ISSN:0301-1569    

DOI:10.1159/000275965

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Histological studies were performed on the temporal bones of 17 persons who died of intracranial abscess as a complication of chronic otitis media and mastoiditis. In all cases the route of intracranial infection was via the dura mater rather than through the labyrinth. During the acute stage of intracranial abscess formation, the site of intracranial invasion showed a destructive inflammatory reaction characterized by the presence of granulations, resorption and sequestration of bone, invasive cholesteatoma, collections of purulent exudate, and necrosis of dura mater. At this stage any attempt at definitive removal of diseased tissue would necessarily result in a larger dural defect at a time when local disease and systemic illness present unsuitable conditions for reparative procedures. For this reason it would seem prudent to limit early otologic surgery to ensuring adequate drainage (e.g., postauricular open-wound drainage) and to perform corrective surgery (e.g., tympanomas-toidectomy with repair of the dural defect) after the intracranial abscess has been brought under control.

ISSN:0301-1569    

DOI:10.1159/000275966

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The nasal passages play a crucial role in the protection and functioning of the lower airways. Consequently the nerve supply of the nasal mucosa is extensive, which is related to an immediate and adequate reaction upon a variety of external and internal stimuli. A brief review of the present knowledge on nasal autonomic innervation and pharmacology will be given. There is special attention to more advanced methods, such as radioligand receptor binding techniques, which might augment our insight in the significance of the nervous system in nasal (patho)physiology. Furthermore data on the secretory activity of the nasal glands in the rat and its neural regulation will be accentuated.

ISSN:0301-1569    

DOI:10.1159/000275967

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The acute and chronic effects of treatment with ethacrynic acid (EA) and furosemide (FU) on the structure of the murine endolymphatic sac were studied by means of light and transmission electron microscopy. The animals were treated with loop diuretics in doses which are known to cause morphological alterations of the stria vascularis and a significant reduction of the endocochlear potential. A single intravenous injection of either EA or FU resulted in immediate morhpological changes such as an increase in cytoplasmic contents of endoplasmic reticulum and more prominent Golgi structures of the light cells. These cells developed membrane-bound granules and a smooth tubular network in the apical cytoplasm. These findings together with the appearance of a precipitate on the luminal aspect of the cell membrane suggested secretory activity. Ten days after daily intraperitoneal injections with loop diuretics in sub toxic doses, the epithelial cytoarchitecture of the endolymphatic sac was altered, with pronounced veiling of the light cells by the dark cells. It is concluded that the changes in the endolymphatic sac epithelium after treatment with ototoxic diuretics may not be a result of a primary toxic effect on the sac per se, but rather be secondary to alterations in fluid and ion homeostasis in the rest of the inner ear.

ISSN:0301-1569    

DOI:10.1159/000275968

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

In young rabbits the growth of the subglottis was studied over a period of 20 weeks after interruption of the circularity of the cricoid on the ventral side. In all cases the cricoid developed into a U-like structure which did not cause an airway narrowing. However, a cricoid lesion combined with an injury to the soft tissue lining led up to a subglottic stenosis. It was concluded that when the soft tissue layer is undamaged, an intact circular structure of the cricoid is not compulsory for the normal development of the subglottis.

ISSN:0301-1569    

DOI:10.1159/000275969

出版商:S. Karger AG    

年代:1988

数据来源: Karger

ISSN:0301-1569    

DOI:10.1159/000275970

出版商:S. Karger AG    

年代:1988

数据来源: Karger

ISSN:0301-1569    

DOI:10.1159/000275971

出版商:S. Karger AG    

年代:1988

数据来源: Karger

ISSN:0301-1569    

DOI:10.1159/000275972

出版商:S. Karger AG    

年代:1988

数据来源: Karger