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Biomedical subjects

B M Jaffe

Publications and source records attributed to B M Jaffe.

At least 181 records · Page 10Linked to original sources
PubMed1978

Exogenous prostaglandins and gastric secretion in the cat.

1. In the conscious gastric fistula cate PGE2 was shown to produce dose-related inhibition of gastric acid and pepsin secreted in response to pentagastrin, histamine and insulin. 2. PGF2alpha had little effect on pentagastrin-stimulated gastric acid and pepsin secretion. 3PGF2 delayed the tachyphylaxis of gastric acid stimulated by pentagastrin and histamine, but not that stimulated by insulin. 4. Although not delaying tachyphylaxis of insulin stimulated acid, PGE2 delayed tachyphylaxis of insulin stimulated pepsin.

Animals↗
PubMed1978

Endogenous prostaglandins and gastric secretion in the cat.

1. The gastric juice outputs of acid, pepsin, PGE and PGF, and the plasma concentrations of PGE and PGF have been measured in response to I.V. infusions of pentagastrin, histamine and insulin in the conscious cat. 2. There were significant correlations between the output of gastric acid and gastric outputs of both PGE and PGF during secretion produced by all stimulants. Furthermore, there were similar significant correlations between the gastric outputs of pepsin and both PGE and PGF. However, during insulin stimulation there was significantly more pepsin output per unit PGE or PGF output than during either pentagastrin or histamine stimulation. 3. The correlations between the outputs of gastric acid and both PGE and PGF were similar during pentagastrin and insulin stimulation whereas those between acid and PGE and PGF altered during the infusion of histamine. 4. It is concluded that these data partially, but not entirely, support the hypothesis that local release of prostaglandins may act as a negative feed-back mechanism on gastric acid secretion. 5. Plasma prostaglandin concentration did not correlate with changes in acid or pepsin secretion.

Animals↗
PubMed1978

Effect of a synthetic analogue of PGE2 on exocrine and endocrine pancreatic function in the rat.

The effect of 16,16-dimethyl PGE2-methyl-ester (di-M-PGE2, a long-acting synthetic analogue of PGE2) on exocrine and endocrine pancreatic secretion was studied in rats with chronic pancreatic fistulas. Under basal conditions as well as after stimulation with secretin and OP-CCK, pancreatic exocrine secretion was inhibited markedly by intravenous injection of di-M-PGE2 at 10 microgram/kg and 100 microgram/kg. Secretory volumes and bicarbonate and protein outputs decreased within 10 minutes after the administration of di-M-PGE2, and this inhibitory effect persisted throughout the following 40 minutes. The smaller dose of di-M-PGE2 (10 microgram/kg) inhibited the volume of pancreatic secretion by an average of 47.7% and decreased bicarbonate and protein output by 41.1% and 70.5%, respectively. The larger dose (100 microgram/kg) caused a mean 48.3% inhibition of pancreatic secretory volume and decreased bicarbonate and protein outputs by 41.7% and 64.5%, respectively. Plasma insulin levels were lowered markedly after injection of di-M-PGE2 under basal conditions (mean inhibition 63.1% by PG-10 and 55.3% by PG-100) as well as after secretin stimulation (mean inhibition 89.5% by PG-10 and 82.4% by PG-100). These observations document that di-M-PGE2 is a potent inhibitor of pancreatic exocrine and endocrine function in the unanesthetized rat. In these actions the PGE2-analogue antagonized the stimulatory effects of both secretin and OP-CCK.

Animals↗
PubMed1977

Gastric complications after radiotherapy for Hodgkin's disease and other lymphomas.

Six patients who originally received radiotherapy for Hodgkin's disease or primary gastric lymphoma developed radiation injury of the stomach requiring surgical management. Only two of these patients had evidence of gastric neoplastic involvement at the time of treatment. Experience with these patients leads us to draw the following conclusions: (1) Symptoms of radiation injury mimic those of recurrent neoplastic disease. (2) The effects of radiation are progressive and may be resistant to medical management. (3) The indications for surgical management include perforation, hemorrhage, obstruction, intractable pain, fistula formation, and inability to rule out recurrence. (4) Parenteral hyperalimentation can be an important adjunct in preparing debilitated patients for operation. (5) Gastric resection with gastrojejunostomy is the preferred operation. (6) Frozen section examination can be useful in determining the proper level of resection.

Adolescent↗
PubMed1977

Dose dependent inhibition of B-16 melanoma growth in vivo by a synthetic analogue of PGE2.

Daily intratumor administration of 16,16-dimethyl-PGE2-methyl ester in two different dosages inhibited tumor growth in C57Bl/6J mice bearing subcutaneous B-16 melanomas. The larger dose (20 microgram/day/mouse) produced a 68% decrease in tumor volume, a 69% decrease in tumor weight and a 60% decrease in the number of cells in mitotic phase. The smaller dose (10microgram/day/mouse) was one fifth less effective than the 20microgram dose but produced similar changes. Histological examination of tumors revealed no significant differences either in the inflammatory cell population or the amount of necrosis in the control and di-M-PGE2-treated tumors.

Animals↗
PubMed1977

Use of calcium and secretin in the diagnosis of gastrinoma (Zollinger-Ellison syndrome).

Sixty-five patients with peptic ulcer disease were evaluated for gastrinoma (Zollinger-Ellison syndrome) by measuring changes in serum gastrin concentration after intravenous (i.v.) administration of calcium or secretin, or both. The presence of gastrinoma was established in all 20 patients whose serum gastrin increased by 395 pg/ml or more after i.v. calcium and in all 18 patients whose serum gastrin concentration increased by 110 pg/ml or more after i.v. secretin. The experience with these 65 patients shows that stimulation by calcium or secretin may confirm the presence of gastrinoma in cases where the diagnosis would otherwise remain obscure. Although a positive response to calcium or secretin is diagnostic for gastrinoma a negative response does not exclude this diagnosis. Stimulation with secretin is preferred for screening for gastrinoma because it is quicker and more reliable than calcium.

Adult↗
PubMed1977

Endogenous serotonin in the control of gastric acid secretion.

In three dogs with Heidenhain pouches (HP), gastric fistulas (GF), and duodenal cannulas, acidification of the duodenum with 0.1N HC1 (5 ml/minute) resulted in significant inhibition of GF output (preacidification, 8.66+/-0.58 mEq/30 minutes; postacidification, 5.47+/-0.66 mEq/30 minutes) and elevated peripheral venous blood levels of serotonin (basal, 226+/-64 ng/ml; peak, 521+/-168 ng/ml). Infusion of exogenous serotonin to comparable blood levels (basal, 208+/-38 ng/ml; mean postacidification, 571+/-153 ng/ml) resulted in similar GF inhibition (preacidification, 9.17+/-0.92 mEq/30 minutes; postacidification, 6.49+/-0.56 mEq/30 minutes). Per increment in peripheral blood serotonin of 1 ng/ml, endogenous serotonin inhibited 54.59+/-12.99 muEq/hour and exogenous serotonin inhibited 46.54+/-10.39 muEq/hour, p greater than 0.05. Neither endogenously released nor exogenous serotonin inhibited HP acid output. Using mesenteric venous infusions of serotonin, significant amounts of immunoreactive serotonin were found to escape hepatic inactivation; basal peripheral venous levels of serotonin, 233+/-103 ng/ml, increased to 455+/-127 ng/ml at 10 minutes. During release of endogenous serotonin, 92+/-21% of portal venous serotonin was bound to platelets; in contrast, during intraportal serotonin infusion, only 59+/-18% of serotonin was platelet bound.

Animals↗
PubMed1977

Inhibition of B-16 melanoma growth in vivo by a synthetic analog of prostaglandin E2.

The effect of systemic administration of 16,16-dimethyl prostaglandin E2-methyl ester (di-M-PGE2) on the growth of B-16 melanoma tumors has been studied in C57BL/6J mice. Daily i.p. injection of 5 mu of di-M-PGE2 commencing on the day of tumor inoculation with 10(5) and 10(6) viable cells delayed appearance of tumors; for the smaller tumor inoculum, it also increased median survival among treated mice from 23 to 33 days. Di-M-PGE2 treatment of mice with established tumors caused significant inhibition of tumor growth, as measured by a number of parameters including tumor diameters and volumes. At the time of sacrifice, di-M-PGE2-treated mice had tumors that were an average of 32% smaller (by weight), contained 60% fewer melanoma cells, and had higher concentrations of cyclic adenosine 3':5'-monophosphate and cyclic guanosine 3':5'-monophosphate (+225% and +100%, respectively).

Animals↗
PubMed1976

Prostaglandins E and F in endocrine diarrheagenic syndromes.

The role of prostaglandins in endocrine diarrheagenic syndromes was evaluated by measuring peripheral concentration of immunoreactive PGE and PGF in patients with non-endocrine diarrhea as well as those with the Zollinger-Ellison (Z-E) syndrome, MCT, carcinoid tumors and the WDHA syndrome. In 21 normals, PGE and PGF levels averaged 272 +/- 18 and 119 +/- 14 pg/ml, respectively. Twenty eight patients with diarrhea of non-endocrine origin (mainly inflammatory bowel disease) had levels indistinguishable from normal, i.e. 353 +/- 25 and 77 +/- 37 pg/ml, respectively. Among 29 patients with the Zollinger-Ellison syndrome (mean gastrin 6127 +/- 3267 pg/ml) only 2 had significantly elevated PGE levels; mean PGE levels, 382 +/- 32 pg/ml, were not significantly different from normal and did not correlate with either diarrhea or the serum gastrin concentration. In contrast, 18 of 22 patients with carcinoid tumors (mean blood serotonin concentration 1655 +/- 604 ng/ml; mean urinary excretion of 5 HIAA 66.8 +/- 16.7 mg/day) had elevated peripheral concentrations of PGE. The mean PGE level (1367 +/- 245 pg/ml) was significantly elevated (P less than 0.001). Nonetheless PGE levels did not correlate with diarrhea, blood concentrations of serotonin, or urinary indole excretion. MCT (mean serum calcitonin 24.5 +/- 6.3 ng/ml) was similarly associated with consistent (18/19) elevation in peripheral concentrations of PGE (mean 1922 +/- 541 pg/ml; P less than 0.001). Inthis syndrome, PGE levels were higher in patients with diarrhea and in those with markedly elevated serum thyrocalcitonin levels. Finally, 8 of 21 patients with the WDHA syndrome had increased levels of PGE. Although 13 of 17 patients had high levels of VIP (mean 8133 pg/ml), 2 patients had hyperprostaglandinemia in the face of normal peripheral concentrations of VIP. In one patient the serum PGE level was elevated prior to resection of the primary pancreatic neoplasm (9939 pg/ml) as well as the subsequent extirpation of a solitary hepatic metastasis (1063 pg/ml); following each procedure the diarrhea abated and the PGE level returned to normal. In none of these syndromes were mean PGF levels elevated. The study has documented hyperprostaglandinemia in some endocrine diarrheagenic syndromes and validated the usefullness of measurements of PGE in patients with unexplained diarrhea.

Adenoma, Islet Cell↗
PubMed1976

Release of immunoreactive serotonin following acid perfusion of the duodenum.

Cannulas were placed in the portal vein, hepatic vein, and infrarenal vena cava in eight anesthetized dogs. The duodenum of each dog was irrigated with saline (control) and 0.1 N HCI (50 ml in 10 min). Heparinized blood samples were taken from each cannula 5 min before, and 1, 5, 10, 30 and 60 min after each irrigation for measurement of immunoreactive serotonin concentrations. Serotonin concentrations did not change during saline irrigation of the duodenum. In contrast, serotonin release was consistently observed after duodenal acidification (pH 1.5-2.0). Portal venous serotonin concentrations were increased at 1 min (356 +/- 147 ng/ml) and following a biphasic pattern remained elevated at 30 and 60 min (499 +/- 131 and 489 +/- 187 ng/ml, respectively). Concentrations in the hepatic vein rose more slowly and to a lower peak (357 +/- 123 ng/ml at 10 min). Caval serotonin concentrations were increased at 10 min (342 +/- 121 ng/ml) but promptly returned to baseline levels. In the canine gastrointestinal tract, immunoreactive serotonin concentrations were highest in the duodenal bulb (15.4 mug/gm). This study demonstrated serotonin release from the duodenum following acid perfusion and documented that some of the released serotonin escaped hepatic inactivation. These findings support the possibility that serotonin may be a gastrointestinal hormone involved in the feedback inhibition of gastric acid secretion.

Animals↗
PubMed1976

Validation and application of a radioimmunoassay for serotonin.

A radioimmunoassay for serotonin (5-hydroxytryptamine) has been developed, validated, and applied to the measurement of serotonin in blood and platelet-rich plasma. Six rabbits immunized with serotonin diazotized to a DL-p-aminophenylalanine-bovine serum albumin conjugate yielded anti-serotonin antibodies. In the radioimmunoassay, antibody-containing plasma (1:100) is incubated with 0.2 pmoles of [3H]serotonin, EDTA, and either serotonin standards or unknown samples (0.1 ml). Blood levels of serotonin are measured in a protein-free supernatant prepared by water lysis of heparinized blood followed by protein precipitation using zinc hydroxide. This assay is sensitive to 100 pg of serotonin and has demonstrated insignificant cross-reactivity with a number of serotonin analogues at their normal circulating concentrations. Validation has been achieved by obtaining comparable values for normal blood serotonin concentrations by radioimmunoassay and by spectrophotofluorometry as well as by demonstrating that dilutions of endogenous serotonin in rabbit blood and blood from a patient with the carcinoid syndrome were superimposable on a standard calibration curve. In 55 normal human subjects the mean whole blood serotonin concentration was 168 +/- 13.4 ng/ml (mean +/- SEM) (range: 31 to 442 ng/ml). In 15 normal volunteers the mean radioimmunoassayable serotonin concentrations in whole blood and platelet-rich plasma were 337 +/- 40 ng/10(9) platelets and 341 +/- 37 ng/10(9) platelets, respectively. Incubation of blood with PGE1 to inhibit in vitro platelet aggregation before radioimmunoassay resulted in a significant fall in measurable serotonin activity in platelet-poor plasma (from 15.3 +/- 3.0 to 6.4 +/- 1.2 ng/ml). Seventeen normal human volunteers demonstrated a rise in circulating serotonin activity to a mean of 362.1 +/- 16.9 ng/ml at 30 min postcibal after a standard test meal, which was significantly (P less than 0.02) greater than the mean fasting level of 198.1 +/- 37.0 ng/ml. Five fasting controls did not show a rise in circulating serotonin levels when sampled at these intervals. These data suggest release of serotonin, presumably from the intestine, after a meal and make serotonin a candidate hormone in gastrointestinal physiology.

Animals↗
PubMed1976

The role of prostaglandin E in the hemodynamic response to aortic clamping and declamping.

The infrarenal aorta was occluded for one hour in 11 control dogs and in eight dogs in which biosynthesis of prostaglandin E (PGE) was inhibited by administration of indomethacin (2.5 mg. per kilogram). The mean arterial pressure (MAP) in the indomethacin group was significantly (p less than 0.001) higher than in the control group at the end of 60 minutes of aortic occlusion (187 +/- 3 vs. 137 +/- 4 mm. Hg, mean +/- S.E.M.) and remained higher (p less than 0.001) after declamping. However, the decline in MAP at the time of aortic declamping was essentially the same for both groups. Total peripheral resistance (TPR) was higher in the indomethacin group than in the control group at the end of one hour of occlusion (159 +/- 13 vs. 124 +/- 12%, p less than 0.001) and remainded higher throughout the period following occlusion. The plasma concentration of PGE in the control group increased significantly (p less than 0.05) above control (630 +/- 110 to 1,299 +/- 261 pg. per milliliter) during the 60 minute period of occlusion with further increases to 1,447 +/- 389 and 1,523 +/- 256 pg. per milliliter (p less than 0.001) at 10 and 60 seconds after declamping, respectively. In the indomethacin group, PGE remained essentially unchanged throughout the clamping and declamping period and therefore was significantly (p less than 0.05) lower than in the control group. A similar pattern was observed in the tissue levels of PGE. This study suggests that PGE is released during and after infrarenal aortic occlusion and may be responsible for maintaining reduced TPR and MAP. However, hypotension after declamping is not affected by inhibition of PGE biosynthesis.

Animals↗