Lymphangiome der Haut

Ohne ZusammenfassungMit 4 Textabbildungen.     

Gastric hypersensitivity induced by oesophageal acid infusion in healthy volunteers

Abstract  Distal oesophageal acid exposure has been shown to increase visceral sensitivity of the proximal oesophagus via central sensitization. Here we evaluated whether acidification of the distal oesophagus also affects the sensorimotor function of the proximal stomach. A gastric barostat study combined with a 30-min acid (HCl 0.15 mol L^br>−1br>) or saline infusion in the distal oesophagus was performed in 18 healthy volunteers. Gastric and cutaneous sensitivity was assessed before and up to 2 h after the start of infusion. Directly after acid infusion, but not after saline, the threshold for discomfort decreased (–6.4 ± 1.7 vs 0.4 ± 0.4 mmHg; P = 0.028) and distension-induced symptoms increased significantly compared with the baseline (122 ± 49% vs −3 ± 9%). Cutaneous sensitivity remained unaffected by acid infusion. In contrast, when the infused liquid was aspirated 3 cm more distally, at the level of the lower oesophageal sphincter, the effect of acid infusion on gastric sensitivity was abolished and the increase in distension-induced symptoms was reduced (61 ± 24%). Distal oesophageal acid infusion induces visceral hypersensitivity without affecting somatic sensitivity arguing against a similar mechanism of central sensitization as observed in non-cardiac chest pain. As reduction of the acid load to the stomach prevented this effect, our findings indicate that either gastric and/or duodenal acidification is involved. It should be emphasized though that aspiration from distal oesophagus may have attenuated the effect by reducing the acid-exposed area or by reducing the contact time.     

Does acute psychological stress increase perception of oesophageal acid?

Abstract Gastro‐oesophageal reflux disease (GORD) patients often report an increase in their reflux symptoms during stressful situations. The aim of this study was to assess the influence of acute psychological stress on oesophageal acid perception. In 15 healthy volunteers and 10 GORD patients with a positive symptom–reflux association an oesophageal acid perfusion test was performed, once with and once without the presence of an acute psychological stressor (IQ test). The order of the measurements was randomized. The time from onset of the acid infusion to first acid perception, discomfort and pain was noted. Blood pressure was measured to assess the effect of the stress task. In healthy volunteers, the time to first perception (control task: 617 ± 174 s vs stress task: 561 ± 162 s), discomfort (control task: 969 ± 158 s vs stress task: 940 ± 151 s) or pain (control task: 1393 ± 122 s vs stress task: 1366 ± 121 s) did not differ significantly between both measurements. In GORD patients, no significant differences between both measurements were found either in time to first perception (control task: 63 ± 26 s vs stress task: 43 ± 15 s), discomfort (control task: 153 ± 44 s vs stress task: 249 ± 62 s) or pain (control task: 558 ± 139 s vs stress task: 633 ± 118 s). Systolic blood pressure rose significantly during the stress task in both the healthy volunteers (6 ± 1 mmHg) and the GORD patients (9 ± 2 mmHg). Neither in the healthy volunteers nor in the GORD patients, the acute psychological stress induced by an IQ test increased oesophageal acid perception. The observed increase in systolic blood pressure shows that the experimental stressors were effective.     

Wertvolles Magnesiumpräparat in der Dermatologie

Ohne Zusammenfassung     

Initial changes in the sensory hair-cell membrane following aminoglycoside administration in a guinea pig model

This study demonstrates the initial changes affecting the sensory hair-cell plasma membranes in the vestibular end organs of gentamicin-treated guinea pigs by using a ruthenium red staining technique. First, 0.1 ml of a solution containing 5 mg gentamicin sulfate was injected into the middle ear. After 7 days, the sensory hair cell cilia were observed to be degenerating. The various stages of this degeneration process were classified into two types: the decrease in glycocalyx was designated type I fusion, while type II fusion was characterized by a bleb formation of the plasma membrane of the sensory hair cells, followed by a decrease in glycocalyx. The latter mechanism allowed plasma membrane contact, with subsequent fusion of the plasma membrane of neighboring sensory hair-cell cilia. The material also illustrates the degeneration of ciliary actin filaments. These findings suggest that the aminoglycoside affects both the glycocalyx and the plasma membrane, and that the decrease in glycocalyx may be the first sign of sensory hair-cell fusion.     

Endolymphatic sac morphology following long-term kanamycin intoxication

The well-known toxicity pattern of aminoglycoside antibiotics has been used with the aim to produce waste products in the inner ear. The endolymphatic sac was studied after daily intraperitoneal injection of 75 mg/kg kanamycin for 10 and 20 days to see whether or not the endolymphatic sac showed signs of increased phagocytic activity. The epithelium of the endolymphatic sac was reduced in height, the cells were swollen and extremely thin. The dark epithelial cells were outnumbering the light cells. The subepithelial tissue showed an edematous swelling containing few blood vessels, collagen fibrils and fibroblasts with an empty appearance. There were few wide lateral intercellular spaces and there were intraluminal free floating cells. There were, in all, no clear morphological signs of increased phagocytic activity in the epithelium of the endolymphatic sac.     

Ultrastructure of the endolymphatic sac in the mongolian gerbil

We describe our findings in an ultrastructural study of the endolymphatic sac of the mongolian gerbil. In conjunction with its specific renal physiology, enabling this animal to withstand long-term water deprivation, we have used our findings to hypothesize the existence of a local monitoring system within the endolymphatic space. The presence of elastic tissue in the subepithelial space of the endolymphatic sac could explain the mechanism through which this structure equilibrates endolymphatic pressure changes. Finally, we propose that a secretion of water-retaining macromolecules may act through osmotic forces to modulate inner ear fluid.