[Megadolichobasilar anomaly causing acute deafness with vertigo]. / Megadolichobasilaris als Ursache einer akuten Taubheit mit Schwindel.

Megadolichobasilar anomaly, a dilatant arteriopathy of the basilar artery attributable to chronic arterial hypertension, can cause cranial nerve compression syndromes of the cerebellopontine angle or infarcts of the vertebrobasilar circulation. In this paper, we report on a patient with known megadolichobasilar anomaly and a partially thrombosed fusiform aneurysm of the basilar artery, who presented with acute-onset vertigo and subsequent deafness due to thromboembolic occlusion of the labyrinthine artery. Because of the vascular origin of the patient's symptoms, his vertigo disappeared over time while the deafness persisted.

Vasomotor responses in cyclosporin A-treated rats after chronic angiotensin blockade.

Chronic angiotensin-converting enzyme (ACE) inhibition prevents endothelial dysfunction in hypertension and hypercholesterolemia. Long-term treatment with cyclosporin A impairs endothelium-dependent relaxations and augments contractions to angiotensin II in the rat aorta. The present study compares vasomotor responses to several vasoconstrictor and dilator stimuli after 6 weeks of oral treatment with either the angiotensin-converting enzyme inhibitor lisinopril (10 mg/kg per day), the angiotensin subtype 1 receptor antagonist D 8731 (10 mg/kg per day), cyclosporin A (15 mg/kg per day), or a combination of cyclosporin A with lisinopril or D 8731 (n = 15 rats per group). Twenty-four hours after the last treatment, aortic rings were mounted in organ chambers for measurement of isometric force. Endothelium-dependent relaxations to acetylcholine and calcium ionophore were impaired by cyclosporin A but not affected by the vasodilators. Cyclosporin A-induced endothelial dysfunction was prevented by cotreatment with lisinopril or D 8731. Relaxations to nitroglycerin, SIN-1, and forskolin were not affected by any treatment. Contractions to phenylephrine and serotonin were reduced by lisinopril but not by D 8731. In contrast, contractions to angiotensin II were augmented by cyclosporin A, lisinopril, and the combination of both but not by D 8731 or D 8731 plus cyclosporin A. The data suggest a role for angiotensin II in cyclosporin A-induced endothelial dysfunction. Chronic ACE inhibition reduces overall smooth muscle contractility. The selective augmentation of angiotensin II effects by ACE inhibition and cyclosporin A suggests upregulation of angiotensin receptors in the aortic smooth muscle by these treatments. Chronic angiotensin subtype 1 receptor blockade does not appear to affect angiotensin receptor function.

[Adonco. A clinical-scientific database system for the acquisition and analysis of oncologic data in head and neck regions]. / AdOnco. Ein klinisch-wissenschaftliches Datenbanksystem zur Erfassung und Auswertung onkologischer Daten im Kopf-Hals Bereich.

BACKGROUND: Our aim was to design and develop a computer database system for head and neck cancer patients for clinical and scientific use. METHODS: A relational database based on Filemaker Pro 6.0 was developed and integrated into our local network. Its precise and easy to handle interface should allow a quick overview of the patient's oncological data. An automatically generated letter was integrated to enhance patient care. For evaluation purposes, statistical analysis functions were incorporated. RESULTS: Over a 7 month period, about 300 patient records were available through the local network. The automated letter function and the well organized display resulted in more efficient patient care. Additionally, the quality of the information presented to referring physicians increased. Statistical analysis provided by the database was reliable and easy to export. CONCLUSIONS: We developed an oncology database for clinical and scientific use and integrated it into our patient documentation system. The combination of clinical and scientific features proved to be very effective in daily patient care routine and research.

Evaluating cochlear implant trauma to the scala vestibuli.

OBJECTIVES: Placement of cochlear implant electrodes into the scala vestibuli may be intentional, e.g. in case of blocked scala tympani or unintentional as a result of trauma to the basilar membrane or erroneous location of the cochieostomy. The aim of this study was to evaluate the morphological consequences and cochlear trauma after implantation of different cochlear implant electrode arrays in the scala vestibuli. DESIGN: Human temporal bone study with histological and radiological evaluation. SETTING: Twelve human cadaver temporal bones were implanted with different cochlear implant electrodes. Implanted bones were processed using a special method to section undecalcified bone. MAIN OUTCOME MEASURES: Cochlear trauma and intracochlear positions. RESULTS: All implanted electrodes were implanted into the scala vestibuli using a special approach that allows direct scala vestibuli insertions. Fractures of the osseous spiral lamina were evaluated in some bones in the basal cochlear regions. In most electrodes, delicate structures of the organ of Corti were left intact, however, Reissner's membrane was destroyed in all specimens and the electrode lay upon the tectorial membrane. In some bones the organ of Corti was destroyed. CONCLUSIONS: Scala vestibuli insertions did not cause severe trauma to osseous or neural structures, thus preserving the basis for electrostimulation of the cochlea. However, destruction of Reissner's membrane and impact on the Organ of Corti can be assumed to destroy residual hearing.

[Evaluation of an electrode design for the combined electric-acoustic stimulation]. / Evaluation eines Elektrodendesigns für die kombinierte elektrisch-akustische Stimulation.

BACKGROUND: The objective of this study was to assess the intracochlear position and the extent of trauma to cochlear structures using the C40(+) M electrode (MED-EL, Innsbruck, Austria), which was especially designed for the combined electric acoustic stimulation. METHODS: Five human temporal bones were implanted using a standard cochlear implant procedure featuring mastoidectomy, posterior tympanotomy, and promontory cochleostomy. For the cochleostomy, an inferior approach with preservation of the endosteum of the cochlea was used to contribute to hearing preservation in the in vivo condition. RESULTS: All insertions of the new electrode array were performed into the scala tympani of the cochlea. The average insertion depth was 288 degrees. Apically, 4 of the 5 implantations were completely atraumatic. One bone showed a rupture of the basilar membrane only at the tip of the electrode. However, 4 of the 5 arrays produced severe trauma to basal cochlear structures. Two pathomechanisms, the direct traumatization through drilling of the cochleostomy or the indirect traumatization via buckling of the array could be distinguished. CONCLUSIONS: Due to the reduced contact spacing and its flexible body, the C40(+) M electrode is suitable for cochlear implantations with hearing preservation and combined electric and acoustic stimulation of the auditory system. Modifications of the surgical pathway to the cochlea should help to minimize the risk of basal cochlear trauma.

Regulation of aortic wall structure by the renin-angiotensin system in Wistar rats.

The effects of long-term angiotensin-converting enzyme (ACE) inhibition, angiotensin II (AT1)-receptor blockade, calcium-entry blockade, or cyclosporin A treatment on rat aortic wall structure were investigated to determine the role of the renin-angiotensin system in the physiologic regulation of vascular structure in vivo. Groups of 15 Wistar rats were treated for 6 weeks either with the ACE inhibitors lisinopril or fosinopril or with the AT1-antagonists D 8731 or losartan (each 10 mg/kg/day) or with the calcium antagonist isradipine, 60 mg/kg/day, or cyclosporin A, 15 mg/kg/day, or a combination of cyclosporin with one of the vasodilators. Media thickness, vascular smooth-muscle cell density, and intima thickening were measured in histologic sections of the abdominal aorta. In addition, aortic contractility and heart weight were determined. Long-term ACE inhibition, AT1-receptor blockade, and calcium-entry blockade reduced aortic media thickness and increased media smooth-muscle cell density. Only ACE inhibition significantly reduced the extent of intima lesions. Media thickness correlated well with the maximal aortic contraction to phenylephrine and serotonin but not to angiotensin II. ACE inhibition and AT1-receptor blockade decreased heart weight, whereas calcium antagonism increased it. Cyclosporin treatment was without effect on any of these parameters. The data demonstrate a significant long-term influence of the renin-angiotensin system on aortic wall structure and function in Wistar rats.

Isolation and characterization of macrovascular and microvascular endothelial cells from human hearts.

In vivo models to investigate mechanisms of local hemostasis in the macro- and microvascular coronary circulation are not available. Therefore, we established a culture system of human macro- and microvascular endothelial cells with high cellular yield and high endothelial cell purity. Microvascular endothelial cells from human hearts were isolated by enzymatic treatment of cardiac muscle preparations obtained during heart transplantation. The isolated microvessels were used to start cultures that were subsequently separated and purified from contaminating nonendothelial cells by paramagnetic beads linked to the lectin Ulex europaeus agglutinin I. Macrovascular endothelial cells were isolated from epicardial coronary arteries and purified by paramagnetic beads as well. With this method high purity (< 2% nonendothelial cells) was achieved as judged from fluorescence-activated cell sorting. Immunochemistry demonstrated the expression of several typical endothelial markers. The two endothelial cell types displayed functional heterogeneity in respect to bradykinin degradation and plasminogen activator inhibitor-1 activity. Thus the ability to selectively isolate and culture human macro- and microvascular cardiac endothelial cells provides a valuable tool to systematically investigate endothelial function in human hearts.