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Biomedical subjects

H Abrahamsson

Publications and source records attributed to H Abrahamsson.

At least 91 records · Page 5Linked to original sources
PubMed1984

Mobilization of 45Ca from insulin-producing RINm5F cells attached to microcarriers.

A technique was designed allowing studies of 45Ca efflux from insulin-releasing cells of a clonal cell line (RINm5F) attached to fibronectin-coated plastic beads. Supporting the existence of Ca2+-Ca2+ and Na+-Ca2+ exchange mechanisms, the efflux of 45Ca in a Ca2+-deficient perifusion medium was increased after introduction of Ca2+ and decreased after removal of Na+. The washout of radioactivity was similar to that from pancreatic islets in also being inhibited by glucose in the presence of low concentrations of extracellular Ca2+. During perifusion with a medium containing 2.56 mM Ca2+, increasing the K+ concentration resulted in an increased 45Ca efflux, a process counteracted by D-600. Also, exposure to tolbutamide resulted in a distinct stimulatory peak. Glucose was a poor stimulator of 45Ca efflux, suggesting that this sugar lacks the ability to depolarize the RINm5F cells sufficiently to induce normal opening of the voltage-dependent channels in the plasma membrane. Such a defect might well explain why the RINm5F cells do not respond to glucose with stimulation of insulin release.

Animals↗
PubMed1984

Reflex inhibition of gastric motility pathophysiological aspects.

Inhibition of gastric motility in response to abdominal trauma was studied in anesthetized cats. Nociceptive stimuli to the gut inhibited the stomach via two different reflex mechanisms. One reflex was strictly spinal and adrenergic inhibiting cholinergic neurons in the stomach. Stimuli to the stomach, small intestine and proximal colon induced stronger adrenergic inhibition than stimuli to distal colon. The second inhibitory mechanism was a vagal nonadrenergic inhibition of gastric tone evoked from all parts of the intestine via spinal afferents. This vagal reflex disturbed gastric electrical control potentials parallel to the motor inhibition. The vagal nonadrenergic and the sympatho-adrenergic reflexes seem to act together in suppressing gastric tone. Adrenal medullary activity was not essential for the gastric response to abdominal trauma.

Abdominal Injuries↗
PubMed1984

Sympathetic nervous control of gastric motility and interaction with vagal activity.

Gastro-gastric reflexes controlling gastric motility were studied in anaesthetized cats. Distensions and contractions of the gastric wall elicited two different inhibitory responses: 1) A spinal adrenergic reflex inhibiting cholinergic neurons in the gastric wall leading to suppression of rhythmic gastric contractions and increasing gastric reservoir capacity. 2) A vago-vagal reflex involving non-adrenergic vagal fibres to the stomach. This latter storage reflex seems to be of major importance for gastric reservoir capacity. It is concluded that stimulation of gastric mechanoreceptors activates sympathetic adrenergic reflexes which together with simultaneously activated vagal inhibitory reflexes can influence gastric contractions and reservoir capacity.

Animals↗
PubMed1983

Purification of mitochondria and secretory granules isolated from pancreatic beta cells using Percoll and Sephacryl S-1000 superfine.

Mitochondria and secretory granules were isolated from beta-cell-rich pancreatic islets of ob/ob mice. Crude fractions obtained by differential centrifugation were subjected to centrifugation on isotonic Percoll. The gradient medium was removed from the resulting fractions by gel filtration on Sephacryl S-1000 Superfine. When compared to the crude fractions, the purified mitochondrial fraction exhibited a 4.5-fold increase in citrate synthase activity, a 70% reduction of lysosomal arylsulfatase, and a 40% decrease of contamination with granular insulin. In the purified secretory granule fraction, the insulin content was as high as 60% of the total protein (albumin standard) with arylsulfatase unchanged and no detectable citrate synthase activity.

Animals↗
PubMed1983

Depolarization-independent net uptake of calcium into clonal insulin-releasing cells exposed to glucose.

Insulin release, net fluxes of Ca2+, and glucose metabolism were studied in a clonal cell line (RINm5F) established from a transplantable rat islet tumor. The insulin content amounted to only 0.03% of that of the total protein and decreased even further with subsequent passages. The insulin secretion was as high as 10 to 20% of the total hormone content per hour. Insulin release was stimulated by K+ depolarization but not by exposure to glucose. In contrast to this secretory pattern, glucose but not K+ stimulated the net uptake of Ca2+ at micromolar concentrations of the ion. The glucose effect was not mimicked by 20 mM 3-O-methylglucose. It was as pronounced at 1 mM as at 20 mM of the sugar and corresponded to an uptake of 119 fmol cm-2 s-1. Glucose metabolism was typical for tumor cells with a high glycolytic flux and an oxidation-to-utilization ratio as low as 0.05-0.15. Maximal oxidative degradation was attained already at 1 mM. This concentration was also equivalent to the Km for glucose utilization, indicating a substantial left-hand shift of the normal dose-response curve. It is suggested that glucose induces a depolarization-independent net uptake of Ca2+ by favouring intracellular buffering of the cation.

Adenoma, Islet Cell↗
PubMed1983

Effects of beta-adrenoceptor blocking drugs on human sigmoid colonic motility.

Effects of propranolol and metoprolol on sigmoid colonic motility were studied in 12 healthy volunteers in a double-blind randomized fashion. Colonic pressure was recorded 15-18 cm from anus and contractile activity quantified for periods of 25 min. On separate days propranolol, metoprolol, and placebo, respectively, was administered intravenously preceded by a control period. After propranolol, 10 mg intravenously, pressure activity increased significantly from 3.8 +/- 1.1 (SEM) kPa X min (28 +/- 8 mm Hg X min) to 5.9 +/- 1.0 kPa X min (44 +/- 8 mm Hg X min) (P less than 0.001). Also, after propranolol, 5 mg intravenously, the pressure activity was increased (P less than 0.05). After metoprolol, 10 mg intravenously, contractile activity increased from 4.3 +/- 0.9 kPa X min (32 +/- 7 mm Hg X min) to 6.1 +/- 1.0 kPa X min (46 +/- 8 mm Hg X min) (P less than 0.01). The two drugs caused equipotent reduction of heart rate. After placebo, no effect on sigmoid pressure or heart rate was observed. The study shows that unselective (propranolol) and beta 1-selective (metoprolol) beta-blocking drugs enhance distal colonic pressure in man. Colonic motility seems to be under sympathetic beta-adrenergic influence even under fairly unstrained conditions.

Adrenergic beta-Antagonists↗
PubMed1981

Influence of external calcium ions on labelled calcium efflux from pancreatic beta-cells and insulin granules in mice.

Addition of Ca2+ to a glucose-free perifusion medium stimulated the efflux of 45Ca from prelabelled pancreatic islets isolated from ob/ob-mice. This effect differed from that of glucose in being transient, markedly stimulated by previous exposure to a Ca2+-deficient medium and resulting in mobilization also of substantial amounts of 45Ca incorporated in the absence of glucose. The glucose action on 45Ca efflux reflected the balance between inhibitory and stimulatory components which differed with respect to their chronological order and sensitivity to glucose. The magnitude of the stimulatory phase was related linearly to the extracellular concentration of Ca2+ up to 2.40 mM. The efflux of 45Ca from isolated secretory granules was stimulated by Mg-ATP. The latter made the 45Ca efflux from the granules sensitive to Ca2+; significant stimulation being seen when increasing the medium Ca2+ from 0.1 to 10 microM. The results support the concept of an efficient Ca/Ca exchange mechanism in the depolarized beta-cells, emphasizing a role for the secretory granules in this process.

Animals↗
PubMed1981

Effects of propranolol on colonic pressure in patients with irritable bowel syndrome.

The effect of propranolol on colonic motility was studied in 10 patients with irritable bowel syndrome. Colonic motility was recorded by pressure measurement 15-18 cm from the anus, and total contractile activity (kPa x min) simultaneously integrated. After rest, motility was recorded for 30 min after injection of saline (control period) and after injection of 5 mg propranolol intravenously. Administration of propranolol was followed by an increase in colonic motility in 9 out of the 10 patients. In one patient no change was observed. During the control period, total contractile activity was 7.7 +/- 18 (S.E.M.) kPa x min (58 +/- 14 mmHg x min), increasing after propranolol to 14.2 +/- 2.3 kPa x min (107 +/- 17 mmHg x min). The difference was significant (p less than 0.01). After propranolol, the colonic pressure waves regularly appeared for longer periods of time and had higher amplitudes than during control activity. Prolonged elevation of basal pressure with superimposed pressure waves was observed in two patients. This study shows that adrenergic beta-blocking agents enhance colonic motility in man. The results may explain abdominal symptoms such as pain and change in bowel habits appearing in patients treated with beta-blocking drugs.

Adult↗
PubMed1980

Spino-vagal nonadrenergic inhibition of gastric motility elicited by abdominal nociceptive stimulation in the cat.

Reflex inhibition of gastric motility in response to intestinal nociception and afferent nerve stimulation was studied in anesthetized cats. Mechanical stimulation of the small and large intestines elicited marked gastric inhibition, which was imitated by direct electrical stimulation of mesenteric or splanchnic afferents. The reflex response was resistant to atropine, guanethidine, and adrenalectomy. Spinal cord transection at the cervical level or spinal anesthesia completely blocked the reflex, as did vagotomy or vagal cold blockade. Chemical peritoneal stimulation by hydrochloric acid induced long-lasting gastric inhibition, which was not blocked by antiadrenergic or anticholinergic drugs. This response was reduced, but not completely blocked by spinal anesthesia or spinal cord transection. It is concluded that various nociceptive intestinal stimuli suppress gastric motility via a spino-vagal reflex mechanism composed of spinal afferents in the sympathetic nerves, spinobulbar ascending pathways, and vagal nonadrenergic inhibitory fibers to the stomach. In addition, vago-vagal reflexes evidently contribute to the gastric suppression induced by diffuse peritoneal irritation. These two reflex mechanisms are suggested to be mainly responsible for postoperative gastric inhibition, together with sympatho-adrenergic reflexes.

Adrenalectomy↗
PubMed1980

Reflex adrenergic inhibition of gastric motility by nociceptive intestinal stimulation and peritoneal irritation in the cat.

The effects on gastric motility of nociceptive stimulation to jejunum and colon were studied in vagotomized anesthetized cats. Mechanical nociceptive stimulation and diathermy of the jejunum and proximal colon elicited reflex gastric inhibition that was significantly more pronounced than that obtained by stimulation of distal colon. Similarly differentiated reflex responses were induced by electric afferent stimulation of nerves from the respective intestinal segments. Strong nociceptive stimuli from the abdominal cavity, induced by peritonitis, completely blocked vagal excitatory influences on gastric motility, as did multiple nerve stimulation. The gastric inhibitory response to abdominal irritation persisted after adrenalectomy but was eliminated during spinal anesthesia or adrenergic blockade. During gastric suppression in animals with abdominal peritonitis cholinergic potentiation with synstigmin administration could only modestly increase gastric tone. It is concluded that intestinal nociceptive stimulation causes gastric inhibition via sympathetic reflex arches that are segmentally differentiated. These adrenergically mediated inhibitory reflexes are powerful enough to block completely myenteric cholinergic neurons. The results suggest that adrenergic blockade or spinal anesthesia is the logical procedure for treating postoperative adrenergic gastric inhibition. The presently studied sympatho-sympathetic adrenergic reflexes seem to work in synergism with sympatho-vagal nonadrenergic reflexes in suppressing gastric motility during paralytic ileus.

Animals↗
PubMed1980

Reflex vagal inhibition of gastric motility by intestinal nociceptive stimulation in the cat.

The effect on gastric motility of various irritative stimuli to the small and large intestine and peritoneum were studied in anesthetized cats. Mechanical stimulation of the jejunum or colon elicited gastric relaxation, which was not blocked by antiadrenergic or anticholinergic drugs but was abolished by vagotomy. Long-lasting gastric relaxation with similar characteristics was observed on jejunal surgery, spontaneous peritonitis, or chemical irritation of the abdominal cavity with acid or methanol. Diathermic lesions of the gut caused less gastric inhibition than mechanical and chemical stimuli. Afferent electric stimulation of jejunal and colonic nerves induced gastric relaxation with similar characteristics as mechanical stimulation in the same regions. It is concluded that mechanical and chemical irritation of the gut and intestinal surgery and peritonitis are accompanied by a gastric relaxation due to activation of the vagal nonadrenergic inhibitory fibers to the stomach. This vagal mechanism is suggested to be important for the suppression of gastric motility in paralytic ileus.

Animals↗
PubMed1980

Ca2+ transport in pancreatic beta-cells during glucose stimulation of insulin secretion.

The role of Ca2+ in the regulation of insulin secretion was evaluated using beta-cell-rich pancreatic islets isolated from ob/ob-mice. The glucose stimulation of the secretory activity is supposed to result from accumulation of Ca2+ in the submembrane cytoplasmic space. It is likely that this process reflects the balance between increased entry of Ca2+ into the beta-cells and an enhanced sequestration of Ca2+ in the organelle sinks. The proposed model can explain the cAMP potentiation of glucose-stimulated insulin release with suppression of the mitochondrial Ca2+ uptake. Furthermore, differences in the Ca2+ buffering capacity of the secretory granules may account for other characteristic features of glucose-stimulated insulin release, in particular its biphasic nature and sensitivity to suppression on withdrawal of nutrients.

Adenosine Triphosphate↗
PubMed1980

Calcium movements in relation to glucose-stimulated insulin secretion.

The influence of glucose on the beta-cell handling of Ca2+ was studied in pancreatic islets isolated from ob/ob mice. Glucose had both stimulatory and inhibitory effects on the washout of radioactivity from islets preloaded with 45Ca. Although the phenomenon of stimulation may be essentially associated with an increased turnover of 45Ca incorporated in response to glucose, the inhibitory effect might merely reflect a lowering of Ca2+ in the cytoplasm following from its accumulation into secretory granules and mitochondria. It is suggested that the Ca2+ uptake by the granules is mediated by an ATP-dependent proton gradient and that these organelles serve as a regulator of the cytoplasmic Ca2+ involved in stimulus-secretion coupling. Alterations in the beta-cell handling of Ca2+ may not only explain the role of glucose as an initiator of insulin release, but also the potentiation by cAMP of the action of glucose. The latter effect can tentatively be ascribed to an increase of cytoplasmic Ca2+ following cAMP-induced inhibition of the net Ca2+ uptake by mitochondria.

1-Methyl-3-isobutylxanthine↗
PubMed1979

Reflex suppression of gastric motility during laparotomy and gastroduodenal nociceptive stimulation.

The effects on gastric motility of laparotomy or of nociceptive stimuli directed to the antro-duodenal area were studied in anaesthetized cats. A diathermic lesion of the duodenal or gastric antral wall induced pronounced gastric relaxation, which could either fade off within 0.5--1.5 h or persist for several hours. This gastric relaxatory response persisted after administration of antiadrenergic and anticholinergic drugs but was eliminated by vagotomy or cold blockade of the vagi. Vagotomy performed during the relaxed gastric state after diathermy immediately resulted in a more or less complete recovery of gastric tone. Blunt mechanical stimulation of the duodenum also caused a prompt gastric relaxation, which showed the same characteristics as the response to diathermy as regards the effects of nerve-blocking drugs and vagotomy. The laparotomy incision per se caused temporary inhibition of rhythmic gastric contraction, but this effect was largely abolished if atropine or guanethidine had been given. It is concluded that nociceptive stimuli against the gastric or duodenal wall induce, besides a sympathoadrenergic reflex inhibition of gastric motility, a profound long-lasting gastric relaxation via a reflex activation of the vagal nonadrenergic inhibitory fibres. This vagally mediated relaxation of the stomach is likely to contribute to the suppression of gastric motility seen in 'paralytic ileus'.

Abdomen↗