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Biomedical subjects

B I Hirschowitz

Publications and source records attributed to B I Hirschowitz.

At least 145 records · Page 8Linked to original sources
PubMed1979

Zollinger-Ellison syndrome unresponsive to cimetidine.

A patient with Zollinger-Ellison syndrome appeared initially to respond to cimetidine with a reduction in gastric acid secretion. Symptoms immediately improved but after three days recurred with increasing severity. Intravenous cimetidine had only a short-lived and partial inhibitory effect on the rate of acid production and because of continuing pain and progressive bleeding from his duodenal ulcer, total gastrectomy was performed. Evidence of the effect of atropine and of oral and intravenous cimetidine is presented. Despite recent optimism, cimetidine is not always adequate treatment for Zollinger-Ellison syndrome.

Administration, Oral↗
PubMed1979

Enzymatic sulfation of glycochenodeoxycholic acid by tissue fractions from adult hamsters.

Using a radiometric assay with glycochenodeoxycholic acid as substrate, bile acid:3'-phosphoadenosine-5'-phosphosulfate sulfotransferase activity was found in 105,000 g supernatant fractions of liver, proximal intestine, and adrenal gland homogenates from adult hamsters. Optimum conditions for measurement of the hepatic enzyme were determined. In both male and female animals sulfation only occurred at the 7 alpha-position. Saturation analysis with glycohenodeoxycholic acid revealed that the higher activity observed in fractions from female compared to male hamsters was due to a 4-fold lower apparent Km (79 muM vs. 317 muM) for this bile acid in the females. The sulfation of glycohenodeoxycholic acid was competitively inhibited by glycolithocholic acid, chenodeoxycholic acid, and ursodeoxycholic acid. The data are consistent with the concept that sulfation of many, if not all, bile acids can occur in vivo.

Adrenal Glands↗
PubMed1979

Utilization of a radioiodinated bile salt for kinetic studies and hepatic scintigraphy. Studies in nonhuman mammals.

An 125I- or 131I-labeled bile salt derivative, cholylglycyliodohistamine, has been synthesized and purified. The bile salt derivative is rapidly cleared from the circulation when injected intravenously into rats and rabbits. Ten minutes after injection, approximately 50% of the recovered bile salt derivative was in the jejunum and ileum, and 36% was found in the liver. Sixty minutes after injection, 99% of the recovered radioactivity was found in the luminal gastrointestinal tract. The isotope was cleared from the circulation of rabbits with a t1/2 of approximately 2 min. Hepatic scintigraphy using rabbits demonstrated rapid uptake by the liver and excretion into the intestine. Quantitative analysis of scintigraphy showed an uptake rate of 14%/min and a subsequent excretory rate of 4.6/min.

Animals↗
PubMed1978

Serum lysozyme activity in inflammatory bowel disease.

Serum lysozyme activity was determined in the sera of 70 patients with inflammatory bowel disease by the lysoplate method. Serum lysozyme levels were significantly elevated only in patients with Crohn's disease of the small bowel. Patients with either granulomatous or ulcerative colitis had serum lysozyme values not different from normals, irrespective of activity of their disease.

Adult↗
PubMed1978

Calcium and secretin as provocative stimuli in the Zollinger-Ellison syndrome.

The effects of calcium and secretin were studied in 8 patients with the Zollinger-Ellison syndrome and 18 patients with duodenal ulcer disease. Intravenous infusion of calcium gluconate produced marked increases in serum gastrin levels in the patients with Zollinger-Ellison syndrome (4,350 +/- 1,625 pg/mg) and very slight increases in the patients with duodenal ulcer disease (140 +/- 49 pg/ml). Secretin given as a single intravenous injection also induced marked elevations in serum gastrin in the group with the Zollinger-Ellison syndrome (4,063 +/- 1,990 pg/ml). By contrast, intravenous secretin resulted in a progressive fall in serum gastrin levels in the duodenal ulcer group (from 119 to 97 pg/mg). These results suggest that both stimuli are very useful dagnostic tools in discriminating between Zollinger-Ellison and non-Zollinger-Ellison patients. The secretin challenge test is felt to be superior to the calcium infusions because it is simpler, safer and very rarely produces false-negative or-positive results.

Adult↗
PubMed1978

Stimulation of gastrin release and gastric secretion: effect of bombesin and a nonapeptide in fistula dogs with and without fundic vagotomy.

Bombesin and a synthetic bombesin nonapeptide were studied by intravenous infusion at a dose of 0.5 microgram.kg-1.h-1 for 4 h in 7 dogs with esophagostomy and gastric fistula. In 3 of the dogs who had highly selective (fundic) vagotomy, mean integrated gastrin output over 4 h was double that in the 4 dogs with vagi intact during both nonapeptide (1,554 vs. 700 pg.ml-1.4 h-1) and bombesin infusion (2,442 vs. 1,440 pg.ml-1.4 h-1). Peak concentrations of serum gastrin reached during bombesin (490 +/- 100 vs. 320 +/- 90) were higher than those during nonapeptide infusion (270 +/- 40 vs. 160 +/- 28 pg/ml) in the vagotomized and intact dogs, respectively. The difference between vagotomized and vagally intact dogs suggests that the fundic vagotomy removed an inhibitor of gastrin release from the innervated antrum. Despite these differences in gastrin release, gastric acid output with the two peptides was the same (49--52 mEq/4 h) whether the fundus was denervated or innervated. This suggests that bombesin may stimulate gastric acid secretion by the release of an additional secretagogue which is not measured by the gastrin assay. Neither of the two inhibitors of gastrin release--antral acidification to pH 1.4 or less or atropine (100 microgram/kg)-- inhibited gastrin release by bombesin, even though the atropine reduced acid output by 80%. Bombesin is a potent gastric stimulus whose action is only partly explained by the measured gastrin release.

Animals↗
PubMed1978

Effect of cimetidine on stimulated gastric secretion and serum gastrin in the dog.

The histamine H-2 receptor antagonist cimetidine was given for 90 minutes to four fistula dogs during a steady dose 270-minute infusion of histamine (50 microgram. base/kg.hr.), urecholine (80 microgram./kg.hr.) or pentagastrin (1.5 microgram./kg.hr). In each case there was gradual but marked (75-95%) inhibition of acid secretion with maximal effects after 60-90 minutes while pepsin secretion was also suppressed but to a lesser extent. These effects persisted for at least the 90 minutes after the end of cimetidine infusion. Serum gastrin was not significantly changed by cimetidine. Kinetics of effect of cimetidine were derived from stepdose responses to histamine (2-150 microgram./kg.hr.), pentagastrin (0.1 to 10 microgram.kg.hr.) and urecholine 20-160 microgram./kg.hr.) which were made alone and with background infusions of cimetidine. Cimetidine acted competitively for acid output with histamine as the stimulus and noncompetitively for pentagastrin or urecholine. With histamine or pentagastrin pepsin was less inhibited than H+ and in the case of urecholine, pepsin secretion was not inhibited by cimetidine.

Animals↗
PubMed1978

Sclerosing cholangitis associated with ulcerative colitis. Light and electron microscopy studies.

The light and electron microscopy findings of liver biopsies from four patients with sclerosing cholangitis and ulcerative colitis are described. The main histologic feature was mesenchymal proliferation involving phagocytic, fibroblastic and immunocytic cells suggestive of an immunologic type of liver injury which may attack bile duct epithelial cells. Other histologic features, included the presence of myelin fibers in both hepatocytes and bile duct epithelial cells and an abundant amount of lysosome-like structures. The significance of these findings is discussed.

Adult↗
PubMed1978

Group-specific component [Gc] levels in chronic liver disease.

Serum Group-specific component (a probable vitamin D transport protein) concentrations have been measured in 72 patients with chronic liver disease. Low mean values were found in groups of patients with cirrhosis and metastatic liver disease. In a group of patients with biliary tract disease the mean value was not significantly different from normal except for seven patients with severe bone disease who were found to have the lowest levels. The mechanism for the reduction remains to be clarified, but low Group-specific component values may play a contributory role in the osteodystrophy of chronic obstructive liver disease.

Adolescent↗
PubMed1977

A critical evaluation of a procedure for measurement of serum bile acids by radioimmunioassay.

A radioimmunoassay for the quantitative determination of cholic acid conjugates has been developed. Antisera were raised in rabbits injected with cholylglycine coupled by amide linkage to bovine serum albumin. The antibodies reported in this communication were not found to be mono-specific in the strictest sense. This assay is relatively simple, rapid, sensitive, reliable, and most importantly, specific for bile acids; the specificity of each antibody, however, must be thoroughly characterized at the dilution in routine use. The range of normal values for cholic acid conjugates in serum was found to be 0.1--1.6 micronmol/l (mean: 0.62, +/- S.D.: 0.4).

Animals↗
PubMed1977

Long-term effects of highly selective vagotomy (HSV) in dogs on acid and pepsin secretion.

Gastric H+ and pepsin studies before and at intervals for 4o months after fundic vagotomy (HSV) in 3 fistula dogs were done with the vagal stimulant 2-deoxyglucose (2-DG), and blocked the secretory response to 2-DG, but secretion began to recover by 5-6 months, and from 16 months on stabilized at 60% H+ and 13-17% pepsin (preoperative = 100%). After HSV the stomach showed hypersensitivity to urecholine with a lower threshold and lower Km, but unchanged Vm, while with histamine the curves were shifted to the right, with Vm unchanged and Km increased. With pentagastrin there was also a small decrease in Vm. Pepsin responses to urecholine recovered and exceeded control by 16 months, but remained relatively unresponsive to histamine or pentagastrin. A cholinergic background provided by urecholine at subthreshold doses (less than 10 mug/kg-hr) restored both pentagastrin and histamine responses to prevagotomy levels. Gastrin release from the innervated antrum by 2-DG was several times greater than in controls and was atropine sensitive. The results indicate that denervation of the secretory mucosa, especially of the peptic cells, is never more than partially reversed even after 3 years. Even though the response to vagal stimulation is partial, the mucosa remains capable of normal response, ie, there is no atrophy, and therefore, the vagus is not directly trophic to the gastric fundus. Moreover, vagotomy was followed by some hypersensitivity to urecholine, indicating changes in cholinergic receptors like those seen in denervated muscle cells.

Acetylcholine↗
PubMed1977

Kinetics of atropine inhibition of pentagastrin-stimulated H+, electrolyte, and pepsin secretion in the dog.

The effects of atropine on pentagastrin-stimulated gastric secretion of water, H, Cl, Na, K, and pepsin were determined by kinetic analysis of dose-response studies in 5 dogs with esophagostomy and gastric cannula. First a dose-response study was done using 7 doses of pentagastrin (1-6 mug/kg hr), each dose given by I.V. infusion for 4 hr at a separate time. The same series of doses was used with atropine sulfate 10 mug/kg hr as background. Atropine inhibited pentagastrin-stimulated secretion competively with a dose ratio change of 20. In a third set of studies pentagastrin was infused alone for 4 hrs in the dose of 1.5 mug/kg hr and then with each of 7 doses of atropine (0.625-40 mug/kg hr), each dose used separately. Atropine competitively inhibited water, H, Cl, and K secretion, with Ki (dose of atropine giving 50% inhibition) of 1.0 mug/kg hr. Pepsin secretion was much more strongly inhibited than acid secretion by atropine with Ki 0.27 mug/kg hr and the inhibition was uncompetitive. Calculated maximal inhibition of H+ secretion by atropine was 89% and of pepsin 95%. Furthermore the shape of the response to pentagastrin was altered by atropine so that the peak response was delayed to the third and fourth hour of pentagastrin infusion.

Animals↗