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Biomedical subjects

C T Richardson

Publications and source records attributed to C T Richardson.

At least 55 records · Page 3Linked to original sources
PubMed1983

Stressful life events, acid hypersecretion, and ulcer disease.

We have evaluated 2 patients with symptomatic gastric disease who dated the onset of their illnesses to stressful events in their lives. In 1 patient, six family members had recently died and our patient feared that he too would die. The other patient was accused of grand theft, was under police surveillance, and had lost his job. Both patients had markedly increased gastric acid secretion rates that decreased to normal after hospitalization and reassurance in the first case and acquittal in the second case. Ulcer symptoms subsided at the same time as the decrease in acid secretion. Although we cannot prove that severe emotional stress in our patients led to acid hypersecretion and ulcer disease, their courses suggest that stressful life events caused increased acid secretion which, in turn, led to ulceration and symptoms.

Adult↗
PubMed1982

Parietal cell vagotomy in a surgical training program.

Parietal cell vagotomy was performed in 48 patients at the Parkland Memorial Hospital and the Dallas Veterans Administration Hospital between April 1977 and January 1981. The maximum follow-up time was 50 months and the average was 28 months. Seventy-five percent of the patients were followed for more than 1 year. There were no operative deaths. Four patients (8.3 percent) had persistent postoperative side effects including two documented ulcer recurrences (4.2 percent). Acid secretion studies were reviewed to characterize the longterm effect of parietal cell vagotomy. These studies demonstrated marked postoperative reductions in gastric acid secretion. The results of this study suggest that with the simplified technique described in this paper, parietal cell vagotomy can be performed with minimal mortality and morbidity by surgical residents under direct staff supervision.

Adolescent↗
PubMed1982

Clinical comparison of cimetidine and ranitidine.

Ranitidine is a histamine H2-receptor antagonist that differs structurally from cimetidine. We assessed its kinetics, potency, and duration of effect in patients with chronic duodenal ulcers. Ranitidine had an absorption lag time of approximately 30 min, an absorption half-life (t 1/2) of approximately 40 min, and an elimination t 1/2 of 3 hr, all differing from those of cimetidine. It is five times as potent, so that equal doses of ranitidine induce considerably longer suppression of both basal and food-stimulated gastric acid secretion than cimetidine.

Adult↗
PubMed1982

Sucralfate.

Explore the source record for details and available documents.

Aluminum↗
PubMed1981

Tiotidine and cimetidine--kinetics and dynamics.

Tiotidine and cimetidine kinetics and dynamics were compared to assess mechanisms of the longer duration of effect of tiotidine in man. Both drugs has similar lag times for absorption. Tiotidine with a meal was more slowly absorbed than when fasting and was also more slowly absorbed than cimetidine with a meal. The elimination rates for both drugs did not differ; they were both approximately 2 to 3 hr. Oral doses of cimetidine achieved areas under the plasma concentration curve approximately three times that of tiotidine but these concentrations were only 1/10 as potent. The cimetidine concentration inducing 50% inhibition of food-stimulated gastric acid secretion was 0.41 +/- 0.04 whereas it was 0.04 +/- 0.003 microgram/ml for tiotidine. The effect of tiotidine lasted longer than that of cimetidine because the doses recommended for use in man resulted in higher concentrations in plasma relative to effective concentration than clinical doses of cimetidine.

Adult↗
PubMed1981

Peptic ulcer: new therapies, new diseases.

Although hospitalizations and deaths attributable to peptic ulcer have decreased notably during the past decade, it is not certain whether this decrease is because of reduced incidence of new cases or changes in other factors, such as the severity of the disease. Several genetic traits associated with peptic ulcer have been recognized. Hyperpepsinogenemia I is the most prevalent. Peptic ulcer is a heterogeneous group of disorders with multiple genetic and environmental causes. One manifestation of the diversity of ulcer disease is the variety of physiologic abnormalities seen in patients. The use of endoscopy has enabled more reliable evaluation of new treatments. Histamine H2-receptor antagonists are the dominant mode of treatment, but increasing attention is being given to agents that enhance the resistance of the mucosa to injury, such as prostaglandins. Because of the lower frequency of side effects, proximal gastric vagotomy is gradually replacing truncal vagotomy with drainage. The possibility that endoscopic treatments, such as laser coagulation, may reduce mortality from bleeding ulcers is being investigated.

Duodenal Ulcer↗
PubMed1981

Tiotidine, a new long-acting histamine H2-receptor antagonist: comparison with cimetidine.

The effects of tiotidine, a new histamine H2-receptor antagonist, and cimetidine on food-stimulated gastric acid secretion were evaluated in duodenal ulcer patients. Homogenized steak meals were infused immediately after, 1 h after, 5 h after, and 10 h after an oral dose of medication, and food-stimulated acid secretion was measured by in vivo intragastric titration. Tiotidine and cimetidine had a similar onset of action; however, tiotidine was more potent and had a longer duration of effect. Increased potency was demonstrated by the fact that from 1 to 2 h after medication 150 mg tiotidine inhibited acid secretion to approximately the same extent as did 300 mg cimetidine, and by the fact that for a given percent inhibition of acid secretion, plasma tiotidine concentration was eight to nine times lower than plasma cimetidine concentration. Longer duration of effect was demonstrated by the fact that from 5 to 7 h after medication, acid secretion was inhibited by 80% and 97% with 150 and 300 mg tiotidine, respectively, whereas 300 mg cimetidine inhibited acid secretion by only 22%. Also, 10-12 h after medication, 150 and 300 mg tiotidine inhibited acid secretion by 22% and 53%, respectively, while 300 mg cimetidine had no inhibitory effect. The long duration of effect was due in part to increased potency and in part to a plateau in plasma concentration of tiotidine, which was maintained from 2 to 6 h after medication. Neither tiotidine nor cimetidine had a significant effect on food-stimulated gastrin release or gastric emptying of a nonabsorbable marker.

Adult↗
PubMed1981

'Partial' sham feeding releases gastrin in normal human subjects.

We determined whether sham feeding which precluded oral contact with food would release gastrin. In 16 experiments in 7 subjects, either an appetizing meal was discussed or subjects were permitted to see and/or smell a meal of their choice being prepared. In response to this 'partial' sham feeding, serum gastrin concentrations increased from 48 +/- 5 to 57 +/- 7 pg/ml (P less than 0.005). Gastric acid output also increased significantly in response to 'partial' sham feeding. These studies indicate that sham feeding releases significant amounts of gastrin in healthy human subjects and that this response is not dependent upon the presence of food in the oral cavity.

Adult↗
PubMed1980

Serum gastrin response to secretin after vagotomy.

It is unknown whether the gastrin response to secretin (secretin test) can distinguish hypergastrinemia due to vagotomy from hypergastrinemia due to Zollinger-Ellison syndrome (ZES). Therefore, we measured serum gastrin concentrations basally and in response to intravenous secretin in 13 vagotomized duodenal ulcer patients without preoperative evidence evidence of ZES and in 5 vagotomized patients with ZES. Following secretin, serum gastrin concentrations increased 40 pg/ml or less [mean (+/- SE) rise 23 +/- 3 pg/ml] in the vagotomized patients without ZES. On the other hand, in the patients with ZES serum gastrin increments after secretin ranged from 105 to 1224 pg/ml. Thus, a large (> 100 pg/ml) rise in serum gastrin concentrations following secretin in a vagotomized patient should suggest Zollinger-Ellison syndrome and not be attributed to vagotomy per se.

Diagnosis, Differential↗
PubMed1980

Effect of sham feeding on gastric emptying.

We studied the effect of vagal stimulation by sham feeding on gastric emptying in normal human subjects. When a saline test meal was infused into the stomach, simultaneous sham feeding did not alter the emptying of a nonabsorbable marker added to the meal or the volume of fluid emptied from the stomach. When a homogenized steak meal was infused, sham feeding caused a slight acceleration of emptying (47 +/- 2 vs. 53 +/- 2% marker recovered from the stomach 45 min after the meal, P less than 0.05). Gastric acid secretion in response to both meals was significantly augmented by sham feeding. Our results suggest that vagal stimulation by sham feeding has no effect on the emptying of isotonic saline and only a monor effect on gastric emptying of homogenized food in humans.

Adult↗
PubMed1980

Experience with sham feeding as a test for vagotomy.

Sham feeding is thought to stimulate gastric acid secretion solely via vagal pathways. We evaluated whether sham feeding can be used as a test for vagotomy. From results in 50 nonvagotomized subjects (28 unoperated duodenal ulcer patients and 22 healthy controls), a ratio of sham feeding-stimulated acid output to peak acid output of 0.10 or less was defined as abnormally low (with 95% confidence). The ratio of sham feeding to peak acid output was abnormally low in 28 of 41 (68%) vagotomized duodenal ulcer patients without clinical evidence of recurrent ulcer, suggesting that most of these patients had indeed had an effective reduction in vagal innervation of the stomach. On the other hand, 11 of 15 (73%) vagotomized duodenal ulcer patients with symptomatic, recurrent ulcers had normal ratios of sham feeding to peak acid secretion. That a normal ratio represented an incomplete vagotomy was independently suggested in 5 of these patients; in 1 an intact vagal trunk was confirmed at a second operation; in the other 4, acid secretion fell strikingly after transthoracic vagotomy, which would not have been expected to happen if vagotomy had initially been complete. In 5 vagotomized patients tested on two occasions, the ratio was reasonably reproducible. We conclude that a ratio of sham feeding-stimulated to peak acid output greater than 0.10 after an attempted vagotomy suggests persistent vagal innervation, whereas a ratio of 0.10 or less suggests, with at least 95% confidence, that vagotomy has been successful.

Adult↗
PubMed1980

Effect of sham feeding on gastric acid secretion in healthy subjects and duodenal ulcer patients: evidence for increased basal vagal tone in some ulcer patients.

Sham feeding augments gastric acid secretion by activating efferent vagal pathways to the stomach. If increased vagal activity in the basal state were the cause of increased basal acid secretion in some patients with duodenal ulcer, these patients might be expected to secrete little or no additional acid in response to sham feeding. To test this, we measured basal and sham feeding-stimulated acid secretion (as well as peak pentagastrin-stimulated acid output) in 29 duodenal ulcer patients and 22 healthy subjects. Four ulcer patients who had markedly increased basal acid secretion (basal/peak acid output > 0.30) and normal basal serum gastrin concentrations failed to augment acid secretion in response to sham feeding. On the other hand, patients with marked basal acid hypersection owing to hypergastrinemia (Zollinger-Ellison syndrome) responded to sham feeding with a large increase in acid secretion above basal rates. Every normal subject responded to sham feeding with an increase in acid secretion above basal rates, even when acid secretion had been stimulated by an intravenous pentagastrin infusion before beginning sham feeding. These findings suggest that in some patients with duodenal ulcer (4 of 29 in this study) increased basal acid secretion is caused by increased vagal tone.

Adult↗
PubMed1979

Duodenal-ulcer disease associated with elevated serum pepsinogen I: an inherited autosomal dominant disorder.

To delineate genetic factors involved in the pathogenesis of duodenal ulcer, serum pepsinogen I levels were determined by radioimmunoassay in two large kindreds with multiple members affected with duodenal ulcer. An elevated serum immunoreactive pepsinogen I concentration (greater than 100 ng per milliliter) segregated as an autosomal dominant trait in these families. Furthermore, 10 of 11 patients with clinical ulcer disease in these families had hyperpepsinogenemia. An elevated serum pepsinogen I concentration appears to be a subclinical marker of the ulcer diathesis in families with this autosomal dominant form of peptic-ulcer disease.

Duodenal Ulcer↗
PubMed1979

Effect of atropine on vagal release of gastrin and pancreatic polypeptide.

We studied the effect of several doses of atropine on the serum gastrin and pancreatic polypeptide responses to vagal stimulation in healthy human subjects. Vagal stimulation was induced by sham feeding. To eliminate the effect of gastric acidity on gastrin release, gastric pH was held constant (pH 5) and acid secretion was measured by intragastric titration. Although a small dose of atropine (2.3 mug/kg) significantly inhibited the acid secretory response and completely abolished the pancreatic polypeptide response to sham feeding, this dose of atropine significantly enhanced the gastrin response. Higher atropine doses (7.0 and 21.0 mug/kg) had effects on gastrin and pancreatic polypeptide release which were similar to the 2.3-mug/kg dose. Atropine (0.78 and 2.3 mug/kg) without sham feeding significantly inhibited basal acid secretion and also led to significant increases in serum gastrin above basal levels. The gastrin response to sham feeding with 2.3 mug/kg atropine was significantly greater than the sum of the gastrin responses to sham feeding alone and to 2.3 mug/kg atropine alone, indicating potentiation of vagal gastrin release by atropine. We conclude: (a) Unlike vagally mediated gastric acid secretion and pancreatic polypeptide release which can be blocked by atropine, vagal gastrin release is potentiated by atropine. This observation suggests the existence of a vagal-cholinergic pathway which normally (i.e., in the absence of atropine) inhibits gastrin release. (b) Because atropine (without sham feeding) increased basal gastrin levels, it is likely that the cholinergic pathway which inhibits gastrin release is active even when the vagus nerve is not stimulated by sham feeding.

Adult↗
PubMed1979

Effect of selective proximal vagotomy on food-stimulated gastric acid secretion and gastrin release in patients with duodenal ulcer.

We studied effects of selective proximal vagotomy on food-stimulated acid secretion and gastrin release in 7 duodenal ulcer patients. Food-stimulated acid secretion was evaluated by sham feeding patients and by infusing food directly into their stomachs. Vagotomy reduced sham feeding-stimulated acid secretion from 28.2 +/- 4.6 to 1.2 +/- 0.7 meq/hr (95% reduction) whereas infused food-stimulated secretion was decreased from 36.1 +/- 4.6 to 17.9 +/- 5.5 meq/hr (50% reduction). In contrast to the reductions in acid secretion, the gastrin response to infused food doubled after surgery. Although selective proximal vagotomy reduced the rate of acid secretion in response to infused food and also reduced by 64% the peak secretory capacity (peak acid output to pentagastrin), fractional secretion (i.e., the secretion rate in response to infused food expressed as a percentage of the peak secretory capacity) increased significantly after vagotomy from 63 +/- 7% to 91 +/- 11%. This increased fractional secretion in response to infused food was probably a result of exaggerated gastrin release after vagotomy.

Adult↗