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E Wenzl

Publications and source records attributed to E Wenzl.

At least 55 records · Page 3Linked to original sources
PubMed1991

Factors influencing the restitution of the duodenal and colonic mucosa after damage.

Rapid epithelial restitution is an important protective mechanism which enables the gastrointestinal mucosa to reestablish epithelial integrity following superficial injury within hours. In this study we examined the influence of an acidic luminal pH, removal of the necrotic layer, nutrient bicarbonate, calcium and sodium desoxycholate (Na-DOC) on restitution in the rabbit duodenum in vitro and the role of Na-DOC and calcium for rapid restitution of the human colon in vitro. Transmucosal potential difference (PD), short-circuit current (lsc) were measured and resistance against passive ion flux (R) was calculated. Electrophysiological changes paralleled morphological injury but did not necessarily reflect restitution in all experiments. The extent of mucosal injury was assessed by computerized real-time morphometry. 5 hrs after luminal exposure to 10 mH HCl for 10 min residual damage (RD) was 14% in the duodenum. Luminal pH of 3.0 (RD of 30%), removal of necrotic layer at acidic luminal pH (RD of 66%), absence of bicarbonate from the serosal solution (RD of 35% at neutral luminal pH; RD of 96% at acidic luminal pH) and removal of calcium from the serosal solution (RD of 58%) impaired restitution in the duodenum. Continuous postinjury luminal Na-DOC exposure did not influence restitution in the duodenum (RD of 19%). 5 hrs after luminal exposure to 0.5 mM Na-DOC for 10 min RD was 26% in the human colon. Continuous postinjury luminal Na-DOC exposure (RD of 51%) and removal of calcium from the nutrient solution (RD of 65%) impaired restitution in the human colon. Thus we conclude that restitution of the rabbit duodenum in vitro requires a necrotic layer and bicarbonate flux to withstand acidic luminal pH, while restitution is not affected by Na-DOC. In the human colon Na-DOC inhibits restitution. Both the duodenum and colon require calcium for rapid restitution.

Animals↗
PubMed1991

[Effect of postoperative aggregation inhibiting therapy following carotid thrombendarterectomy on patient survival. Analysis after more than 15 years follow-up].

The patients in the clinical series as well as in the group with preoperative known cardiac risk receiving postoperative ASA medication yielded a significant better long-term survival results. ASA prolongs long-term survival after carotid endarterectomy. A postoperative ASA-therapy decreases the incidence of lethal cardiac complications.

Aspirin↗
PubMed1990

[Intracellular pH regulation in human SW-620 colon cancer cells].

Intracellular pH (pHi) regulation is essential for basic functioning of the cell and activation of pHi regulatory mechanisms appears to be involved in the initial stage of cell division. Little is known about pHi regulation in human colonic carcinoma cells. We investigated SW-620 (CCL 227) cells, a cell-line derived from a human colonic adenocarcinoma. pHi changes were recorded by computer-assisted spectrofluorimetric monitoring of the pH-sensitive, fluorescent dye BCECF (2',7'-bis(carboxyethyl)- 5(6)carboxyfluorescein). Resting pHi in HEPES (N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid) buffered solution was 7.53 +/- 0.01. Intracellular acidification after an ammonium prepulse produced a pHi decline of 0.5 units and pHi returned to normal value in NaCl Ringer's. Both 1 mM amiloride and Na-free solution completely inhibited recovery for 8 minutes. This inhibition was reversible in NaCl Ringer's. Na-free solution led to a pHi decrease to 7.39 +/- 0.04 after 16 min, pHi was also lowered by 8 minute incubation of cells with 1 mM amiloride (7.40 +/- 0.02). In HCO3/CO2-buffered solution resting pHi was 7.42 +/- 0.01 (n = 35). Recovery from an acute acid load, induced by NH4 prepulse or switching from HEPES- to bicarbonate-buffered solution, was Na dependent, Cl independent, reversible and only partially blocked by 1 mM amiloride - pHi slowly recovered from 6.83 +/- 0.03 to 7.00 +/- 0.06 in 8 minutes. In the presence of amiloride and 200 microns H2DIDS (dihydro-4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid) pHi recovery was completely inhibited for 8 minutes. In Na-free solution pHi decreased from 7.44 +/- 0.04 to 7.29 +/- 0.03 within 8 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1990

[Blunt pancreatic trauma].

21 blunt pancreatic injuries were reviewed over a 22 year period. Only four of them were admitted directly to the Trauma Center, while the others were referred because of pancreatic complications. Twelve of the patients developed significant pancreatic complications. Sepsis causing death in two cases were attributed directly to the pancreatic injury. The subsequent report examines the question of distal resection with drainage, which was performed eight times and the clinical outcome after an average posttraumatic period of 11.6 years.

Acute Disease↗
PubMed1990

Antiplatelet therapy following carotid bifurcation endarterectomy. Evaluation of a controlled clinical trial. Prognostic significance of histologic plaque examination on behalf of survival.

To determine whether antiplatelet therapy following carotid bifurcation endarterectomy influences postoperative survival and whether signs of progression in the plaques harvested at the time of surgery might be a prognostic indicator, a controlled clinical trial was undertaken. During 1982 to 1985, 66 patients were recruited, operated on (carotid endarterectomy) and assigned, using the method of adaptive randomisation to the therapy group (n = 32) receiving 1.0 g acetylsalicylic acid (ASA) per day, starting day two prior to surgery, or to the control group (n = 34), which remained without antiplatelet medication. The plaques harvested at the time of surgery were processed using standard histopathological methods and examined "blindly" by light microscopy for signs of arterio-sclerotic progression. The final endpoint was patient survival. The last assessment of the participants survival status was done by June 1989. During follow-up, 20 patients died, six in the treatment group and 14 in the untreated group, the difference being statistically significant (P less than 0.013 Breslow, P less than 0.029 Mantel). In 27 instances the histo-pathological examination showed signs of progression. In this subgroup ASA yielded a significant prolongation of patient survival (P less than 0.017 Breslow, P less than 0.048 Mantel). In the remaining patients no signs of cellular infiltration were evident and no influence of ASA on patient survival was demonstrable (P less than 0.503 Breslow, P less than 0.390 Mantel).

Aged↗
PubMed1990

Antiplatelet treatment prolongs survival after carotid bifurcation endarterectomy. Analysis of the clinical series followed by a controlled trial.

To examine the role of antiplatelet drugs in the secondary prevention of arteriosclerotic arterial disease following carotid endarterectomy, a clinical series (n = 252) was analyzed. Based on these results a prospective randomized trial was initiated, comparing the effect of antiplatelet drugs (acetyl-salicylic acid [ASA] 1000 mg/day) versus untreated controls. In both investigations patient survival was the primary end point. A cardiac risk (n = 91) implied a significant reduction in patient survival (p less than 0.019 Breslow, p less than 0.052 Mantel). Antiaggregating drugs prolonged survival in the collective series (p less than 0.0001 Breslow, p less than 0.0002 Mantel) and in the subgroup of patients with cardiac risk (p less than 0.014 Breslow, p less than 0.020 Mantel) as well. In the prospective trial 66 patients were recruited, receiving ASA (n = 32) versus no therapy (n = 34). During follow-up 15 patients died, 4 in the treatment, and 11 in the control group. Between both groups there was a significant difference in the probability of survival (p less than 0.021 Breslow, p less than 0.048 Mantel).

Aspirin↗
PubMed1990

Mechanisms of stress ulceration and implications for treatment.

The incidence of stress ulceration and its complications has decreased over the last decade significantly. The reason for this development is the better understanding of the protective mechanism of stomach and duodenum as well as the prophylactic treatment. This can be achieved by antacids, H2-blockers, and sucralfate, whereas prostaglandins are not effective.

Antacids↗
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

Regulation of intracellular pH in resting and in stimulated parietal cells.

Microspectrofluorimetry of the pH-sensitive, fluorescent dye 2',7'-biscarboxyethyl-5 (6)-carboxyfluorescein (BCECF) was used to measure intracellular pH (pHi) in single parietal cells (PC) of intact rabbit gastric glands during resting and stimulated conditions. In 61% of PC, histamine plus isobutylmethylxanthine (IBMX) (both 100 microM) caused a small increase in pHi, ranging from 0.04 to 0.21 pH units (average delta pHi = 0.09 +/- 0.04 units over a 6-min period). In the other 39% of PC, pHi remained constant or decreased slightly (maximum decrease was 0.10 unit). The specific inhibitors omeprazole (50 microM, blocks H+- K+-ATPase), 4,4'-diisothiocyanodihydrostilbene-2,2'-disulfonic acid (H2DIDS; 100-200 microM, blocks Cl-HCO3 exchange) and amiloride (1 mM, blocks Na-H exchange) were added to both resting and stimulated PC. In stimulated PC, omeprazole caused pHi to decrease by 0.08 unit, but this inhibitor had no effect on pHi of resting PC. H2DIDS caused pHi to increase in stimulated PC five times faster compared with resting PC. Amiloride or Na-free solution (which should reverse the Na-H exchanger and cause cellular acidification) caused pHi to decrease 2.5 or 5 times, respectively, more slowly in stimulated PC compared with resting PC. Also, recovery from NH4-induced acidification (due primarily to Na-H exchange) was 1.8 times faster (measured at pHi 6.7) in resting vs. in stimulated PC. During histamine plus IBMX-induced stimulation, increased H secretion by the H+-K+-ATPase at the apical membrane is accompanied by an increase in activity of the Cl-HCO3 exchanger at the serosal membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1989

Intracellular pH regulation in IEC-6 cells, a cryptlike intestinal cell line.

Regulation of intracellular pH, pHi, was studied using microspectrofluorimetry of the pH-sensitive, fluorescent dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein in the rat intestinal crypt cell line, IEC-6. In N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-buffered solutions with pHi 7.25, treatment with a pulse of NH4Cl caused cells to acidify and then recover to control level. Because recovery was Na dependent, blocked by 1 mM amiloride, and unaffected by the presence and absence of Cl, it was likely because of a Na+-H+ exchanger. Cells were also acid loaded by changing from HEPES to HCO3-CO2-buffered solutions. pHi again recovered, but 1 mM amiloride reduced the rate of H+ efflux by only 47%. This HCO3-dependent, amiloride-insensitive H efflux required Na+ but not Cl- and was completely blocked by 200 microM [H2] 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). We conclude that a Na+-HCO3- cotransporter was operative. Cl-free solutions caused pHi to increase from 7.19 to 7.41; this effect required the presence of exogenous HCO3-CO2 but not Na and was blocked by 200 microM [H2]DIDS. A Cl- -HCO3- exchanger is the most likely explanation for these data. All the pHi regulatory mechanisms are operative in NaCl-HCO3-CO2-buffered solutions. The Na+-H+ and Na+-HCO3- mechanisms are acid extruders, whereas the Cl- -HCO3- exchanger is an acid loader. These transporters may be important for generating HCO3 secretion by intestinal crypt cells.

Acids↗
PubMed1989

Intracellular pH dependence of buffer capacity and anion exchange in the parietal cell.

When parietal cells (PC) are stimulated with histamine, the anion exchanger rate increases three to five times to compensate for alkaline loading induced by H+-K+ adenosinetriphosphatase (ATPase) and to provide Cl for acid secretion. It has been hypothesized that this increased activity is caused by the increase in intracellular pH (pHi) that often occurs in stimulated PC (from 7.1 to a maximum of 7.3). The dependence of the anion exchanger on pHi was studied using microspectrofluorimetry of the pH-sensitive dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-buffered solutions were used because the anion exchanger can transport OH- (or HCO3) in exchange for Cl- even with [HCO3]o = 200 microM. It was found that when solutions were changed either from NaCl to Cl- free or Cl- free to NaCl, rates of change of pHi (delta pH/delta t) were strongly dependent on pHi: nearly 0 at pHi 6.6 and 1.25 pH/min at pHi 8.0. To convert these pHi changes into anion flux rates, the intrinsic buffer capacity (beta i) was determined over the same pHi range by making small changes of [NH4]o to determine the resulting changes of [NH4]i and pHi (i.e., beta i = delta[NH4]i/delta pHi) in PC that had been pretreated with 1 mM amiloride and 200 microM [H2]4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) [to block Na+-H+ and Cl- -OH-(HCO3-) exchange]. beta i was also strongly dependent on pHi: at pHi 6.5 beta i = 48 mM/pH, and this decreased as pHi increased; at pHi 7.75 beta i = 8 mM/pH. The derived anion fluxes (i.e., JOH = beta i x delta pH/delta t) were roughly linearly related to pHi between 6.6 (JOH near 0) and 8.1 (JOH = 13 mM/min). Between pHi 7.1 and 7.3, the range normally observed during stimulation of PC, rates of anion exchange increased by 75%. This pHi sensitivity cannot explain the 300-500% increase in anion exchanger activity observed during secretagogue stimulation of PC.

Animals↗
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

[What does after care in colorectal cancer accomplish? A prospective study over an 8-year period].

Results of a computer supported follow-up-program on patients with colorectal cancer are demonstrated. Between 1978 and 1985 1024 patients underwent these program, the drop-out-rate was 18%. 231 recurrences in 137 patients were discovered (40% local recurrence, 30% liver metastases and 30% others). 54% of patients with local recurrence and 43% with liver metastases were without symptoms. Radical surgery could be performed in 47% of local recurrences and in 31% of liver metastases. The 3 years survival rate after radical surgery for recurrence was 28% for local recurrences and 31% for liver metastases.

Colonic Neoplasms↗
PubMed1988

Influence of postoperative anticoagulant treatment on patient survival after femoropopliteal vein bypass surgery.

To examine whether anticoagulants given after autologous saphenous bypass surgery influenced patient survival 119 patients who received such a graft for obliterative arterial disease were recruited for a controlled clinical trial. Patients were randomly assigned to start, in the second postoperative week, phenprocoumon (60 patients) or no treatment (59 patients). The median duration of survival for all patients was greater than 60 months, and the 75%-quartile was 39.0 (SE of the median 3.9) months. 10 patients died in the treated group and 20 in the control group. The treated group had a greater probability of survival (p less than 0.023, Breslow; p less than 0.043, Mantel). Graft occlusions occurred in 11 patients in the treatment group and in 17 controls. When these patients were excluded from the analysis, the difference in probability of survival between the two groups remained significant (p less than 0.009, Breslow; p less than 0.013, Mantel).

Aged↗