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M Ritter

Publications and source records attributed to M Ritter.

At least 163 records · Page 9Linked to original sources
PubMed1992

Omeprazole-induced pseudohypertrophy of gastric parietal cells.

Paraffin-embedded and haematoxylin-eosin-stained sections of biopsy material obtained from patients taking omeprazole reveal a characteristic "hypertrophy" of the parietal cells; these are taller than the chief cells, and project, with convexly bulging apical cell membrane, into the lumen of the body glands, producing a serrated internal gland profile. We have found this phenomenon in 92.9% of 198 patients with non-operated stomachs. After Billroth I or II resection, this phenomenon was found in the body mucosa of the stomach remnant in only 35.3% of the cases (n = 17). The specificity of the diagnosis "hypertrophy" of the parietal cells under omeprazole therapy was 89.4%, the sensitivity 91.0%. A comparative morphometric analysis in forceps biopsy material investigated after paraffin and epoxide embedding, showed that this "hypertrophy" was a pseudohypertrophy. Apparently, as a result of an increase in intracytoplasmic secretory canaliculi, the gastrin-stimulated parietal cell shrinks less than the non-stimulated parietal cell. This pseudohypertrophy of the parietal cells can readily be used to monitor the compliance of the patient prescribed omeprazole. A question that has yet to be clarified is how quickly pseudohypertrophy develops, and how long it takes to regress after discontinuation of omeprazole. The phenomenon can also be seen in active autoimmune gastritis with no atrophy of the gland, since the parietal cell antibody also binds selectively to the proton pump of the parietal cell.

Cell Membrane↗
PubMed1991

Prevention of high-altitude pulmonary edema by nifedipine.

BACKGROUND: Exaggerated pulmonary-artery pressure due to hypoxic vasoconstriction is considered an important pathogenetic factor in high-altitude pulmonary edema. We previously found that nifedipine lowered pulmonary-artery pressure and improved exercise performance, gas exchange, and the radiographic manifestations of disease in patients with high-altitude pulmonary edema. We therefore hypothesized that the prophylactic administration of nifedipine would prevent its recurrence. METHODS: Twenty-one mountaineers (1 woman and 20 men) with a history of radiographically documented high-altitude pulmonary edema were randomly assigned to receive either 20 mg of a slow-release preparation of nifedipine (n = 10) or placebo (n = 11) every 8 hours while ascending rapidly (within 22 hours) from a low altitude to 4559 m and during the following three days at this altitude. Both the subjects and the investigators were blinded to the assigned treatment. The diagnosis of pulmonary edema was based on chest radiography. Pulmonary-artery pressure was measured by Doppler echocardiography and the difference between alveolar and arterial oxygen pressure was measured in simultaneously sampled arterial blood and end-expiratory air. RESULTS: Seven of the 11 subjects who received placebo but only 1 of the 10 subjects who received nifedipine had pulmonary edema at 4559 m (P = 0.01). As compared with the subjects who received placebo, those who received nifedipine had a significantly lower mean (+/- SD) systolic pulmonary-artery pressure (41 +/- 8 vs. 53 +/- 16 mm Hg, P = 0.01), alveolar-arterial pressure gradient (6.6 +/- 3.8 vs. 11.8 +/- 4.4 mm Hg, P less than 0.001), and symptom score of acute mountain sickness (2.0 +/- 0.7 vs. 3.9 +/- 1.9, P less than 0.01) at 4559 m. CONCLUSIONS: The prophylactic administration of nifedipine is effective in lowering pulmonary-artery pressure and preventing high-altitude pulmonary edema in susceptible subjects. These findings support the concept that high pulmonary-artery pressure has an important role in the development of high-altitude pulmonary edema.

Adult↗
PubMed1991

Cellular mechanisms of bradykinin-induced hyperpolarization in renal epitheloid MDCK-cells.

Previous studies have demonstrated that bradykinin hyperpolarizes the cell membrane of subconfluent MDCK cells by increase of the potassium conductance. The present study has been performed to elucidate the intracellular mechanisms involved. To this end, the effects of bradykinin on the potential difference across the cell membrane (PD), on formation of inositol phosphates, and on intracellular calcium concentration (Cai) have been analyzed in cells without or with pretreatment with pertussis toxin or 12-O-tetradecanoylphorbol 13-acetate diester (TPA). In untreated cells, bradykinin leads to a transient increase of inositol 1,4,5-trisphosphate and inositol 1,3,4,5-tetrakisphosphate, increase of Cai, activation of potassium channels and hyperpolarization of the cell membrane. The effects of bradykinin on PD and Cai are still present in the absence of extracellular calcium. In cells pretreated with pertussis toxin the effect of bradykinin on inositol trisphosphate formation is almost abolished but bradykinin still leads to a transient increase of Cai and PD in the presence and absence of extracellular calcium. In cells pretreated with TPA the bradykinin-induced increase of inositol trisphosphate formation is blunted, the bradykinin-induced increase of Cai abolished, but the bradykinin-induced hyperpolarization still present. The observations indicate that bradykinin increases Cai in part by phorbol ester and pertussis toxin sensitive activation of phospholipase C. In addition, bradykinin is capable of enhancing Cai by utilizing pertussis toxin insensitive mechanisms. Furthermore, bradykinin is able to transiently enhance the potassium conductance without a general increase of intracellular calcium.

Animals↗
PubMed1991

Activation of cell membrane potassium conductance by mercury in cultured renal epithelioid (MDCK) cells.

To elucidate mechanisms of mercury toxicity, the cell membrane potential has been determined continuously in cultured kidney (MDCK)-cells during reversible application of mercury ions to extracellular perfusate. Exposure of the cells to 1 microM mercury ions is followed by rapid, sustained, and slowly reversible hyperpolarization of the cell membrane, increase of cell membrane potassium selectivity, and decrease of cell membrane resistance. Thus, mercury ions enhance the potassium conductance of the cell membrane. Half maximal hyperpolarizing effect is elicited by approximately 0.2 microM. Higher concentrations of mercury ions (greater than 10 microM) eventually depolarize the cell membrane. At extracellular calcium activity reduced to less than 0.1 microM, 1 microM mercury ions still leads to a sustained hyperpolarization and increase of potassium selectivity of the cell membrane. As evident from fluorescence measurements, 10 microM, but not 1 microM mercury ions leads to a rapid increase of intracellular calcium activity. Pretreatment of the cells with either pertussis toxin or cholera toxin does not blunt the hyperpolarizing effect of mercury ions. In conclusion, mercury ions activate the potassium conductance by a mechanism independent of increase of intracellular calcium activity and of cholera toxin- or pertussis toxin-sensitive G-proteins. This activation of potassium conductance may account for early effects of mercury intoxication, such as kaliuresis.

Animals↗
PubMed1991

Further characterization of volume regulatory decrease in cultured renal epitheloid (MDCK) cells.

In Madin Darby canine kidney (MDCK) cells volume regulatory decrease (VRD) is paralleled by a variable, transient hyperpolarization followed by a sustained depolarization of the cell membrane. In the depolarized cells, the cell membrane selectivity is decreased for potassium and increased for chloride. Without knowledge of the cell membrane resistance (Rm), these changes of cell membrane selectivity cannot be translated into conductances, i.e. the observed alterations of ion selectivity could have been due to inhibition of potassium conductance or activation of anion conductance. In the present study Rm has been determined by cellular cable analysis. To this end, three microelectrodes were impaled into three different cells of a cell cluster, current (up to 3 nA) was injected into one cell and the corresponding voltage deflections determined in the other two cells. As a result, exposure of the cells to hypotonic perfusates leads to a marked, sustained reduction of Rm. In the absence of chloride and in the absence of bicarbonate and chloride, the decrease of Rm is only transient. The data indicate that cell swelling leads to a transient increase of potassium conductance followed by a sustained increase of anion conductance. As evident from BCECF fluorescence, exposure of MDCK cells to hypotonic perfusates leads to a significant decrease of intracellular pH, which may in part be due to loss of bicarbonate through the anion conductive pathway.

Animals↗
PubMed1991

Regulation of potassium conductance by prostaglandins in cultured renal epitheloid (Madin-Darby canine kidney) cells.

Madin-Darby canine kidney (MDCK) cells form arachidonic acid metabolites following stimulation of several hormones known to modify the ion conductances at the plasma membrane. The present study has been performed to elucidate the influence of arachidonic acid on the electrical properties of subconfluent MDCK cells. As a result, arachidonic acid (1 or 10 mumol/l) leads to a transient hyperpolarization of the cell membrane, followed by a transient depolarization and a second, sustained hyperpolarization. The effects are inhibited by cycloxygenase inhibitor indomethacin (1 mumol/l). The initial transient hyperpolarization is mimicked by prostaglandin E2 (PGE2, 0.1 mumol/l), the sustained hyperpolarization by both PGE2 (0.1 mumol/l) and PGF2 alpha (0.1 mumol/l). The transient hyperpolarization is paralleled by an increase of potassium selectivity and a decrease of cell membrane resistance and is thus the result of increased potassium conductance. The transient depolarization is paralleled by an increase of chloride selectivity, reflecting an increase of chloride conductance. The sustained hyperpolarization is paralleled by an increase of cell membrane resistance, and increase of potassium selectivity and a decrease of chloride selectivity, and is thus the result of decreasing chloride conductance. The observations reveal a role of prostaglandins in the regulation of ion conductances in MDCK cells, which could well participate in the transport regulation by hormones.

Animals↗
PubMed1991

Hepatorenal reflex regulating kidney function.

In anesthetized male rats, infusion of glutamine (2 mumol/min) into the superior mesenteric vein at a rate known to induce liver cell swelling leads to marked decreases in renal glomerular filtration rate, renal para-aminohippurate clearance and urinary flow rate. Glutamine infused at identical rates into the jugular vein does not elicit any of these effects. The effect of glutamine is mimicked by serine but not by glutamate. Spinal transection, renal denervation or section of the vagal hepatic nerves abolishes the effect of mesenteric venous glutamine infusion. Mesenteric application of glucagon (1 ng/min) or of both glutamine and glucagon enhances glomerular filtration rate and urinary flow rate. Infusion of 1 ng/min glucagon through the jugular vein does not significantly alter glomerular filtration rate or urinary flow rate. The data disclose a powerful liver-borne mechanism regulating kidney function that is mediated by the hepatorenal innervation.

Animals↗
PubMed1991

Coronary reserve in patients with aortic valve disease before and after successful aortic valve replacement.

In patients with aortic valve disease and normal coronary angiograms coronary reserve was determined by the coronary sinus thermodilution technique. Three groups of patients were studied: 37 preoperative patients; 18 different patients 12-52 months after aortic valve replacement and seven control subjects with no cardiac disease. Coronary flow ratio (dipyridamole/rest) was diminished in preoperative compared with postoperative patients (1.66 +/- 0.44 vs 2.22 +/- 0.85; P less than 0.05) as well as with controls (2.80 +/- 0.84; P less than 0.01), and corresponding coronary resistance ratio (dipyridamole/rest) was higher in preoperative patients than in both other groups (0.61 +/- 0.17 vs 0.48 +/- 0.14; P less than 0.05 vs 0.37 +/- 0.10; P less than 0.01). Differences in the flow ratio, but not in the resistance ratio, were significant (P less than 0.05) in patients after aortic valve replacement compared with controls. Total coronary sinus blood flow at rest was elevated in preoperative compared with both postoperative patients and controls (252 +/- 99 vs 169 +/- 63; P less than 0.01; vs 170 +/- 35 ml.min-1, P less than 0.05), whereas flows after maximal vasodilation did not differ among the three groups (416 +/- 184 vs 361 +/- 150 vs 488 +/- 235 ml.min-1). Postoperative patients showed a distinct, though not total regression of left ventricular angiographic muscle mass index and wall thickness. Nine of the 18 postoperative patients showed a normal coronary flow reserve and nine showed subnormal response. These two subgroups did not differ with respect to preoperative macroscopic and microscopic measures of hypertrophy. Thus in aortic valve disease, the reduced coronary vasodilator capacity is mainly due to an elevated coronary flow at rest, while the maximal coronary blood flow achieved is identical to that of postoperative patients and controls. With regression of left ventricular hypertrophy, flow at rest decreases and this leads to a distinct improvement of coronary flow reserve.

Aged↗
PubMed1991

Impaired balance of interleukin-4 and interferon-gamma production in infections with Schistosoma mansoni and intestinal nematodes.

In chronic infection with Schistosoma mansoni, IL-4 and IFN-gamma are co-modulated in opposite directions. This was shown when testing sera and cell culture supernatants from 31 Brazilian patients with schistosomiasis before, and three months after treatment with praziquantel. Thorough examinations were undertaken to account for polyparasitism with intestinal nematode infections involving tissue migrating larval stages that may induce analogous changes. Controls free of S. mansoni included a group (n = 17) matching the schistosomiasis patients' parasitation by intestinal nematodes and a group (n = 16) free of helminths other than T. trichiura. Serum IL-4 was greater than 20 pg/ml in 81% of schistosomiasis patients but in only 35 and 25%, respectively, of controls with and without intestinal nematodes. IL-4 data correlated inversely with the mitogen-induced IFN-gamma synthesis. Generation of IL-4 in response to phorbol esters was related to the intensity of infection by schistosomes and intestinal nematodes. The parasitological status three months after therapy with either praziquantel or mebendazole revealed a dichotomy: whereas the ratio of IFN-gamma to IL-4 generated in vitro was identical in uninfected controls and in patients who cleared the parasites, failure to eliminate the parasites was associated with lower IFN-gamma/IL-4 ratios generated in vitro.

Female↗
PubMed1991

Effect of bradykinin, ATP and adrenaline on cell membrane resistances of Madin-Darby canine kidney cells.

1. Previous studies have shown that bradykinin, ATP and adrenaline hyperpolarize the cell membrane of Madin-Darby canine kidney (MDCK) cells by activation of calcium-sensitive K+ channels. The present study has been performed to determine the effect of these hormones on the resistance of the cell membrane and the cellular coupling. To this end, cellular cable analysis has been performed. 2. As a result, all three hormones lead to the expected, marked decrease of cell membrane resistance. 3. However, the bradykinin-induced reduction of cell membrane resistance was sustained, contrasting with only transient hyperpolarization induced by bradykinin and only transient activation of the K+ channels. Thus, the cable analysis reveals the sustained activation of an additional conductance. 4. ATP, but not the other two hormones, leads to a delayed increase of the intercellular coupling resistances. 5. Prolonged exposure of the cells to adrenaline leads to oscillations of the cell membrane potential, apparently by oscillatory activation of the K+ channels.

Adenosine Triphosphate↗
PubMed1991

Inhibition of ion conductances by osmotic shrinkage of Madin-Darby canine kidney cells.

Osmotic swelling of Madin-Darby canine kidney (MDCK) cells enhances the ion conductances of the cell membrane, which allows release of cellular ions and subsequent regulatory cell volume decrease. The present study has been performed to test whether cell shrinkage similarly affects the ion conductances of MDCK cell membranes. Increase of extracellular osmolarity by addition of 50 mM NaCl or 100 mM mannitol leads within 3 min to a hyperpolarization of the cell membrane, a marked increase of cell membrane resistance [by 223 +/- 38% (n = 8) and 228 +/- 21% (n = 5), respectively], as well as a moderate increase of the K+ selectivity of the cell membrane (by 37 +/- 13%, n = 9). Thus exposure to hypertonic extracellular fluid decreases the cell membrane conductances including the K+ conductance. Cell volume measurements reveal a regulatory cell volume increase, which is sensitive to both furosemide and dimethylamiloride. Extracellular ATP (10 microM), which activates calcium-sensitive K+ channels, hyperpolarizes the cell membrane close to the K+ equilibrium potential. The respective values are -69.9 +/- 3.1 mV (n = 9) in isotonic fluid, -79.4 +/- 1.8 mV (n = 9) within 3 min, and -76.4 +/- 1.8 mV (n = 7) within 16-h exposure to hypertonic extracellular fluid. This observation points to a sustained increase of intracellular K+ activity after exposure to hypertonic extracellular fluid.

Adenosine Triphosphate↗
PubMed1991

Progesterone inhibits K conductance in plasma membrane of cultured renal epitheloid MDCK cells.

Progesterone causes natriuresis, an effect largely attributed to displacement of aldosterone from its receptor. The present study, however, demonstrates that progesterone (0.1, 1, and 10 mumol/1, respectively) also causes a rapid, fully reversible depolarization of Madin-Darby canine kidney (MDCK) cells (by 1.3 +/- 0.5, 4.1 +/- 0.7 and 12.3 +/- 1.5 mV, respectively). 17 alpha-Hydroxyprogesterone and dihydroxytestosterone are, by two orders of magnitude, less effective, whereas cholesterol, aldosterone, hydrocortisone, and estradiol (each up to 10 mumol/l) did not significantly alter the potential difference across the cell membrane. The effect of progesterone is blunted by antiprogestogen RU 486 (5 mumol/l). The progesterone-induced depolarization is paralleled by a decrease of potassium selectivity and an increase of cell membrane resistance and is abolished in the presence of the potassium channel blocker barium (10 mmol/l), as well as in the presence of 40 mmol/l potassium in the extracellular fluid. Neither removal of extracellular chloride or bicarbonate nor amiloride, ouabain, or pretreatment with pertussis toxin abolish the depolarizing effect of 5 mumol/l progesterone. In conclusion, acute administration of progesterone depolarizes MDCK cells by decreasing the potassium conductance of the cell membrane.

Animals↗
PubMed1991

Influence of mercury ions on electrical properties of rat proximal and distal renal tubules.

The present study was designed to elucidate the acute effects of mercury ions on electrogenic transport systems in rat proximal and distal convoluted tubules. Male Munich Wistar rats were anesthetized with Inactin and prepared for micropuncture in the usual way. Under control conditions, the transepithelial potential difference (PDte) approaches -3.2 +/- 0.6 mV in early proximal tubules, +2.1 +/- 0.3 mV in late proximal tubules, and -17.8 +/- 1.8 mV in distal convoluted tubules. PDte of neither early nor late proximal tubules was significantly affected by the acute application of mercury ions. In the distal tubules, mercury ions (10 mumol/l) lead to a gradual depolarization of the epithelium from -17.8 +/- 1.8 to -9.3 +/- 2.7 mV within 8 min. A linear correlation between PDte under control conditions and depolarization caused by amiloride is seen. The slope of this correlation is significantly reduced during the application of mercury ions. In conclusion, mercury ions decrease the distal PDte an effect possibly contributing to altered renal electrolyte excretion following the acute administration of mercury ions. The depolarization is, at least in part, due to an inhibition of amiloride-sensitive sodium channels at the luminal cell membrane of principal cells.

Amiloride↗
PubMed1991

[Collagenous duodenitis and ileitis in a patient with collagenous colitis].

Collagenous colitis is a disease accompanied by chronic watery diarrhea, of which the etiology is unknown. Sporadic cases of collagen deposits in the upper gastrointestinal tract are meanwhile reported. We here report the case of a 53-year-old female patient suffering from collagenous colitis with additional collagen deposits in the duodenum and ileum. The favourable effect of a therapeutical trial with bismuth nitrate is described.

Basement Membrane↗
PubMed1990

[Quantitative Doppler echocardiography in the evaluation of heart diseases].

Doppler ultrasound is an established noninvasive method in cardiology. The most important indications are: 1. stenosis/insufficiencies of atrioventricular/semilunar valves, 2. dysfunction of artificial valves, 3. atrial and ventricular septal defects, 4. intraventricular pressure gradients, e.g. in hypertensive cardiomyopathy, 5. determination of the systolic pulmonary artery pressure. Color Doppler and pulsed wave Doppler as mainly used for quantitative and semiquantitative-, continuous wave Doppler mainly for quantitative analyses. Doppler it can be obtained qualitative and semiquantitative, from continuous wave Doppler quantitative information about the velocity of blood flow.

Cardiomyopathies↗
PubMed1990

[The quality of life following esophagectomy. The results of a psychosocial study of 80 cancer patients].

Of 235 patients who, between 1982 and 1988, had undergone an oesophagectomy for cancer of the oesophagus, 80 (64 men, 16 women; mean age 54.6 [39-67] years) were re-assessed for the quality of their life since surgery. Three standardized questionnaires were used ("general physical complaints" [PC], "satisfaction with life" [SL], "psychosocial stress" [PS]), plus data from a representative random group of the normal population (n = 1761; PC), a group of 48 healthy persons (SL) and a group of 788 cancer patients (PS) with different types of malignancy. The point score for PC was, as expected, significantly higher for the patients than the random controls (23.5 vs. 14.3; P less than 0.001), but was lower than that of cardiac (30.2) and psychiatric patients (30.0; P less than 0.001). As for quality of life, the postesophagectomy patients scored 68.17, compared with 56.75 (P less than 0.001) for the healthy controls. The main psychosocial stress was less in the areas of anxiety and depression than in a loss of social activity and impairment of physical capacity.

Esophageal Neoplasms↗
PubMed1990

Utilization of preventive services by pregnant women in Jerusalem--a cross sectional study.

A study was made of health service utilization patterns during pregnancy of 279 young mothers, a representative sample of the Jewish population in Jerusalem. Only 47% reported that they used the municipal family health centers (FHCs) for prenatal care. Some 82% reported that they had resorted to more than one source of care during pregnancy. Sources other than the FHC were: regular Sick Fund doctor service (33%); private practitioners (25%); hospital-based services (25%). Among the FHC users, there was an unexpectedly high percentage of women of Asian-African origin and of those living in remote neighborhoods. Under-utilization was frequent among wealthy women, those with higher education and members of the Orthodox religious sector. While there was general satisfaction with the service, lower gratification was associated with higher utilization. This phenomenon may intimate that there may be a process of negative selection among women who use the service, when other alternatives are not readily available.

Adult↗