration into the pulmonary interstitium in experimental pneumoconioses.

Pneumoconioses produced by intratracheal applications of various dusts (quartz, coal, cadmium and lead sulfide) in rats were investigated by electron microscopy in order to follow the pathway of the dust particles from the alveoli into the pulmonary interstitium. As postulated by Spencer in 1977 on the basis of light microscopic investigations, the dust particles produce necroses of the alveolar septae ('alveolar ulcers'). TWo forms of necroses appear to occur: with a less severe dust exposure, individual pneumocytes and their basement membrane are destroyed by dust particles. Dust-laden, macrophages are deposited here which are displaced into the stroma after re-epithelization of the alveolar defect. On the other hand, with massive dust exposure, almost all pneumocytes of the affected alveoli become necrotic. The affected alveoli collapse and are replaced by connective tissue, so that the dust is situated in the connective tissue stroma. A transcellular penetration of the dust particles into the pulmonary interstitium or an immigration of dust-laden macrophages into the pulmonary stroma through the intercellular junctions of intact pneumocytes was not observed in any of the pneumoconiosis models.

Animals↗

Morphological alterations to the bronchial mucosa in high-dosage long-term exposure to sulfur dioxide.

Light- and electron-microscopic studies were carried out on chronic bronchitis in the rat, produced by high-dosage long-term exposure to sulfur dioxide. Particular attention was given to the advanced stages of the disease. Inflammatory intramural infiltration and fibrosis developed in the regions of the bronchial tree near the hilus and in the peripheral sections. The highly differentiated cells of the bronchial epithelium perish at the same time. After a loss of the goblet and ciliate cells, extensive epithelial metaplasias with dysplasias develop in the central regions of the bronchus. Bronchiolitis obliterans develops in the peripheral regions of the bronchus. In the bronchiolar epithelium, the Clara cells, which play a crucial role in the maintenance of bronchial secretion in the advanced stages of the disease, are preserved.

Animals↗

[Determination of organic elements in histological sections (author's transl)].

In the microscopic differential diagnosis of fibrosing lung processes organic deposits are often encountered which defy identification by histological methods. Assessment of the aetiological significance of these deposits depends on an accurate analysis. Energy-dispersive X-ray microanalysis with an electron microscope provides the means to identify organic deposits in the tissues. Such analyses, which do not require elaborate techniques, show up the type and structure of the deposits and the topographical relation to the lung lesion. They provide detailed information for assessing pulmonary lesions caused by fibrosis-inducing dusts.

Asbestos↗