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S Bar-Meir

Publications and source records attributed to S Bar-Meir.

At least 19 recordsLinked to original sources

Vanadate has no effect on insulin-extraction by the rat liver.

The mechanism(s) responsible for the insulin-like effects of vanadate are still unclear, although several possible explanations have been raised. However, the possibility that vanadate induces inhibition of insulin degradation in the liver was not examined yet. Therefore, in the present study we examined the effect of vanadate on the extraction of insulin by the perfused rat liver using an open, non-recycling system. Baseline insulin extraction (44 +/- 2% and 37 +/- 3%) was not affected by the administration of 1 and 5 microM vanadate (decreased to 42 +/- 2% and 36 +/- 1, respectively, p = NS). Vanadate had no adverse effects on liver viability, and the bile flow remained stable during and after vanadate administration (0.87 +/- 0.08 microliter/min/g liver prior to Vs. 0.084 +/- 0.11 microliter/min/g liver following vanadate administration). This study shows that vanadate does not inhibit insulin extraction by the perfused liver, and that does of vanadate that effectively inhibit hepatic glucose production possess no adverse effects on liver viability.

Animals

Recovery of hepatic clearance and extraction following a release of common bile duct obstruction in the rat.

The rate of recovery for hepatic clearance and extraction following release of common-duct obstruction was investigated in the rat. Male Wistar rats underwent ligation of a cannulated common bile duct. Two weeks later, the cannula was opened and implanted into the duodenum, thus re-establishing enterohepatic circulation. Hepatic extraction and indocyanine green clearance were determined in three groups of six rats each, which differed by the time elapsed from the re-establishment of communication between the common bile duct and duodenum, i.e., 1, 48 and 168 h, respectively. A fourth group, in which a sham operation was performed, served as a control. Clearance was reduced from 16.9 +/- 2.5 ml/min per kg in the control group to 2.9 +/- 0.8, 5.4 +/- 2.4, and 8.5 +/- 3.3 ml/min per kg 1, 48, and 168 h, respectively, after release of common-bile-duct obstruction. Extraction rate was reduced from 37.3 +/- 5.9% to 17.5 +/- 2.7% in the 1st hour and recovered completely at 1 week. Thus, in the rat, release of a 2-week common-bile-duct obstruction is associated with complete recovery of the extraction capacity of the liver within a week, but only incomplete recovery of clearance. This decrease in clearance seems to be due to a decrease in effective hepatic blood flow, mostly probably due to the development of porto-systemic shunts.

Animals

Vanadate inhibits glucose output from isolated perfused rat liver.

Previous studies have demonstrated that vanadate ions mimic many of the actions of insulin in in vitro systems. Also, vanadate administered to diabetic hyperglycemic rats lowers their blood glucose levels to normal values. In this study we demonstrate that vanadate inhibits glucose output in the isolated perfused rat liver. Glucose production was suppressed maximally (about 50% to 60%), on addition of extremely low vanadate ion concentrations (0.5 to 1 mumol/L). This concentration is about two log units lower than the vanadate ion concentrations that are required to activate hexose uptake and glucose metabolism in vitro and is within the range of endogenous intracellular vanadium concentration. Insulin had little or no effect in inhibiting hepatic glucose output in this experimental system. The effect of vanadate ions is rapid in onset and is not accompanied by any signs of liver toxicity as assessed by various criteria. In conclusion, the study indicates that (a) vanadate ions inhibits hepatic glucose output, maximally and at extremely low, nontoxic concentrations (ID50 = 0.7 +/- 0.1 mumol/L). (b) The modulation action of the ion is fast and probably occurs at point(s) distal to the insulin receptor itself. (c) The liver participates in the process of maintaining euglycemia in diabetic rats receiving optimal doses of vanadate orally.

Animals

Cimetidine and omeprazole have different effects on hepatic extraction of lidocaine in rats.

The effect of two antisecretory drugs, omeprazole and cimetidine, on the hepatic extraction of indocyanine green and lidocaine was studied in the isolated perfused rat liver. Both indocyanine green and lidocaine are removed by the liver with high extraction efficiency in a flow-dependent manner. The elimination of lidocaine, but not indocyanine green, involves metabolism by the mixed-function oxidase in the liver. A selective effect on the hepatic extraction of lidocaine, but not indocyanine green, may therefore indicate an inhibition of hepatic mixed-function oxidase. To test this hypothesis, a nonrecycling system at a fixed perfusion flow rate was used to measure the extraction of lidocaine. Under control conditions, the extraction rate of lidocaine was 83% +/- 8%. In the presence of omeprazole at concentrations of 0.9, 2.0, and 4.5 micrograms/mL, the extraction rates were 81% +/- 9%, 82% +/- 7%, and 75% +/- 7%, respectively. These changes were not significantly different than control rates. In contrast, the increasing concentrations of cimetidine caused significant decreases in the hepatic extraction of lidocaine to values of 78% +/- 8%, 63% +/- 14%, and 48% +/- 14% at concentrations of 0.25, 0.50 and 1.25 micrograms/mL, respectively. The hepatic extraction of indocyanine green, 39% +/- 6%, was not affected by the administration of either omeprazole or cimetidine. Thus, in the rat, omeprazole seems to be a less potent inhibitor of cytochrome P-450 than cimetidine.

Animals

The effect of chronic captopril administration on hepatic blood flow of the rat.

The effect of chronic captopril administration on indocyanine green (ICG) clearance and hepatic extraction has been studied in the rat using the intact liver for ICG clearance and the isolated perfused liver for ICG extraction. The captopril was added to the drinking water to give a calculated daily intake from 0-45 mg kg-1. Hepatic clearance of ICG was dose related from 16.5 +/- 2.4 (control) to 7.2 +/- 1.6 mL min-1 kg-1, respectively. The hepatic extraction of ICG was not significantly different (37 +/- 6%) from the control value in groups on 4 and 45 mg kg-1 daily. Since ICG clearance and extraction are dependent on hepatic blood, a change in ICG clearance without a change in the extraction reflects a similar change in the hepatic blood flow. This remained unchanged at daily captopril intakes of 1 and 4 mg kg-1 and decreased when the daily intake was 10 mg kg-1 or higher. If these results in the rat are applicable to man, the chronic administration of therapeutic doses of captopril (0.5-2 mg kg-1) will not affect the hepatic blood flow.

Animals

The effect of PGE2 on hepatic blood flow and bile indocyanin green in the rat.

The effect of Prostaglandin E2 (PGE2) on hepatic blood flow and bile excretion has been only partially investigated. We studied in the rat the effect of PGE2 on indocyanine green (ICG) clearance, bile flow and ICG recovery in the bile. PGE2 administered to rats at a rate of 2 micrograms/kg/min had no effect on ICG clearance as compared to vehicle-treated rats (14.6 +/- 2.5 Vs, 16.9 +/- 2.5 ml/min/kg) and on bile flow (1.23 +/- 0.15 Vs. 1.24 +/- 0.11 microliters/min/gm liver). However, ICG excretion in bile was significantly increased as compared to a vehicle-treated group, 0.48 +/- 0.09 and 0.25 +/- 0.02 micrograms/microliters bile, respectively (P less than 0.005). This effect of PGE2 on ICG recovery in bile was found to be dose-dependent, and when PGE2 was administered at a rate of 1 microgram/kg/min, bile ICG decreased to 0.33 +/- 0.10 microgram/microliter bile. The effect of PGE2 on bile ICG is not due to an increased extraction of ICG by the liver since using the isolated perfused rat liver, the mean ICG extraction rate over a 20 minute period, with and without PGE2 infusion, was very similar, 33 +/- 3.5 and 37 +/- 6.2 percent, respectively. The lack of effect of PGE2 on ICG clearance and extraction and on bile flow, with an increase in biliary excretion of ICG, suggests a decreased hepatic storage of ICG induced by PGE2 possibly due to an accelerated rate of ICG excretion from the hepatocytes to the bile canaliculi.

Animals

Effects of upper dorsal sympathectomy on esophageal motility in humans.

To evaluate the role of the sympathetic nervous system in modulating esophageal motility, esophageal manometry was performed on two groups of patients who underwent upper dorsal sympathectomy for relief of palmar hyperhydrosis. In six patients sympathectomy was done by the supraclavicular approach, with removal of T2 and T3 ganglia. Manometry was performed before the operation and three weeks after it. In seven other patients sympathectomy was done by the axillary approach, with removal of T2-T4 ganglia. Manometry in this group was performed 28.4 +/- 22.4 months after the operation. Fifteen individuals with an intact sympathetic system served as controls. Manometric parameters evaluated were esophageal contraction amplitude and duration and lower esophageal sphincter pressure. The difference between the results obtained in the pre- and postoperative periods in the first group was not statistically significant. The differences between the two patient groups and between the patient groups and the control group were not statistically significant either. We conclude that upper dorsal sympathectomy does not affect esophageal motility in man.

Adolescent

The significance of unexplained dilated common bile duct at endoscopic retrograde cholangiopancreatography.

The clinical significance of unexplained dilation of the common bile duct (CBD) seen at endoscopic retrograde cholangiopancreatography (ERCP) in non-jaundiced patients with abdominal pain, was studied in a group of 14 patients. A CBD diameter of more than 15 mm was associated with choledocholithiasis (29%), periampullary carcinoma (14%), papillary stenosis (14%), or no definite pathology (43%) during a follow-up of 20 months. Dilation of the CBD exceeding 20 mm, was associated with periampullary carcinoma or papillary stenosis in 80% of the patients. It is recommended that such a group of patients be followed very closely, and the ERCP examination repeated within a few months.

Aged

The role of short-term multilumen duodenojejunal manometry in patients with intestinal motor dysfunction.

Short-term duodenojejunal manometry, using a multilumen perfused tube, was performed in 12 patients with symptoms of motor dysfunction, 6 patients with irritable bowel syndrome and predominant diarrhea and 6 patients with chronic constipation. Ten healthy individuals served as controls. The durations, in minutes, of the various phases of the migratory motility complex in the three groups were: phase I: 24.4 +/- 22.1, 26.9 +/- 17.3, and 27.2 +/- 18.5; phase II: 86.7 +/- 25.2, 132 +/- 93, and 73.1 +/- 40.8, and those of phase III: 6 +/- 2.5, 6.8 +/- 5, and 6.4 +/- 1.7, respectively. The differences between patients and controls were not statistically significant. Variables of contractions of phase III in the different groups were: frequency (per minute): 10.9 +/- 0.8, 10.7 +/- 0.4, and 11.3 +/- 0.4; Summation of amplitudes per minute: 205.2 +/- 55.7, 288 +/- 57.9, and 337.8 +/- 76.5; Mean amplitude (mm Hg): 19.1 +/- 4.2, 28.6 +/- 5, and 33.5 +/- 7.1, respectively. Results in the patient groups were not significantly different from controls. Short-term duodenojejunal manometry was normal in patients with irritable bowel syndrome and in those with chronic constipation.

Adult

[Duodenitis].

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Duodenitis

Cancer family syndrome of Lynch.

This report describes a family in whom eight cancers (six colonic and two endometrial) occurred in seven relatives. The colonic cancer was diagnosed in five of the six affected patients at an unusually young age, had a predilection for the proximal colon, and was of the mucinous type in four patients. Polyposis was not found in any colon. The occurrence of cancer in this kindred is characteristic of the "cancer family syndrome" of Lynch.

Adenocarcinoma, Mucinous