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Biomedical subjects

S Brosch

Publications and source records attributed to S Brosch.

24 records · Page 2Linked to original sources
PubMed1999

[Medication-induced vocal cord paralysis as an uncommon cause of cord paralysis].

A case is reported of a 57-year-old man who was found to have a right vocal cord paralysis that most likely followed prolonged treatment with the anti-arrythmic medication Amiodaron-HCl (Cordarex). Phoniatric treatment was given for 5 1/2 months, during which time microlaryngoscopy and stroboscopy were performed. With the help of speech therapy, mobility of the paralyzed cord was seen to begin to return 3 1/2 months after discontinuing the Amiodaron-HCl. Full cord mobility has not returned to date.

Amiodarone↗
PubMed1999

Clinical course of acute laryngeal trauma and associated effects on phonation.

We report the clinical course of blunt laryngeal trauma in three young patients. All three patients underwent several phoniatric examinations as well as indirect microlaryngoscopy and microstroboscopy. The follow-up period ranged from three to eight months. In the first case, there was isolated haemorrhage of the left vocal fold; in the second, dislocation of the arytenoid cartilage with formation of an adhesion in the area of the anterior commissure; and, in the third, non-dislocated fracture of the thyroid cartilage with development of haematoma in the right hemilarynx and transient vocal fold paralysis. One patient required surgical treatment; however, repositioning of the arytenoid cartilage, attempted seven weeks following the injury, proved unsuccessful. In conclusion, all three patients showed significant limitation of vocal fold vibration many months after trauma which was unrelated to the extent of resulting tissue damage. In all three cases, patients developed secondary posttraumatic functional dysphonia requiring treatment.

Accidental Falls↗
PubMed1998

The effect of alendronate on cytokine production, adhesion molecule expression, and transendothelial migration of human peripheral blood mononuclear cells.

Since both osteoclasts and macrophages belong to the mononuclear phagocytic system it is conceivable that bisphosphonates not only affect bone metabolism but also inflammatory responses. The migration of mononuclear cells into perivascular tissue is a central event in inflammatory reactions. We studied the effects of the aminobisphosphonate alendronate on the transendothelial migration of human peripheral blood mononuclear cells in an in vitro model. Alendronate (at a concentration of 100 microM) significantly increased the percentage of peripheral blood mononuclear cells that migrated through endothelial cell monolayers. Similar results were obtained with another aminobisphosphonate, viz, pamidronate. An overnight treatment of the endothelial cell monolayers with alendronate did not alter the rate of peripheral blood mononuclear cells that subsequently migrated. The overnight cultivation of the peripheral blood mononuclear cells in the presence of alendronate resulted in an increased surface expression of CD54 (intercellular adhesion molecule-1, ICAM-1) in both CD14(+) and CD3(+) cells; in CD14(+) cells also the expression of CD49d (alpha4 subunit of late activation antigen-4, VLA-4) increased after alendronate treatment. Alendronate treatment of peripheral blood mononuclear cells also resulted in an increased production of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma). We conclude that alendronate has a distinct effect on the transendothelial migration of human peripheral blood mononuclear cells in vitro. Alendronate may either directly or indirectly, e.g., by augmenting the production of proinflammatory cytokines, influence the expression of certain adhesion molecules and thereby facilitate transendothelial migration. These effects could be related to the transient leukopenia reported following intravenous administration of relatively high doses of aminobisphosphonates for the treatment of hypercalcemia of malignancy.

Alendronate↗
PubMed1995

The effects of veratridine and BDF 9148 on the action potentials and contractility of the rat right ventricle.

1. The effects of veratridine, BDF 9148 and lignocaine on the action potentials and contractile force of the electrically-driven rat right ventricle have been determined. 2. Veratridine at 10(-7)-10(-6) M and BDF 9148 at 10(-7)-10(-5) M had no effect on the threshold potential or amplitude but prolonged the ventricular action potentials. 3. In contractility studies, veratridine at 10(-7)-10(-6) M augmented the cardiac stimulation responses and the augmenting effects with 3 x 10(-7) and 10(-6) M were greater at 2 than 4 Hz. In the presence of veratridine at 3 x 10(-6) M, the ventricle would not pace. 4. BDF 9148 at 10(-7)-10(-5) M augmented the cardiac stimulation responses and the augmenting effects with 10(-7) and 3 x 10(-7) M were greater at 2 than 4 Hz and the effect was maximal at 3 x 10(-7) M and submaximal at 10(-5) M. The effects of BDF 9148 at 10(-5) were not readily reversible. 5. Lignocaine at 10(-4) M had no effect on the ventricular action potential duration but decreased the threshold potential and amplitude and also reduced the cardiac stimulation force responses. In the presence of lignocaine, the augmenting effects of veratridine and BDF 9148 on ventricular force were reduced. 6. In summary this study has shown that BDF 9148 prolongs the action potential and augments the contractile force responses of the rat right ventricle by a lignocaine-sensitive mechanism. BDF 9148 or similar drugs may have potential as positive inotropes in the treatment of heart failure.

Action Potentials↗