PubMed Health⌕ Search

Biomedical subjects

U M Farack

Publications and source records attributed to U M Farack.

18 recordsLinked to original sources
PubMed2000

Effect of loperamide on mucosal guanylyl cyclase activity in rat jejunum following Escherichia coli heat-stable toxin-induced fluid accumulation.

Loperamide has antidiarrhoeal activities against secretagogues with different mechanisms of action. Besides its opioid-like effect on intestinal motility and secretion it might exhibit additional antisecretory properties which may not be completely elucidated yet. Direct effects of loperamide on mucosal guanylyl cyclase have never been observed. We therefore investigated the effect of loperamide on intestinal fluid transport altered by heat-stable Escherichia coli enterotoxin which acts by stimulating mucosal guanylyl cyclase. Net fluid movement was determined during a 1 hr incubation period in ligated jejunal loops of anaesthetised female Wistar rats. Transport rates of net fluid movement were calculated from the loop contents measured gravimetrically at the beginning and the end of the experiments. Addition of heat-stable Escherichia coli enterotoxin to the luminal solution resulted in a net secretion of water which was significantly reversed into net absorption by loperamide. The specific activity of the particulate guanylyl cyclase was determined in mucosal scrapings of the jejunum without and with the addition of heat-stable Escherichia coli enterotoxin and/or loperamide. Additions of loperamide of up to 10 micromol/l did not change guanylyl cyclase activity. We conclude that the effect of loperamide counteracting heat-stable Escherichia coli enterotoxin induced changes of intestinal fluid transport does not involve a direct effect on guanylyl cyclase.

Animals↗
PubMed1989

Inhibition by loperamide of mucus secretion in the rat colon in vivo.

The effect of loperamide on mucus secretion and the net transport of fluid, sodium and potassium was investigated in the perfused rat colon in vivo. Prostaglandin E2 (PGE2, 1 mg/kg per h intraarterially) and deoxycholic acid (2 mM intraluminally) were used as secretagogues. Mucus secretion was determined as the total amount of protein-bound hexose in the effluent. Under basal conditions, loperamide (6 mg/kg subcutaneously) slightly decreased mucus secretion and increased the absorption of fluid and sodium. PGE2 and deoxycholic acid stimulated mucus secretion about 4- and 9-fold, respectively. Loperamide abolished the mucus secretory response to PGE2 and reduced the response to deoxycholic acid by 50%. It also reduced the fluid secretion following PGE2 but did not affect the diminished fluid absorption following deoxycholic acid. Potassium secretion was not significantly influenced by loperamide and therefore was independent of the secretion of mucus. The data suggest that loperamide is a potent inhibitor of colonic mucus secretion, a property that possibly contributes to the antidiarrheal effect of this opiate analogue.

Animals↗
PubMed1988

Discrepancy between effects of cholera toxin on net fluid movement and cAMP levels in rat jejunum, ileum, and colon.

Regional differences in the response to cholera toxin were evaluated in rat jejunum, ileum, and colon in vivo. Ligated intestinal loops were exposed to a supramaximal concentration of cholera toxin for 5 hr, and net fluid transport, adenosine 3',5'-monophosphate (cAMP) concentrations, and adenylate cyclase and phosphodiesterase activities of mucosal homogenates were determined. The fluid transport response and the specific activities of adenylate cyclase (with and without cholera toxin) and phosphodiesterase declined progressively from the jejunum to the colon. In contrast, cAMP concentrations (with and without cholera toxin) were lowest in the jejunum and highest in the colon. These results demonstrate that cAMP concentrations of the total mucosal homogenate do not parallel cholera toxin-induced fluid secretion in the three intestinal segments. Rather, the activities of adenylate cyclase and phosphodiesterase suggest a relation between fluid secretion and the turnover of cAMP.

Adenylyl Cyclases↗
PubMed1987

Influence of vasoactive intestinal peptide, secretin, and Ala4, Val5-secretin on the net movements of electrolytes, fluid, and mucus in the rat colon in vivo.

The effect of vasoactive intestinal peptide (VIP), secretin, and VIP-secretin (Ala4, Val5-secretin) on the net movements of sodium, potassium, fluid, and mucus was investigated in the rat colon perfused in vivo. Peptides (1-100 micrograms/kg.h) were infused intra-arterially. VIP influenced electrolyte and fluid movements at a threshold dose 10- to 100-fold lower than secretin, whereas the secretory efficacy was not significantly different. Replacing the NH2-terminal hexapeptide of secretin by that of VIP did not markedly alter the effect of secretin. Mucus output was stimulated weakly by all three peptides. The results indicate that the larger colonic secretory activity of VIP as compared to secretin is not primarily due to the difference in their NH2-terminal sequence but probably requires the intact molecule.

Animals↗
PubMed1987

Hepatobiliary fibropolycystic diseases. Two cases of Caroli's disease.

Two case reports of Caroli's disease type I are given. The main clinical features were recurrent severe cholangitis, biliary colics, and persistent cholestasis. Both cases demonstrate the predominance in males and the prevalence of symptoms in adults up to the sixth decade. No features of congenital hepatic fibrosis or biliary cirrhosis and no renal pathomorphological changes could be detected. Investigations of their family members did not reveal genetic aspects.

Bile Duct Diseases↗
PubMed1985

The influence of bisacodyl and deacetylbisacodyl on mucus secretion, mucus synthesis and electrolyte movements in the rat colon in vivo.

The effect of the diphenolic laxatives bisacodyl and deacetylbisacodyl on mucus secretion and fluid, sodium and potassium net transport was studied in rat colon perfused in vivo. Mucus output in the effluent was determined as total protein-bound hexose. Deacetylbisacodyl was more potent than the parent compound and was used to investigate dose-response relationships. At a low concentration (0.1 mg/dl), mucus and potassium secretion were stimulated whereas sodium and fluid absorption were inhibited, or converted to secretion, only at higher concentrations (0.5-3.0 mg/dl). All effects were dose-dependent and reversible within 1 h. With longer lasting perfusion of deacetylbisacodyl, mucus appeared in two peaks, one initial peak and another after 4 h. The late peak contained newly synthetized glycoproteins as indicated by the incorporation of intravenously injected [14C]galactose. It is concluded that stimulation of mucus secretion and synthesis contributes to the laxative action of bisacodyl. The effects of low versus high concentrations suggests that part of the potassium secretion is due to mucus release.

Animals↗
PubMed1985

[Rhino-cranial mucormycosis in acute leukemia].

The diagnosis of acute lymphatic non-T-non-B leukaemia of common ALL type was confirmed in a 22-year-old woman. Cytostatic treatment brought full remission for 21/2 years. Renewed cytostatic treatment for recurrence brought about a mucormycosis in the mid-face region during a period of protracted agranulocytosis, despite antibiotic prophylaxis with ketoconazole and cotrimoxazole. The causative mucor organism was demonstrated in smears and biopsy material. The infection was successfully treated with i.v. amphotericin B and débridement of the affected tissue. There remained large tissue defects in the region of gum, nose, upper lip and right oral cavity. Previously the mortality rate of mucormycosis in the course of leukaemia was 100%.

Adult↗
PubMed1985

Treatment of HBsAg-,HBeAg-positive chronic active hepatitis with adenine arabinoside. A case report with clinical remission and seroconversion to anti-HBs.

A 26-year-old patient developed HBsAg-, HBeAg-positive chronic active hepatitis arising from an acute infection 6 months earlier. Treatment with adenine arabinoside (Ara-A), 15 mg/kg/day administered as overnight infusions for three weeks, resulted in clinical and complete biochemical remission with normalisation of aminotransferases, loss of HBsAg, HBeAg and DNA polymerase, and appearance of Anti-HBs during follow-up for 9 months. Treatment of chronic hepatitis B infection using Ara-A for several weeks may be especially effective when initiated early in the course of the disease.

Adult↗
PubMed1984

Inhibition by loperamide of deoxycholic acid induced intestinal secretion.

The effect of loperamide on deoxycholic acid (DOC)-induced secretion was studied in ligated loops of the rat jejunum and colon in vivo. In controls, loperamide slightly augmented fluid absorption. 3 mmol DOC caused net fluid secretion. Loperamide reduced this secretion in the colon and reversed it to absorption in the jejunum. Na-K-ATPase specific activity and cAMP levels were measured in the jejunum, and [14C]erythritol clearance as an index of mucosal permeability in the colon. In the jejunum this opiate analogue affected neither basal or DOC-depressed Na-K-ATPase, nor mucosal cAMP. In the colon it reduced a large increase of the erythritol clearance caused by DOC. It is suggested that loperamide interferes with DOC-induced intestinal secretion in part by lowering mucosal permeability.

Animals↗
PubMed1984

Mechanism of action of diphenolic laxatives: the role of adenylate cyclase and mucosal permeability.

Net fluid movement and mucosal 14C-erythritol clearance were measured in ligated colonic loops of the rat in vivo. The diphenolic laxatives, oxyphenisatin and bisacodyl, dose-dependently inhibited net fluid absorption or caused secretion, both increased the 14C-erythritol clearance. Pretreatment with the adenylate cyclase inhibitor, RMI 12 330 A, did not change these results. It is concluded that diphenolic laxatives mainly influence intestinal fluid transport not by stimulation of mucosal adenylate cyclase but rather by augmenting epithelial permeability.

Adenylyl Cyclase Inhibitors↗
PubMed1983

Differentiation of secretagogue drugs by chlorpromazine in rat intestine in vivo.

The effect of chlorpromazine (CPZ) on passive epithelial permeability and net fluid movement induced by secretagogues was tested in the rat intestine in vivo. CPZ, in a dose of 20 mg/kg intramuscularly, did not alter colonic permeability either in control conditions or during increased permeability caused by deoxycholic acid (DOC) or bisacodyl. Fluid secretion induced by cholera toxin and theophylline was strongly reduced by CPZ. The effects of oxyphenisatin and bisacodyl were only slightly but significantly inhibited by CPZ, whereas the action of DOC was unaffected. It is concluded, that the increase of the epithelial permeability is the main reason for the augmented fluid secretion caused by DOC. Bisacodyl and oxyphenisatin seem to act partly via an increase in permeability and to some degree via an induction of an active secretory process.

Animals↗
PubMed1983

Is the secretagogue effect of deoxycholic acid mediated by the adenylate cyclase-cAMP system.

The role of the adenylate cyclase (Ac)-cAMP system in mediating deoxycholic acid (DOC)-induced fluid secretion was studied in the rat jejunum and colon in vivo using the AC inhibitor, RMI 12 330 A. A potent inhibitory effect of RMI 12 330 A on fluid secretion induced by cholera toxin was demonstrated in ligated rat jejunal loops. On the contrary, the changes of fluid movement in jejunal and colonic loops caused by DOC could not be influenced by RMI 12 330 A, and mucosal cAMP levels of colonic loops were not increased. Colonic mucosal permeability estimated by the 14C-erythritol clearance increased significantly during a 45-min exposure to 3 mmol DOC, and was not affected by RMI 12 330 A. These results do not support the theory that the AC-cAMP system plays an important role in DOC-induced intestinal fluid secretion and suggest that an increase in mucosal permeability is the predominant factor responsible for the secretagogue effect.

Adenylyl Cyclase Inhibitors↗
PubMed1982

Independence of the activation of mucus and potassium secretion on the inhibition of sodium and water absorption by deoxycholate in rat colon.

The dose dependence of the influence of deoxycholic acid (DOC) on fluid and sodium absorption, transmural potential difference (PD), permeability of 14C-erythritol and secretion of potassium and mucus (protein bound hexoses) was measured in the in vivo perfused rat colon. The following results were obtained: 1. The threshold concentration for the inhibitory effect of DOC on fluid and sodium absorption is 2 mmol. In order to decrease PD and increase the colonic permeability for 14C-erythritol the same concentration was needed. 2. In contrast, DOC stimulated potassium and mucus secretion even in a fourfold lower concentration (0.5 mmol). No difference in the responsiveness of the descending and ascending colon was observed. 3. It is concluded that the identical dose dependency of the effect of DOC on fluid and sodium movement, PD, and permeability of the colonic mucosa is consistent with the interpretation that the secretagogue effect of DOC is mediated by an increase in permeability. However, because of their greater sensitivity, mucus and potassium secretion obviously are affected by a different mechanism. It is speculated that mucus and potassium are secreted together by the mucus producing cells of the colonic mucosa under the influence of DOC.

Animals↗
PubMed1981

Loperamide reduces the intestinal secretion but not the mucosal cAMP accumulation induced by choleratoxin.

The effect of loperamide on net fluid transport and epithelial cAMP accumulation was tested in choleratoxin-exposed ligated colon loops of the rat in vivo. Purified choleratoxin (50 micrograms/ml saline, for 5 h) induced net secretion and doubled cAMP levels in comparison with saline-treated controls. Loperamide (4 mg/kg intragastrically) reduced this secretion by 75%, without diminishing cAMP accumulation; it had no effect on basal fluid transport or cAMP. The data suggest that the opiate analogue interferes with the secretory process at a point beyond the cAMP increase caused by activation of adenylate cyclase.

Animals↗
PubMed1979

[Alpha 1-antitrypsin deficiency, liver cirrhosis and pulmonary emphysema (author's transl)].

It is well known that incidence of chronic obstructive lung disease in adult patients with alpha 1-antitrypsin deficiency (ATD) is high. Adult carriers of this genetic trait with cirrhosis of the liver, and also with fibrosis of the liver and hepatoma, have been reported. A causal relationship between ATD and liver lesions has been suspected. In most cases liver disease has been recognized at post morten, - in a few cases, however, intra vitam, when severe symptoms of the liver disease had become apparent. The case of a 59 year-old patient is reported with PIZZ-homozygous ATD, moderate pulmonary emphysema and with marked portal fibrosis and focal transition in cirrhosis of the liver without any sequelae. The clinical course has been rather benign so far.

Electrocardiography↗