Search PubMed⌕ Search

Biomedical subjects

G Stacher

Publications and source records attributed to G Stacher.

At least 109 records · Page 6Linked to original sources
PubMed1976

Effect of alterations of blood glucose levels on gastric acid secretion, plasma gastrin, and plasma osmolality in man.

In 16 experiments on 4 healthy subjects, the effect of procedures which alter blood glucose, ie, infusion of 0.2 units/kg body wt/hr insulin and/or 0.66 g/kg body wt/hr glucose, on gastric acid secretion, plasma gastrin, and plasma osmolality was studied, Each subject underwent four different experimental procedures, each lasting 4 hr. All had in common one basal hour and the infusion of insulin in the second hour, but differed in the time of infusion of glucose or isotonic saline. To control for order effects, the four procedures were applied to the subjects in the form of a Latin square. Acid output was measured continuously be means of intragastric titration and a telemetering capsule; blood glucose, plasma gastrin, and plasma osmolaity were determined in 15-min intervals. An inverse relationship between blood glucose and acid output was found: Low glucose levels were associated with high rates of acid secretion, high glucose levels with low acid secretion. No noticeable changes occurred in either plasma gastrin or plasma osmolality. These results reveal a determining influence of blood glucose levels on acid secretion. On the basis of earlier work in animals it is concluded that this influence is exerted via the reciprocal activities of the hypothalamic satiety and feeding centers.

Adult↗
PubMed1976

Effect of bromazepam on gastric acid secretion related to hypnotically induced anxiety.

The effects of bromazepam (0.1 mg/kg b.w. i.v.) and of placebo on gastric acid secretion related to hypnotically induced anxiety were evaluated in a double blind study, 22 experiments were carried out on 4 healthy volunteers. Drugs were injected after one basal hour. Hypnosis was induced immediately thereafter, and a sequence of anxiety-charged situations out of the subjects past was recalled. After one hour, posthypnotic amnesia was suggested, the subjects awakened and observation continued for another hour. Acid output was measured by means of intragastric titration and a telemetering capsule. During hypnosis and recalling of anxiety in both series, acid output decreased. In the posthypnotic hour there was a significant increase of secretion in the placebo-series, while there was virtually no change in the the bromazepam-series. The pattern of acid output in the placebo-series seems to result from an activation of the sympathetic system under anxiety and a rebound vagal activation in the posthypnotic hour. By contrast, under the sedating effect of bromazepam, no anxiety could be evoked and no rebound vagal activation and thereby no increase of acid secretion resulted.

Adult↗
PubMed1976

Inhibitory effect of an intravenous glucose load on basal and insulin-stimulated gastric acid secretion in man.

The effect of intravenous glucose on basal and insulin-stimulated gastric acid secretion was investigated in a crossover study on four healthy subjects. Acid output was measured by means of intragastric titration and a telemetering capsule; serum-gastrin and blood glucose levels were measured in 15-minute-intervals. Two different experiments were carried out on each subject. After one basal hour in series (a), 2 ml saline, and in series (b), 0.2 U/kg b. w. glucagon-free insulin were injected intravenously. Two hours later, in both series 0.66 g/kg b. w. glucose were given by rapid i.v. infusion, and the experiment continued for another hour. Hyperglycemia was found to depress significantly basal as well as insulin-stimulated acid secretion, while serum-gastrin levels showed no systematic variation. On the basis of these findings and of earlier studies in animals, it is concluded that the inhibitory effect of hyperglycemia is due to a central action, i.e., an increased activity of the satiety center.

Adult↗
PubMed1976

Gastric acid secretion, serum-gastrin levels and psychomotor function under the influence of placebo, insulin-hypoglycemia, and/or bromazepam.

Gastric acid output, blood-glucose, serum-gastrin and psychomotor-performance were measured in four healthy subjects one hour before and two hours after the intravenous injection of (a) 2ml saline, (b) 0.2 U/kg b.w. insulin, (c) 0.1 mg/kg b.w. bromazepam. Each subject underwent one experiment of each type. The study was layed out as a Latin-square and analysed accordingly. Gastric acid secretion was measured by means of intragastric titration and a telemetering capsule; blood-glucose and serum-gastrin levels as well as psychomotor performance as a measure of vigilance were determined in 15-minute-intervals. In the saline series (a), none of the four parameters showed any systematic variation. In series (b), a bimodal response of acid output to insulin, initial inhibition and subsequent stimulation was observed in all subjects. Serum-gastrin levels showed only a slight and transient increase in the first thirty minutes. Psychomotor performance decreased markedly with progressing hypoglycemia, and increased when glucose levels rose again. In the bromazepan series (c), acid output and psychomotor performance decreased and, after the first hour, increased almost parallely, while glucose and gastrin levels remained unchanged. In series (d), an additive effect of insulin and bromazepam occurred: acid output and psychomotor performance were lower than after insulin alone; peak acid secretion, maximal hypoglycemia and peak of serum-gastrin were shifted to the right. It is concluded that the lowered basal as well as insulin-stimulated acid secretion after bromazepam is due to the central effect of the drug, and that this effect is mediated to the gastric glands directly via autonomic nervous pathways without involving a release of endogenous gastrin.

Adult↗
PubMed1975

Inhibitory effect of bromazepam on insulin-stimulated gastric acid secretion in man.

The action of bromazepam on insulin-stimulated gastric acid secretion was examined in 5 healthy volunteers in a randomized study. To measure acid output, the intragastric titration technique and a pH-sensitive telemetering capsule were used. Three series of experiments were performed: (1) insulin (0.2 U/kg body weight), stimulation alone; (2) simultaneous injection of insulin and bromazepam (0.1 mg/kg body weight), subjects kept awake; (3) synchronous injection of insulin and bromazepam but with subjects allowed to fall asleep after drug administration. In all three series after insulin administration a significant initial inhibition of gastric secretion occurred. There were no significant differences between the three series regarding the intensity of hypoglycemia. Blood glucose levels lower than 25 mg/100 ml were reached in all experiments. Bromazepam in subjects kept awake caused drowsiness and a lower gastric acid response to hypoglycemia as compared to insulin alone, but the difference was not significant. In subjects allowed to sleep, this reduction was marked and gastric acid output was significantly lower than in both other series. These findings suggest that sleep and drowsiness, rather than bromazepam itself, cause inhibition of insulin-induced gastric secretion.

Analysis of Variance↗
PubMed1975

Effect of acupuncture of pain threshold and pain tolerance determined by electrical stimulation of the skin: a controlled study.

The effect of needling traditional acupuncture loci (Ho-Ku, LI4; Nei-Kuan, EH-6) compared to arbitarily chosen points was measured in twelve healthy subjects. In a crossover blind study pain tolerance and pain threshold were measured by electrical stimulation of the skin in the thyroid area. Traditional acupuncture was found to be significantly more effective in elevating pain threshold than needling of arbitarily chosen points. Pain tolerance also rose more under "real" acupuncture, the difference, however, being statistically not significant. In one subject, threshold and tolerance increased more under needling of nonacupuncture loci, while two subjects did not show any changes under either procedure.

Acupuncture Therapy↗
PubMed1975

Gastric acid secretion and sleep stages during natural night sleep.

Gastric acid secretion during natural sleep was studied in 4 healthy female volunteers for 11 nights. Acid output was measured by means of intragastric titration and a telemetering capsule, and sleep was monitored continuously by recording EEG and eye movements. Compared to the waking state, sleep was found to be associated with significantly lower levels of acid secretion. Although there were no significant differences between acid secretion during sleep stages 1 to 4 and rapid eye movement (REM), acid secretion decreased with deeper stages of sleep. During all REM phases only small amounts of acid were produced. Arousal or periods of waking in the course of the night, as well as waking in the morning, were associated with an increase in acid output.

Adult↗
PubMed1975

Action of six commonly used benzodiazepines on isolated guinea-pig ileum preparation.

The spasmolytic activity of six commonly used benzodiazepines was investigated on isolated guinea-pig ileum preparation. All six substances proved to be non-competitive antagonists of carbachol and barium chloride, the pD'2 values ranging between 3.23 and 4.37 in the presence of either agonist. The significance of these findings is discussed.

Animals↗
PubMed1974

Inhibitory effect of bromazepam on basal and betazole-stimulated gastric acid secretion in man.

Basal, as well as betazole-stimulated gastric acid secretion in man is reduced after the intravenous administration of bromazepam. In subjects staying awake, this reduction is limited to the first two 15-minute periods. The reduction is highly significant in subjects who fall asleep after receiving the drug. Natural sleep causes the same depression. The low level of acid secretion is maintained until the subjects are awakened when there is a sharp and highly significant rise. Acid secretion in subjects who fall asleep after the simultaneous administration of betazole and bromazepam is significantly higher than after the administration of bromazepam alone. Sleep causes a much greater depression of basal and betazole-stimulated acid secretion than does the benzodiazepine itself. Acid secretion was measured by continuous intragastric titration and a pH-sensitive endoradiosonde.

Adult↗