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Biomedical subjects

M Feldman

Publications and source records attributed to M Feldman.

At least 289 records · Page 16Linked to original sources
PubMed1986

Inhibitory effects of beta-adrenergic agonists on gastric acid secretion in dogs.

We evaluated the effect of two beta-adrenergic agonists, isoproterenol (nonselective agonist) and terbutaline (selective beta 2-agonist), on gastric acid secretion stimulated by intravenous pentagastrin, bethanechol, or histamine in dogs with gastric fistulas. Intravenous infusion of isoproterenol or terbutaline inhibited pentagastrin-stimulated acid secretion to a significantly greater extent than they inhibited bethanechol- or histamine-stimulated acid secretion. For example, isoproterenol (12 micrograms X kg-1 X h-1) reduced mean pentagastrin-, bethanechol-, and histamine-stimulated acid output by 86, 63, and 14%, respectively. Percent inhibition of acid secretion with terbutaline (30 micrograms X kg-1 X h-1) averaged 60, 17, and 24% for pentagastrin, bethanechol, and histamine, respectively. Terbutaline also inhibited pentagastrin-stimulated acid secretion from vagally denervated fundic pouches in a dose-related manner. Plasma somatostatin-like immunoreactivity was significantly higher during infusion of terbutaline plus pentagastrin than during infusion of pentagastrin alone. However, an intravenous infusion of 0.3 microgram X kg-1 X h-1 somatostatin-14 had no effect on pentagastrin-stimulated acid secretion from the gastric fistula, even though this infusion increased plasma somatostatin-like immunoreactivity to the same extent as terbutaline plus pentagastrin infusion. Thus the amount of somatostatin released during terbutaline infusion was not sufficient to explain the inhibition of pentagastrin-stimulated acid secretion observed.

Adrenergic beta-Agonists↗
PubMed1986

Comparison of acid secretory responsiveness to gastrin heptadecapeptide and of gastrin heptadecapeptide pharmacokinetics in duodenal ulcer patients and normal subjects.

Serum gastrin concentrations and gastric acid secretion were measured during intravenous infusion of gastrin heptadecapeptide (G-17) (0, 7, 22.1, 70, 221, and 700 pmol/kg X h) in 15 duodenal ulcer patients and 15 healthy controls. Ulcer patients developed higher serum gastrin concentrations during G-17 infusion due to nearly twofold slower clearance of gastrin (8.8 vs. 15.7 ml/kg X min; P less than 0.01). Despite slower clearance of G-17, ulcer patients had plasma elimination half-times for G-17 similar to controls (6.0 vs. 6.1 min, respectively). Thus, calculated volume of distribution for G-17 was lower in ulcer patients than controls (78.5 vs. 140.7 ml/kg; P less than 0.025). For any serum gastrin during gastrin-17 infusion, acid secretion (millimoles per hour) was higher in ulcer patients than in controls. However, when acid secretion was expressed as a percentage of peak acid output to G-17 (to correct for differences in parietal cell mass), curves relating acid secretion to serum gastrin were identical in ulcer patients and controls.

Adult↗
PubMed1986

Psychiatric, neurological, and psychoeducational characteristics of 15 death row inmates in the United States.

The authors present the results of clinical evaluations of 15 death row inmates, chosen for examination because of the imminence of their executions and not for evidence of neuropsychopathology. All had histories of severe head injury, five had major neurological impairment, and seven others had other, less serious neurological problems (e.g., blackouts, soft signs). Psychoeducational testing provided further evidence of CNS dysfunction. Six subjects had schizophreniform psychoses antedating incarceration and two others were manic-depressive. The authors conclude that many condemned individuals probably suffer unrecognized severe psychiatric, neurological, and cognitive disorders relevant to considerations of mitigation.

Adult↗
PubMed1986

The significance of recurrent childhood respiratory disorders in flight training applicants.

A random sample of 1700 18-year-old applicants for flight training, who had been free from respiratory symptoms for 1 year or more, was screened for respiratory symptoms in the past. Those who denied such a history had a questionnaire sent to their parents for further verification. Altogether 70 subjects with a past history of "wheezing," "asthma," or "spastic bronchitis" were thus identified. Abnormalities in either FEV1/FVC, Vmax50 or Vmax75 were found in 40% of the subjects with a history of childhood "wheezing," "asthma," or "spastic bronchitis," but only in 8% of controls without such a history. A history of wheezing had no effect on the RV/TLC ratio. The age at which the last bout had occurred had no apparent effect on the degree of flow abnormalities. The most sensitive index for a flow abnormality was Vmax50, which was less than 74% of the predicted values in 2/(30%) of the 70 subjects tested. It is concluded that, in subjects with a history of "wheezing," "asthma," or "spastic bronchitis," flow abnormalities may persist even after prolonged remissions.

Adolescent↗
PubMed1986

General anesthesia during excision of a mouse tumor accelerates postsurgical growth of metastases by suppression of natural killer cell activity.

Our previous studies indicated that anesthetic drugs cause acceleration of postoperative metastasis of mouse tumors. We tested whether this augmentation could be attributed to a decrease in natural killer (NK) activity. The results indicated that two of the anesthetic drugs used during excision of the Lewis lung carcinoma (3LL) tumor, halothane and ketamine, decreased NK activity, whereas the other two, thiopental sodium and N2O, had no effect on NK activity in in vitro assays. The observed decrease in NK cell activity was reversed following treatment with polyinosinic-polycytidylic acid (poly I:C), which is an NK cell potentiator. Treatment of mice with poly I:C abolished the accelerated growth of metastases following excision of the tumor under ketamine or halothane anesthesia. On the other hand, treatment with poly I:C seemed to have no effect on acceleration of postoperative metastasis in mice anesthetized with N2O or thiopental sodium.

Anesthesia, General↗
PubMed1986

Filicidal abuse in the histories of 15 condemned murderers.

This paper describes the family characteristics of 15 Death Row inmates. It documents extraordinary physical and/or sexual abuse in 13 cases. It describes murderous behaviors of parents toward children in 8 cases and documents ongoing hostility and neglect throughout childhood and adulthood. The paper explores the mechanisms by which such abuse may contribute to violent behaviors. It highlights the relevance of these findings to the outcome of sentencing in capital cases.

Capital Punishment↗
PubMed1985

Effect of atropine on plasma gastrin and somatostatin concentrations during sham feeding in man.

The purpose of these studies was to measure circulating gastrin and somatostatin concentrations during sham feeding in humans and to evaluate the effect of two doses of intravenous atropine on circulating concentrations of these peptides. Gastric acid and bicarbonate secretion and pulse rate were also measured. Sham feeding increased plasma gastrin concentrations by approximately 15 pg/ml but had no effect on plasma somatostatin-like immunoreactivity (SLI). A small dose of atropine (5 micrograms/kg) augmented plasma gastrin concentrations during sham feeding significantly (P less than 0.01), but did not affect plasma SLI. Atropine also significantly inhibited gastric acid secretion and gastric bicarbonate secretion (by 62% and 52%, respectively), but pulse rate was not affected. A larger dose of atropine (15 micrograms/kg intravenously) suppressed plasma gastrin concentrations significantly compared to the smaller 5 micrograms/kg atropine dose (P less than 0.02), so that plasma gastrin concentrations when 15 micrograms/kg atropine was given were not significantly different from those during the control study. 15 micrograms/kg atropine reduced gastric acid and bicarbonate secretion by 81% and 66%, respectively, and also increased pulse rate by 15 min-1. These studies indicate that small doses of atropine enhance vagally mediated gastrin release in humans, probably by blocking a cholinergic inhibitory pathway for gastrin release. Although the nature of this cholinergic inhibitory mechanism is unclear, we found no evidence to incriminate somatostatin. Our finding that the larger dose of atropine reduced serum gastrin concentrations compared with the smaller dose suggests that certain vagal-cholinergic pathways may facilitate gastrin release.

Adult↗
PubMed1985

Treatment of Zollinger-Ellison syndrome with exploratory laparotomy, proximal gastric vagotomy, and H2-receptor antagonists. A prospective study.

Twenty-two patients with Zollinger-Ellison syndrome were managed by a combined medical and surgical approach. Patients were treated initially with cimetidine or ranitidine. A laparotomy was performed to remove easily resectable tumors and to carry out a proximal gastric vagotomy. Tumors were found in 9 patients (41%) and all visible tumors were removed from 6 of the 9 patients. Fasting serum gastrin concentrations and serum gastrin responses to intravenous secretin were normal 6 wk after surgery in each of the patients from whom all visible tumors were resected and are normal in 4 patients, 6 wk to 5 yr after surgery. Acid secretion was reduced after vagotomy in each patient, even when tumors were not found or completely resected. Thus, vagotomy decreased the acid secretory response to endogenous hypergastrinemia. In addition, vagotomy augmented the inhibitory effect of H2-receptor antagonists on acid secretion. Follow-up has ranged from 6 wk to 6 yr (median, 2 yr). Dosages of cimetidine or ranitidine have been reduced, compared with preoperative amounts, in all but 1 patient. Two patients are taking no antisecretory drugs. Only 3 patients have had occasional symptoms of ulcer disease. Complications such as bleeding, perforation, or obstruction have not occurred in any patient. Endoscopy was performed in all patients to estimate the point prevalence of active ulcers and an ulcer was found in 1 patient. Based on these results, it is our opinion that this combined medical and surgical approach is an effective treatment for patients with Zollinger-Ellison syndrome.

Adolescent↗
PubMed1985

Effect of histamine and cimetidine on amino acid meal-stimulated gastrin release at a controlled intragastric pH in healthy human beings.

Results of several experiments have suggested that histamine-2 receptors play an inhibitory role in regulating gastrin release. We evaluated this prospectively in healthy human beings by infusing intravenously either histamine (0.33 micrograms/kg/min) or cimetidine (3.33 mg/min) during a continuous 3-h intragastric infusion of a 3% mixed amino acid meal, a potent stimulus of gastrin release. In order to be certain that effects of histamine or cimetidine on gastrin release were independent of their known effects on gastric acid secretion, intragastric pH was maintained at 5.0 by in vivo intragastric titration with sodium bicarbonate or hydrochloric acid. Although histamine and cimetidine had significant effects on gastric acid secretion, neither significantly affected the rises in serum gastrin concentrations during intragastric amino acid infusion. For example, mean gastrin rises above basal concentrations were 39 +/- 9 pg/ml on the control day, 39 +/- 9 pg/ml on the histamine day and 44 +/- 11 pg/ml on the cimetidine day (P greater than 0.05). Thus, blockade or stimulation of H2-receptors at the doses tested had no effect on gastrin release in response to an amino acid meal in humans when intragastric pH was maintained at 5.0.

Adult↗
PubMed1985

Effect of oral nalmefene, an opiate-receptor antagonist, on meal-stimulated gastric acid secretion and serum gastrin concentration in man.

We evaluated whether nalmefene, an orally administered opiate-receptor antagonist, would inhibit gastric acid secretion in response to a meal in healthy humans. On separate days either 50 mg nalmefene or a placebo tablet was administered by mouth 90 min before a blenderized steak meal was infused into the stomach through a nasogastric tube. Compared to placebo, nalmefene inhibited meal-stimulated acid secretion in each of 6 subjects studied (P less than 0.05). During the second and third hours after the meal, nalmefene inhibited mean acid secretion by 16%. Nalmefene also resulted in significantly higher meal-stimulated serum gastrin concentrations than placebo (P less than 0.05) even though intragastric pH was kept constant at 5.0 in both experiments. These studies indicate that an orally administered opiate-receptor antagonist can inhibit gastric acid secretion in response to a meal in humans, yet increase meal-stimulated serum gastrin concentrations.

Adult↗
PubMed1985

Gastric bicarbonate secretion in patients with duodenal ulcer.

The gastric mucosa secretes both acid and bicarbonate. In patients with duodenal ulcers, gastric acid hypersecretion is well-established. However, gastric bicarbonate secretion rates in these patients have not been reported. Accordingly, we calculated gastric acid and bicarbonate secretion rates in 13 patients with duodenal ulcer and 13 healthy subjects (controls) using a recently validated method that uses measurements of gastric juice volume, acidity (hydrogen-ion concentration), and osmolality. Non-parietal and parietal gastric volume secretion were also calculated. Although ulcer patients secreted significantly more acid than controls under basal conditions and during a submaximal intravenous pentagastrin infusion, they secreted similar amounts of bicarbonate. Ulcer patients secreted significantly more parietal and nonparietal fluid than controls. Increased nonparietal secretions in duodenal ulcer patients diluted excessive, acidic parietal secretions, preventing significant differences in gastric acidity in ulcer patients and control subjects (50.1 +/- 8.7 vs. 44.0 +/- 9.7 mmol/L basally; 111.0 +/- 3.1 vs. 102.4 +/- 7.5 mmol/L during pentagastrin infusion, respectively). These studies indicate that gastric bicarbonate secretion is close to normal in patients with duodenal ulcer, whereas acid secretion from parietal cells and nonparietal volume secretion are greater than normal.

Adult↗
PubMed1985

Transthoracic vagotomy for postoperative peptic ulcer. Effects on basal, sham feeding- and pentagastrin-stimulated acid secretion, and on clinical outcome.

Transthoracic vagotomy was performed in 16 patients with postoperative peptic ulcer diagnosed by endoscopy. Transabdominal vagotomy had been attempted at a previous operation in 10 patients. Five patients had been treated previously by subtotal gastrectomy without vagotomy and one had had gastrojejunostomy without vagotomy. Three of the 16 patients had had no previous gastric resection. Before transthoracic vagotomy, the ratio of sham feeding-stimulated acid output (SAO) to peak pentagastrin-stimulated acid output (PAO) was greater than 0.10 in each patient, suggesting intact vagal innervation of the stomach (mean ratio: 0.44; range: 0.17-0.79). After transthoracic vagotomy, SAO and PAO decreased by 98 +/- 1% and 73 +/- 8%, respectively. There was no operative mortality, and a clinically important postoperative complication developed in only one patient. Two patients had delayed gastric emptying transiently, and three have developed diarrhea. No patient has developed recurrent peptic ulceration or ulcer complications during a mean follow-up period of 3.9 years (range: 1.0-7.5 years). This study indicates that: (1) sham feeding is useful for identifying patients to undergo transthoracic vagotomy, and (2) transthoracic vagotomy is a safe and effective means of reducing acid secretion and preventing peptic ulcer recurrence, regardless of previous operation.

Adult↗
PubMed1985

Gastric H+ and HCO3- secretion in response to sham feeding in humans.

Sham feeding (SF) was used to evaluate the effect of physiological vagal stimulation on gastric acid (H+) and bicarbonate (HCO3-) secretion in humans, as well as on parietal and nonparietal volume secretion. A recently validated method, derived from a two-component model of gastric secretion, was employed. SF increased both H+ secretion from parietal cells (P less than 0.001) and HCO3- secretion from nonparietal cells (P less than 0.01), although the H+ response was greater and more prolonged. Atropine significantly inhibited not only H+ secretion but also HCO3- and nonparietal volume secretion. Peak H+ secretion during SF averaged approximately 27 mmol/h, whereas peak HCO3- secretion averaged approximately 6 mmol/h. When H+ secretion was already maximally stimulated by an intravenous pentagastrin infusion, SF actually reduced gastric juice acidity and osmolality due to neutralization of H+ by HCO3- and to dilution of H+ by nonparietal secretions. These studies therefore indicate that vagal stimulation induced by SF increases both H+ and HCO3- secretion in humans and that this process is cholinergically dependent.

Adult↗
PubMed1985

Effect of pentagastrin on gastric mucosal histamine in dogs.

We studied the effect of pentagastrin on histamine content of gastric mucosa obtained from dogs with gastric fistulas to determine whether pentagastrin mobilizes cellular stores of histamine. Experiments were also performed on canine gastric mucosa in vitro to investigate the effects of pentagastrin on histamine release, per se. During in vivo studies basal histamine content averaged 0.9 nmol/mg wet wt tissue or 18.8 nmol/mg tissue prot. No significant difference in gastric mucosal histamine content occurred during intravenous administration of pentagastrin (6 or 16 micrograms . kg-1 . h-1) or saline (control), even though acid output from the gastric fistula increased significantly above control during pentagastrin infusion. Moreover, pentagastrin (10(-5) and 10(-8)M) did not release more histamine from gastric mucosa in vitro than the buffer (control), whereas Triton X-100 and the phorbol ester 4 beta-phorbol 12 beta-myristate 13 alpha-acetate, alone and in combination with calcium ionophore A23187, released significant amounts of histamine above control values. From these experiments we conclude that pentagastrin did not alter histamine content of canine gastric mucosa in vivo, even though acid secretion was stimulated maximally, nor did pentagastrin release histamine in vitro.

Animals↗
PubMed1985

Effect of human beta-endorphin on plasma aldosterone concentrations in normal human subjects.

beta-Endorphin recently was proposed as a possible physiological stimulus of aldosterone secretion based on studies in animals. Since human beta-endorphin (beta h-endorphin) does not contain the ACTH-(4-10) homology common to other ACTH-related neuropeptides that stimulate aldosterone, its mechanism of stimulation might differ from that of the other peptides. In the present study, we infused beta h-endorphin into six normal subjects under carefully controlled conditions at dosage levels several orders of magnitude higher than endogenous levels. No increase in plasma aldosterone was found in these subjects ingesting a normal sodium intake despite the fact that other biological actions of beta h-endorphin were manifest. By contrast, an equimolar infusion of ACTH-(1-24) caused a significant increase in plasma aldosterone. These studies do not support a significant role for beta h-endorphin in control of aldosterone secretion in man and are consistent with the concept that the ACTH-(4-10) amino acid sequence, common to ACTH, beta-lipotropin, gamma-lipotropin, beta MSH, and alpha MSH, is a major determinant of their aldosterone-stimulating capacity.

Adult↗