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Biomedical subjects

M Starlinger

Publications and source records attributed to M Starlinger.

At least 55 records · Page 3Linked to original sources
PubMed1990

[Crohn's disease: disease activity and recurrence following surgery].

The data from 238 patients (108 men, 130 women, mean age 29 [15-71] years), who had undergone operations for Crohn's disease between 1968 and 1988, were analysed retrospectively with the purpose of ascertaining the significance of an endoscopically demonstrated "early recurrence". In 170 patients postoperative colonoscopy had been performed at least once. In 130 patients the activity of the disease in the years before and after operation was compared in terms of such parameters as haemoglobin, erythrocyte sedimentation rate, serum albumin, body weight and the frequency of acute flare-ups of the disease and admissions to hospital. The probability of an endoscopically demonstrable recurrence was 90% after 5 years, while the corresponding figure for a symptomatic recurrence was 40%. This indicates that the routine performance of postoperative colonoscopies is of no value in assessing the prognosis. The probability of a reoperation was 21% after 5 years; in cases where both the ileum and colon were involved the probability was three times as high as in those with isolated involvement of either the small or the large intestine. Post-operatively, a substantial reduction in disease activity of several years' duration was achieved in the overall majority of cases.

Adolescent↗
PubMed1990

[Meckel's diverticulum and lower gastrointestinal bleeding. Problems of preoperative diagnosis].

A hitherto perfectly healthy 28-year-old man suddenly passed stools containing bright red blood, and haemoglobin concentration fell at first to 10.1 g/dl. No bleeding source was found on gastroscopy and coloscopy. Nor was the source found by enteroclysis during a bleeding-free interval. Emergency laparotomy was performed after a recurrence of massive bleeding and revealed, 60 cm oral of the ileocaecal (Bauhin's) valve, a Meckel's diverticulum with ulcerated heterotopic gastric mucosa, 5 x 3 x 2 cm in size, and this was resected. 17 red blood cell concentrates had to be infused pre- and postoperatively, but there were no further complications.

Adult↗
PubMed1990

Role of alkaline secretion and cell restitution in duodenal mucosal protection.

Duodenal alkaline secretion is a protective mechanism that is sensitive to changes in mucosal blood flow and arterial bicarbonate concentration (i.e. bicarbonate delivery to the mucosa). Alkaline secretion has been shown to prevent or limit damage and to facilitate the repair process once damage has occurred. A rapid restitution of the epithelial integrity has been demonstrated in the duodenum. This repair process is sensitive to alterations in nutrient HCO3- supply. Removal of the necrotic cell layer before repair is complete inhibits the re-establishment of epithelial continuity at low luminal pH. However, under optimal conditions repair is completed within a few hours, even with repeated acid challenge.

Acid-Base Equilibrium↗
PubMed1989

[The role of alkaline secretion of the duodenal mucosa in protecting the mucosa from hydrochloric acid].

In animal experiments, an in vivo comparison was made of the alkaline secretion (AS) of the duodenal mucosa and of its ability to defend against hydrochloric acid. An i.v. infusion of NaHCO3 and glucagon was applied to stimulate AS, and one of NH4Cl, vasopressin and furosemide to depress it. In the stage of AS influenced via various mechanisms and to different extents, the luminal surface of the duodenum was exposed with HCl. The extent of mucosal damage was determined by quantitative morphometry. The mucosa-damaging effect of standardized HCl-exposure was significantly lower in the stage of enhanced AS than in the control experiments. In contrast, during inhibition of AS hydrochloric acid caused more extensive and deeper mucosal damage. A linear correlation was observed between the degree of AS of the duodenum and the proportion of damaged intestinal villi. In the opinion of the authors, inhibition of the As of the duodenum is accompanied by a decreased acid tolerance of the mucosa, while its stimulation enhances the ability of the mucosa to defend against hydrochloric acid.

Alkalies↗
PubMed1989

[Regulation of intracellular pH by Na+/H+ exchange in human lymphocytes].

Spectrofluorimetry and the pH-sensitive fluorescent dye 2',7'-bis(carboxyethyl)-5(6)carboxyfluorescein (BCECF) was used to measure the intracellular pH (pHi) of suspended human lymphocytes. A linear relationship exists between pHi and the fluorescent spinal-ratio (I490nm/I435nm, emission 526 nm) between pH 6.5 and pH 7.8. At the end of each experiment the ratio was calibrated using the high [K+] nigericin technique. All solutions were HEPES buffered. The pHi in resting cells was 7.27 +/- 0.02 (n = 37) at 25 degrees C. Na+ free solution caused a pHi decrease to 6.81 +/- 0.08. The ammonium prepulse technique (25 mM NH4Cl) dropped the pHi to pH 6.80. A rapid recovery of the pHi after this acidification was observed in NaCl Ringer solution. Na+ free solution completely blocked the recovery. 1 mM amiloride led to a partial block of recovery. pHi was restored to the basal value after readdition of Na+. We conclude that in HEPES buffered solutions human lymphocytes recover pHi via a mechanism dependent on extracellular Na+ and largely accomplished by an amiloride inhibitory Na+/H+ exchanger.

Acid-Base Equilibrium↗
PubMed1989

Rapid epithelial restitution of human and rabbit colonic mucosa.

Rapid epithelial restitution is now considered one of the primary defense mechanisms of the stomach and duodenum. Because there is currently no evidence as to whether restitution occurs in human tissue, this study examined human and rabbit colonic mucosa after superficial injury and monitored the potential difference, alkaline flux, and speed and mechanisms of mucosal restitution as observed with light and electron microscopy. Luminal exposure of the in vivo rabbit colon to 100 mM HCl for 5 min or the in vitro human colon to 10 mM HCl for 10 min caused superficial mucosal injury to 76% of the epithelial surface in the rabbit and 95% in the human. The necrotic epithelial cells detached in sheets from the intact basal lamina and formed a protective mucoid layer. Morphologic evidence of restitution occurred within 15 min after injury in the rabbit and 30 min in the human, as viable nongoblet cells projected lamellipodia and migrated over the denuded basal lamina at a speed of approximately 2 microns/min. One hour after damage 61% of the mucosal surface was still damaged in the rabbit, and 86% of the human mucosal surface was damaged after 2 h. In the following 60 min restitution progressed rapidly, so that only 10% of the surface remained unrepaired in the rabbit after 2 h and 19% in the human after 3 h. Small areas with deeper injury did not repair until 5 h after damage. The potential difference dropped after mucosal injury and did not recover despite morphologic repair. Rapid epithelial restitution is considered to be a basic defense mechanism of the gastrointestinal mucosa that is obviously not necessarily related to the presence of an acidic environment in the stomach or duodenum.

Animals↗
PubMed1989

Importance of an alkaline microenvironment for rapid restitution of the rabbit duodenal mucosa in vitro.

Rapid epithelial restitution after superficial damage of the gastroduodenal mucosa consists of the migration of remaining intact epithelial cells beneath a necrotic layer of mucus and shed cells. Complete reepithelialization occurs within 60 min (rat stomach) to 7 h (rabbit duodenum) and does not involve cell division. The present study investigated rapid restitution of the acid-damaged rabbit duodenal mucosa in vitro under various conditions. Alkaline flux and transmucosal potential difference were measured simultaneously, and computerized morphometry was performed. Rapid restitution was nearly completed 5 h after damage at neutral luminal pH, but it was retarded when the luminal pH (pHL) was kept at 3. Removal of the necrotic layer did not impair restitution at neutral luminal pH but caused delay at acidic pH (pHL = 3.0). Removal of nutrient bicarbonate slightly delayed restitution at pHL = 7.4 and caused complete inhibition at pHL = 3.0. Alkaline secretion was usually stable but was nearly totally abolished after removal of nutrient bicarbonate. The potential difference decreased after acid damage and showed a tendency to recover in parallel with mucosal restitution. This gradual recovery correlated directly with morphometry. The authors assume that rapid restitution of the duodenal mucosa at an acidic luminal pH depends on the presence of a protective necrotic layer and sufficient alkaline secretion to maintain an optimal environment adjacent to the mucosa. Disturbance of this alkaline microenvironment could be important for the development and healing of duodenal ulcer.

Alkalies↗
PubMed1989

Role of acid base balance and mucosal blood flow in alkaline secretion of rabbit duodenum.

Alkaline secretion of the duodenal mucosa is thought to be an important protective mechanism against luminal acid. This study was designed to investigate the role of acid base balance and mucosal blood flow for duodenal alkaline secretion in an in vivo preparation. Segments of proximal duodenum of anaesthetised New Zealand white rabbits were canulated and perfused in situ. Alkaline secretion (pH-stat method), mucosal blood flow, arterial pO2, pCO2 and HCO-3 were measured. We have found that metabolic alkalosis and glucagon led to a significant increase in alkaline secretion, while metabolic acidosis and vasopressin significantly reduced it. Mucosal blood flow was significantly changed under glucagon and vasopressin.

Acid-Base Equilibrium↗
PubMed1989

Role of passive HCO3(-)-diffusion in duodenal acid-stimulated alkaline secretion.

We investigated acid-stimulated alkaline secretion (AS) under different luminal acid concentrations and its relation to mucosal damage on isolated proximal rabbit duodenal mucosa. Luminal HCl caused an increase of AS depending on their concentration, and it was not specific for acid, but occurs also with luminal ethanol. Histology showed [H+]-dependent mucosal damage ranging from villus tip lesions to deep mucosal injury. Ouabain- and/or anoxia-sensitive (active) AS constituted 80% and 100% respectively of basal AS. After exposure to various luminal acid concentrations passive diffusion (sensitive only to removal of nutrient HCO3-) was solely responsible for the rise in AS. We conclude that in the in vitro rabbit duodenum passive diffusion of HCO3- associated with increasing mucosal damage is the major component of the rise in AS.

Animals↗
PubMed1988

[Repair of the duodenal mucosa following acid damage. A protective mechanism as an approach to new therapeutic principles?].

Epithelial repair after luminal acid exposure was studied in the rabbit duodenum in vivo, HCl (200 mM for 30 min) caused uniform damage of the mucosa confined to the villi, 50% of the total villus height was affected by the acid-induced lesion in the proximal, and 70% in the distal duodenum. After demarcation and detachment of the necrotic tissue the defect was bridged by the remaining viable epithelial cells underneath a layer of mucus and necrotic debris (= necrotic layer). Mucosal repair resulted in a reduction of villus height by 62% in the proximal, and 77% in the distal duodenum. This process of mucosal repair progressed continuously, so that 9 hours after acid damage only 33% of villi in the proximal, and 41% in the distal duodenum were not yet fully restored, irrespective of luminal pH(pHL = 7 or pHL = 3). The difference between proximal and distal duodenum is due to the higher acid susceptibility of the distal duodenum. Rapid epithelial repair of the duodenal mucosa in vivo provides an important protective mechanism against the aggression from luminal acid.

Animals↗
PubMed1988

Acid stimulated alkaline secretion in the rabbit duodenum is passive and correlates with mucosal damage.

Low luminal acid concentrations stimulate alkaline secretion (AS) by the duodenal mucosa. We investigated acid stimulated alkaline secretion by proximal rabbit duodenal mucosa in an Ussing-chamber under different luminal acid concentrations and its relation to mucosal damage. Luminal alkalinisation and potential difference (PD) were measured and mucosal damage was investigated histologically. Luminal acid caused an increase of alkaline secretion over baseline (0.95 +/- 0.19 mu Eq/cm2/10 min; n = 55): 0.1 mmol: 7%, 1 mmol/l: 17%, 5 mmol/l: 22%, 10 mmol/l: 33%, 20 mmol/l: 34%, 50 mmol: 39%, 100 mmol/l: 27%. At acid concentrations of 10 mmol/l and above the PD fell from 2.0 +/- 1.0 mV to zero. Histology showed [H+]-dependent mucosal damage ranging from villus tip lesions to deep mucosal injury. Stimulation of alkaline secretion was not specific for acid. Ethanol (14%) stimulated alkaline secretion by 26%, and 28% ethanol by 40% over baseline. Ouabain and/or anoxia sensitive (active) alkaline secretion constituted 80% and 100% respectively of basal alkaline secretion. After exposure to various luminal acid concentrations passive diffusion (sensitive only to removal of nutrient HCO3-) was solely responsible for the rise in alkaline secretion. Only after 14% ethanol a small rise in ouabain and/or anoxia sensitive HCO3- transport was observed. Under the conditions of this study stimulation of duodenal alkaline secretion is not specific for luminal acid, but occurs also with luminal ethanol; both agents stimulate alkaline secretion depending on their concentration. In this model passive diffusion of HCO3- associated with increasing mucosal damage is the major component of the rise in alkaline secretion.

Animals↗
PubMed1988

[Long-term bougienage treatment of corrosive strictures of the esophagus].

The value of long term bougienage of corrosive esophageal strictures is analysed in 21 patients. 67 bougienages have been performed with a 7.4 percent risk of perforation (5 cases), 4 patients whose symptoms were refractory to bougienage underwent operative therapy. Esophageal cancer developed in 2 patients and was operated in one of them. 70 percent of the 14 patients, who are still in the bougienage program report a good quality of life. We believe bougienage therapy of chronic corrosive esophageal strictures to be the method of choice in patients with high operative risk and satisfying response to the dilatations.

Adolescent↗