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Biomedical subjects

P Czygan

Publications and source records attributed to P Czygan.

At least 19 recordsLinked to original sources
PubMed1978

Hormone-sensitive adenylate cyclase in human colonic mucosa.

Human colonic adenylate cyclase has been shown to be sensitive to vasoactive intestinal polypeptide (VIP) and prostaglandins of the E- and F-type. Maximal activation of enzyme activity averaged 200% for VIP and 300-350% for the E-prostaglandins. Both classes of hormones had an additive effect on enzyme activity indicating the existence of two distinct hormone-sensitive adenylate cyclases in human colonic mucosa.

Adenylyl Cyclases↗
PubMed1978

Pool size, synthesis, and turnover of sulfated and nonsulfated cholic acid and chenodeoxycholic acid in patients with cirrhosis of the liver.

In 5 patients with cirrhosis of the liver sulfated and nonsulfated [14C]cholic acid and [14C]chenodeoxycholic acid were administered intravenously and the specific activity curves were determined. Specific activities declined exponentially and pool sizes, synthesis rates, and turnover rates of bile acids were calculated on the basis of a one-pool system. The biological half-life of cholic acid was 4.3 +/- 1.6 days (mean +/- SEM) and of chenodeoxycholic acid was 2.8 +/- 1.2 days. The half-life of cholic acid sulfate was 0.7 +/- 0.5 day and of chenodeoxycholic acid sulfate was 0.8 +/- 0.5 day. The pool size of cholic acid was 513 +/- 103 mg, of chenodeoxycholic acid, 477 +/- 77 mg, of cholic acid sulfate, 4.7 +/- 1.0 mg, and of chenodeoxycholic acid sulfate, 38.7 +/- 4.0 mg. The daily synthesis of cholic acid was 90 +/- 14 mg, of chenodeoxycholic acid, 118 +/- 6 mg, of cholic acid sulfate, 7.2 +/- 2.1 mg, and of chenodeoxycholic acid sulfate was 32.6 +/- 3.2 mg. The data indicate that sulfate esters of bile acids are significantly more rapidly excreted than are unsulfated bile acids. More than one-fourth of the chenodeoxycholic acid but less than one-tenth of the cholic acid formed was sulfated. The preferential sulfation of chenodeoxycholic acid is responsible for the more rapid turnover of chenodeoxycholic acid in comparison to cholic acid. Sulfation enhances the excretion and thereby prevents the accumulation of hepatotoxic concentrations of chenodeoxycholic acid in patients with cirrhosis of the liver.

Alkaline Phosphatase↗
PubMed1977

[Treatment of intrahepatic cholesterol stones by chenodeoxycholic acid (author's transl)].

Intrahepatic gallstones were demonstrated by operative cholangiography in two men, aged 34 and 46 years, respectively. The cholesterol stones were dissolved in both patients within eight and two months, respectively, by retrograde instillation of chendeoxycholic acid via a T-drain. Additional endoscopic papillotomy was performed because of a papillary stenosis in one instance, and extrahepatic occlusion during treatment in the other. During treatment there was a rise of transaminases of 5-fold levels, of gamma-glutamyl transferase up to 10-fold of normal. Since chenodeoxycholic-acid instillations both patients have been receiving the drug orally to prevent recurrence of gallstones. So far all biochemical values are within the normal range, the patients are without symptoms and have a normal exercise tolerance.

Adult↗
PubMed1977

Demonstration of a liver abscess by ERC.

In a patient with septic fever and elevated alkaline phosphatase an ERC was conducted to explore the biliary system. Contrast media could be demonstrated within the hepatic parenchyma, establishing the diagnosis of a liver abscess in communication with the intrahepatic biliary system.

Adult↗
PubMed1977

Topographical studies on histamine- and adrenaline-sensitive adenylate cyclases in gastric and duodenal mucosa of human beings.

The distribution of histamine- and catecholamine-sensitive adenylate cyclases in human gastric and duodenal mucosa was studied. Basal enzyme activities averaged 155 pmol cAMP/mg prot./15 min in fundic gastric mucosa, 305 pmol cAMP/mg prot./15 min in the antral and 344 pmol cAMP/mg prot./15 min duodenal mucosa. 1 mM histamine induced a more than 2-fold increase of enzyme activity in fundic homogenates, whereas this secretagogue was nearly ineffective in similar preparations from the antral region (1.2-fold increase of enzyme activity). The response towards adrenaline was virtually identical in fundic and antral mucosa preparations. The duodenal enzyme was insensitive toward this catecholamine as well as to histamine. The data are suggestive for a messenger function of cAMP in histamine-stimulated gastric acid secretion.

Adenylyl Cyclases↗
PubMed1977

[Morphologic studies on the toxicity of sulfated and nonsulfated lithocholic acid in the isolation-perfused rat liver].

The isolated liver of male Sprague-Dawley rats was perfused by means of media containing lithocholic acid, taurolithocholic acid, lithocholic acid sulfate and taurolithocholic acid sulfate. 150 minutes later the tissue was being examined light- and electrone microscopically. After LC and TLC perfusion considerable alterations were found in the bile capillaries, in the ergastoplasm and minor ones in mitochondria. After perfusion with sulfate esters the tissue was unchanged. Our investigations have shown that sulfation provides a highly effective mechanism of detoxication in rats; but detoxication results not only in a decrease of reabsorption of excreted lithocholic acid sulfate esters but sulfation tenders the very lithocholic acid untoxic for the liver cell. The primary point of action of lithocholic acid seems to be the lipoprotein membrane.

Animals↗
PubMed1976

Induction and activation of rat liver microsomal bile salt glucuronyltransferase.

In vivo induction and in vitro activation of the recently described bile salt glucuronyltransferase were investigated in rat. A radioactive assay for the determination of glucuronyltransferase activity was used. 14C-Labeled bile salts served as substrates, and the glucuronides were separated by thin layer chromatography. Lithocholate glucuronyltransferase activity was determined in liver microsomes of phenobarbital- and 3-methylcholanthrene-treated rats and of untreated controls. Pretreatment with phenobarbital induced lithocholate glucuronyltransferase activity to 150.5% of controls. In contrast, 3-methylcholanthrene treatment decreased activity to 29.6% of controls. In vivo activation of lithocholate glucuronyltransferase by Triton X-100 was observed in controls and in the 3-methylcholanthrene group, but not in the phenobarbital group. Substrate activation of the enzyme by lithocholate was demonstrated in microsomes of untreated controls. Pretreatment with 3-methylcholanthrene, but not phenobarbital, increased the latency of lithocholate glucuronyltransferase. The results indicate that rat liver microsomal bile salt glucuronyltransferase activity is increased by in vivo induction with phenobarbital and by in vitro activation with detergents like Triton X-100. The induction of bile salt glucuronide formation by phenobarbital is most likely one of the factors contributing to the increased biliary and fecal excretion of bile salts in patients with cholestasis following phenobarbital therapy.

Animals↗
PubMed1976

[Electron miscoscopy studies of liver tissue in patients with amanita phalloides poisoning].

Electron microscopic findings of the liver are being described found in 4 patients aged from 12 months to 26 years after poisoning with Amanita phalloides. Marked alterations were seen in nuclei, in the endoplasmic reticulum, and in mitochondria. Morphologic criteria of cholestasis were observed in one patient. Extreme cellular edema was found in two patients. Since our findings differ considerably in several points from those patients with Amanita phalloides poisoning previously reported, one may suppose, that e.g. age, sex, preexisting damage and liver function might be highly important for the extent and form of resulting liver damage.

Adolescent↗