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Biomedical subjects

B I Hirschowitz

Publications and source records attributed to B I Hirschowitz.

At least 127 records · Page 7Linked to original sources
PubMed1980

Determination of the pool size and synthesis rate of bile acids by measurements in blood of patients with liver disease.

1. A simplified technique for the measurement of bile-acid pool size and synthesis rate has been developed in patients with liver disease. Isotope dilution studies in blood and bile were performed after intravenous injection of [24-14C]cholic acid with radioimmunoassay for the measurement of the bile-acid concentration. The interpolated pool sizes and synthesis rates, determined from results from both blood and bile, were not significantly different. The concentration of bile acids in the blood of healthy controls was not sufficiently elevated to permit application of this technique. 2. Three out of six patients with cirrhosis had a markedly reduced pool size compared with that of controls, whereas those with cholestasis had an unchanged pool size. The daily synthesis rate was reduced in both groups. Liver disease caused a redistribution (0.5-16%) of the bile-acid pool to the blood, which was associated with enhanced urinary excretion of cholic acid and its metabolites.

Adult↗
PubMed1980

Within-day fluctuations in serum bile-acid concentrations among normal control subjects and patients with hepatic disease.

Under carefully controlled conditions in a clinical research ward, conjugated primary bile-acid concentrations were measured by a 125I-radioimmunoassay every eight hours for four days in seven healthy control subjects and ten patients with hepatic disease (five with cirrhosis, three with primary biliary cirrhosis and two with sclerosing cholangitis). Two meals of approximately equal composition were consumed daily at 10 A.M. and 6 P.M., and blood was drawn at 4 A.M., 12 noon and 8 P.M.. With the exception of one patient, all subjects had greater postprandial than fasting serum bile-acid concentrations, with all healthy control subjects and most of those with hepatic disease showing evening values equal to or greater than the noon values. For the healthy control subjects, the mean values were 0.8, 1.4 and 1.9 microM, and for those with hepatic disease, 108, 140 and 133 microM. There were large fluctuations in serum bile acids (up to sevenfold) among patients with hepatic disease. These fluctuations were independently validated by finding corresponding changes in serum radioactivity derived from injection of a tracer (24-14C cholic acid) at the start of each study. To be consistent, especially for serial measurements, bile acids should be measured in blood taken at the same time of the day and at the same time relative to meals.

Analysis of Variance↗
PubMed1980

Disordered esophageal motility in Wilson's disease.

We describe the manometric findings in a patient with hepatolenticular degeneration (Wilson's disease). After 21 years of penicillamine therapy, one of the principal neurological problems remaining in a 49-year-old white man with Wilson's disease is food-induced dysphagia. Barium contrast studies showed gross incoordination of the upper esophagus; the manometric study revealed dysmotility of the mid and distal esophagus.

Deglutition Disorders↗
PubMed1980

Use of impromidine to define specific histamine H-2 effects on gastric secretion, heart rate and blood pressure in conscious dogs.

Histamine H-2 receptor-mediated effects of the very selective H-2 agonist (H-1:H-2 < 1:1000) impromidine on gastric acid, chloride and pepsin secretion and on heart rate (HR) and systolic blood pressure were compared to those of histamine in five conscious gastric fistula dogs. In each dog, impromidine in a step-dose response (0.46 to 46 nmol/kg.hr) in 45-min steps was given without and with a background infusion of cimetidine (2 mumol/kg.hr). Histamine acid phosphate was given in a seven step-dose response (18 to 1350 nmol/kg. hr). Impromidine produced the same maximum stimulation of gastric HCI output, increase of HR and fall in systolic blood pressure as histamine. Impromidine was some 38 times more potent than histamine in stimulation of acid (ED50 3.8 vs. 145 nmol/kg.hr) and 30 times more potent in raising HR (ED50 5.6 vs. 172 nmol/kg.hr). Cimetidine competitively inhibited the effects of impromidine with similar pA2 values for each effect (acid, 5.99; chloride, 6.03; change in HR, 6.03; and change in systolic blood pressure, 6.32). The effects of impromidine on pepsin secretion were qualitatively and quantitatively similar to those of histamine and other H-2 agonists with weak stimulation at low doses and progressive inhibition with increasing doses of impromidine. Coupling the results with the known high specificity of impromidine, gastric acid secretion, chronotropism and hypotension all seem to be purely H-2-mediated effects of histamine in the intact conscious dog.

Animals↗
PubMed1979

Familial nonhemolytic jaundice with free and conjugated hyperbilirubinemia, elevated serum bile acids, and liver pigmentation.

We have described an 11-year-old patient with nonhemolytic hyperbilirubinemia, elevated serum bile acids, and liver pigmentation. The Bromsulphalein clearance was not typical of that seen in the Dubin-Johnson syndrome, but there was a secondary rise at 120 min. The abnormalities involving several organic anions and liver histology are compared to those seen in other types of familial nonhemolytic jaundice.

Bile Acids and Salts↗
PubMed1979

Augmented vagal release of antral gastrin by 2-deoxyglucose after fundic vagotomy in dogs.

To study the relation between gastrin released by vagal excitation and the secretion of H+ and pepsin under various conditions, central vagal excitation was induced by 2-deoxyglucose (2DG) in doses of 50, 100, and 200 mg/kg body wt given as a single intravenous injection in seven gastric fistula dogs, three with fundic vagotomy and four with intact vagi. Serum gastrin increased linearly with dose doubling in both groups but was twice as high in the vagotomized dogs. Total acid output for 3 h was related linearly to integrated gastrin output in both groups, but the slope, H+/gastrin, was 10 times steeper in the vagally intact dogs (330 vs. 34 mueq/pg gastrin-ml-30 min) and pepsin output almost 20 times greater [5,400 peptic units (PU) vs. 296 PU]. Acidification of the antrum to pH 1.2-1.4 eliminated the gastrin response to 2DG in both groups of dogs. Atropine (100 microgram/kg iv) reduced serum gastrin in the vagotomized and increased it in the intact dogs. Atropinization uncovers stimulation by 2DG by pathways that do not involve muscarinic cholinergic receptors. Stimulation by both pathways is suppressible by acid. We conclude that fundic vagotomy removes an inhibitor of vagal gastrin release.

Animals↗
PubMed1979

Modification of D-galactosamine-induced liver injury in the rat by spironolactone.

Spironolactone, a competitive inhibitor of mineralocorticoid effects on the distal tubule of the kidney, has recently been found to have other metabolic effects. In these studies, spironolactone (200mg/kg intraperitoneally) for 3 days was found to have a marked protective effect against the hepatotoxic effect of D-galactosamine (275 mg/kg) in rats. Further progress in defining the mechanism of protection from D-galactosamine hepatic necrosis by spironolactone will require assessment of effects of spironolactone on uridine nucleotide metabolism.

Animals↗
PubMed1979

Effect of cimetidine on gastric hypersecretion and diarrhea in systemic mastocytosis.

Two patients had systemic mastocytosis and histamine excess, marked gastric acid and pepsin hypersecretion, and diarrhea. Cimetidine inhibited gastric acid secretion in both, but with only partial initial control of diarrhea. The other manifestations of mastocytosis were only partly controlled, even by combined H-1 and H-2 antagonist therapy. Basal and pentagastrin-stimulated acid and pepsin secretion before and after 5 and 14 months, respectively, of continuous and effective cimetidine therapy were essentially the same. Thus there was no evidence for an increase in the number of H-2 receptors during the long period of blockade or of involution of the parietal or peptic cell mass.

Adult↗