Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008370 (cholestasis)
 9,378 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma cyclic AMP levels were determined during a 40 minute secretin infusion (1 Cl.U kg-1h-1) followed by a 40 minute combined secretin (1 Cl.U kg-1h-1) caerulein (75 ng kg-1h-1) infusion. In nine healthy subjects, both secretin alone and secretin in combination with caerulein did not affect plasma cyclic AMP levels. The same was observed in six patients with chronic pancreatitis. By contrast, in patients suffering from liver disease (nine cases) or extrahepatic cholestasis (six cases), secretin elicited large increases in plasma cyclic AMP concentration; the mean values attained being, respectively, seven and four times higher than before the infusion. On the other hand, increases in plasma cyclic AMP 10 minutes after a bolus injection of glucagon (1 mg) were four times lower in the liver disease group as compared to the controls. The results reported here suggest that the liver plays a major role in the degradation of plasma cyclic AMP produced by target tissues responding to secretin, and in the release of cyclic AMP under glucagon. Liver disease reduce the capacity of the liver to clear cyclic AMP from the blood. The pancreas does not contribute significantly to the cyclic AMP in the blood.
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PMID:Plasma cyclic AMP levels during a secretin-caerulein pancreatic function test in liver and pancreatic disease. 20 44

Pancreatic function can only be determined exactly via the pancreozymin-secretin test. We conducted this test in two versions: (1) under conditions of continuous perfusion with the possibility of volume correction and (2) as a simple tubing. We compared the results of 86 tubings with the results of 87 examinations under perfusion. For that purpose all patients were classified into four groups: group a) with 46 and 10 examinations, respectively, in patients suffering from cholestasis in early infancy, group b) with 7 and 12 examinations, respectively, in older patients with liver diseases, group c) with 8 and 17 examinations, respectively, in patients suffering from cystic fibrosis or Shwachman's syndrome and group d) with 25 and 48 examinations, respectively, in children with normal pancreatic function. Both examination methods nearly identical mean values of the enzyme activities in all four patient groups. However, mean variations were found to be higher in case of tubing. Therefore the lower limits (x - 2s) of this test were defined at a lower level than those of the tests under perfusion.
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PMID:[Determination of exocrine pancreatic function in childhood with the pancreozymin-secretin test]. 128 98

Secretin is known to stimulate bile flow from the bile duct epithelium. To investigate the effects of secretin in cholestasis, we studied the response of the bile flow and the excretion of biliary components to secretin using two cholestatic models with or without damage to the bile duct epithelium. The model without bile duct epithelial damage was a choledocho-caval (CC) fistula over a 24-hour period, and the model with bile duct damage was a bile duct ligation over a 48-hour period. Secretin was administered by intravenous infusion for 30 minutes and bile was collected for 120 minutes. Controls were given saline similarly. The bile flow and biliary bicarbonate excretion rate were significantly increased after secretin infusion in the CC fistula rats when compared with the control rats, but no stimulation by secretin was observed in the ligated rats. These data indicate that secretin-induced bile production was enhanced under cholestatic conditions with no bile duct epithelial disturbance.
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PMID:Effects of secretin on bile production in two kinds of cholestatic models by choledocho-caval fistula and bile duct ligation in rats. 162 81

Bile is an aqueous isotonic solution of bile acids, cholesterol, phospholipids, bile pigments and inorganic electrolytes. It is secreted by the hepatocytes into the bile canaliculi and modified by the bile ducts and gallbladder. The chief mechanisms of bile formation are: 1. active transport of bile acids, responsible for the bile acid-dependent flow. This is the consequence of an osmotic flux of water and electrolytes in response to bile acid secretion. Ursodeoxycholic acid (and other bile acids) have an hypercholeretic effect, probably through a chole-hepatic circulation. 2. Transport of other compounds, responsible for the bile acid-independent flow. These compounds are incompletely identified: organic compounds (such as glutathione) or inorganic electrolytes could be involved. 3. Reabsorption of water and electrolytes in the bile ducts and in the gallbladder, and secretion of bicarbonate by the bile ducts, stimulated by secretin. Cholestasis may be extra or intrahepatic. Extrahepatic cholestasis is always due to obstruction of bile ducts. Intrahepatic cholestasis may result from obstruction of intrahepatic bile ducts or alteration of secretory mechanisms by the hepatocyte.
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PMID:[Formation of the bile]. 179

To examine whether intravenous bilirubin infusion causes cholestasis and impairs liver metabolism, bile secretion and ethanol clearance were measured in 34 anaesthetized pigs before and after intravenous infusion of 0.5 mumol kg-1 min-1 bilirubin for 4.5 hours. Bilirubin infusion increased plasma bilirubin to 556 +/- 76 mumol l-1 and hepatic tissue bilirubin to 3.5 +/- 1.3 mmol kg tissue weight-1. Bilirubin infusion depressed bilirubin secretion and net hepatic uptake of cholate and taurocholate, and caused a 86 +/- 6% reduction of cholate-induced bile secretion. Bilirubin caused formation of large cytoplasmic vacuoles in hepatocytes and dilatation of bile canaliculi. Ethanol clearance and secretin-dependent ductular bile secretion were unaffected by bilirubin. We conclude that intravenous infusion of unconjugated bilirubin causes accumulation of bilirubin in the liver, vacuolization of the hepatocyte cytoplasm and canalicular but not ductular cholestasis. The canalicular cholestasis is not due to impaired hepatic mitochondrial energy metabolism, but may be due to inhibition of a common pathway for lipid, bilirubin and bile salt secretion from hepatocytes.
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PMID:Intravenous bilirubin infusion causes vacuolization of the cytoplasm of hepatocytes and canalicular cholestasis. 181 76

Bile flow may be considerably increased in human cirrhosis. The mechanism of this increase has not been established. Two mechanisms have been proposed: a) increased canalicular filtration because of sinusoidal hypertension, or b) secretion by proliferated bile ductules. To distinguish between these two possibilities, we examined the determinants of bile secretion in rats with secondary biliary cirrhosis after bile duct obstruction. Sham-operated animals served as controls. Four weeks after bile duct ligation, all animals had cirrhosis. Bile flow was significantly higher and bile salt secretion significantly lower in cirrhotic animals than in controls. Biliary bicarbonate concentration was significantly higher in cirrhotic animals than in controls. Bile-to-plasma concentration ratio of erythritol was significantly lower in cirrhotic animals than in controls, suggesting a dilution of erythritol by a secretion distal to bile canaliculi. Bile-to-plasma ratio of sucrose was not significantly different in cirrhotics and controls, suggesting that paracellular permeability was not modified. Secretin, at the dose of 3 clinical units/100 g, induced an increase of approximately 75 percent in bile flow, and 70 percent in biliary bicarbonate concentration in cirrhotics. In conclusion, bile flow was increased in biliary cirrhosis in rats. The dilution of erythritol, the increase in biliary bicarbonate concentration and the increased response to secretin strongly suggest that increased choleresis was due, at least in part, to secretion by bile ductules or ducts. These results confirm that secondary biliary cirrhosis is a good experimental model for the study of alterations of bile secretion in cirrhosis.
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PMID:[An increase of choleresis in secondary biliary cirrhosis in rats is caused by bile duct secretion]. 235 Dec 43

In patients carrying a Kehr tube choledochostomy, the surgeon may observe, but rarely, important hypercholeresis, non-bile-acid dependent, in people with severe advanced chronic hepatic diseases or persistent cholestasis. The amount of bile flowing to the outside can reach two liters and more daily. We have seen this in two patients with compensated hepatic disorders and in another suffering from light cholestasis produced by choledocholithiasis. We have also found the same in three other people with liver and the main biliary extrahepatic tract completely normal. This hypercholeresis is continuous and subject to rapid increases relative to the ingestion of food. Such increases are related to gastrointestinal hormones, specially secretin, which is produced when portions of gastric chyme enters the duodenum.
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PMID:[Biliary secretion. Significance of hypercholeresis from the surgical point of view]. 259 67

Many animal experiments have been studied on the choleretic effects of secretin. We intended to estimate secretin choleresis in human (15 patients) who had received PTCD or T-tube insertion into the common bile duct. Based upon these data of secretin and choleresis, secretin was administered to 11 patients with prolonged jaundice due to intrahepatic cholestasis in order to evaluate this as a new therapy for intrahepatic jaundice. As controls, eleven patients with intrahepatic cholestasis treated with steroid hormones and/or phenobarbital were used. In all cases with biliary drainage, secretin produced a remarkable choleretic effect with a high concentration of bicarbonate. In 9 out of 11 patients with intrahepatic cholestasis who were treated with secretin, levels of serum bilirubin decreased linearly and other liver function tests returned to the normal range. The mean values of T1/2 (number of days required for reduction by half) of serum bilirubin in 9 effective cases to secretin was 10.8 days. On the other hand, that in 11 effective cases treated with steroid hormones and/or phenobarbital was 23.2 days. These results suggest that secretin therapy may be an effective treatment for intrahepatic cholestasis.
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PMID:A new therapeutic trial of secretin in the treatment of intrahepatic cholestasis. 266 8

For biliary atresia portoenterostomy with externally draining conduit provides a model for quantitation of hepatic excretory function and for assessment of the physiologic response of the intrahepatic biliary system to gastrointestinal hormones in a human hepatopathologic condition. Four patients with biliary atresia were serially evaluated from 2 weeks to 43 months following total bile diverting portoenterostomy. A fifth patient with no bile flow provided a control for these studies. The pattern of Rose Bengal excretion for three patients with a satisfactory clinical course was different from that of a fourth patient with highly variable flow and persistent cholestasis. Marked volume and bicarbonate concentration increases in bile were noted 30 to 45 minutes after secretin infusion but only in the four patients with bile flow. The volume response to glucagon was more diffuse. Bilirubin and bile acid concentrations decreased in the stimulated bile flow periods and hourly outputs of these cholephils were not increased above basal. During two intervals of low bile output, secretin markedly increased bile flow in the patient with persistent cholestasis establishing the patency of the hepatoenteric anastomosis (functional obstruction) in contrast to the lack of secretin response in the control (structural obstruction).
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PMID:Stimulation of bile output by gastrointestinal hormones following portoenterostomy for biliary atresia. 648 96

In patients with primary biliary cirrhosis, the chronic cholestasis, salivary, and lacrimal hyposecretion suggest that the disease is a "dry gland" syndrome. To determine whether or not pancreatic damage occurs in primary biliary cirrhosis and other forms of chronic cholestasis, we have studied pancreatic structure and function in primary biliary cirrhosis, and primary sclerosing cholangitis. In a retrospective study, retrograde pancreatograms were abnormal in 43% of 35 patients with primary biliary cirrhosis and 15% of 20 patients with primary sclerosing cholangitis (p less than 0.02). In a prospective study, serum pancreatic isoamylase was abnormal in 56% of 41 patients with primary biliary cirrhosis and 36% of 22 patients with primary sclerosing cholangitis (NS), indicating pancreatic damage in both diseases. After secretin-pancreozymin stimulation, patients with primary biliary cirrhosis, but not patients with primary sclerosing cholangitis, showed a significant reduction in duodenal juice flow rate (p less than 0.01) and immunoreactive trypsin output (p less than 0.01). The reduced trypsin output in patients with primary biliary cirrhosis indicates pancreatic hyposecretion. In neither patients with primary biliary cirrhosis nor patients with primary sclerosing cholangitis was the immunoreactive trypsin concentration, or tryptic activity in duodenal juice, significantly different from controls. Pancreatic involvement in primary biliary cirrhosis is closely associated with Sjogrens syndrome, and it is likely that the pancreatic hyposecretion is a component of the sicca complex. This association was not obvious in primary sclerosing cholangitis.
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PMID:The pancreas in primary biliary cirrhosis and primary sclerosing cholangitis. 712 26


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