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Biomedical subjects

P Thor

Publications and source records attributed to P Thor.

At least 37 records · Page 2Linked to original sources
PubMed1994

Nitric oxide and the interrelation between intestinal motility and pancreatic secretion in fasted and fed dogs.

Intestinal motility and pancreatic secretion show synchronous cyclic changes (MMC) that are interrupted by feeding. The aim of this study was to determine the possible implication of nitric oxide (NO) (that was proposed as nonadrenergic noncholinergic neurotransmitter) in the motor and secretory components of MMC in 5 conscious dogs equipped with monopolar electrodes implanted along the small bowel and pancreatic fistulas. In fasted dogs with typical MMCs, L-NNA (an inhibitor of NO synthase) (5 mg/kg-h i.v.) decreased the MMC interval from control value of 80 +/- 7 to 60 +/- 4 min while increasing significantly the slow waves with spikes and suppressing the phase III-related increase in pancreatic secretion. Infusion of L-arginine (L-Arg) (a substrate of NO synthase) (10 mg/kg-h i.v.) increased the MMC interval from control 79 +/- 7 to 96 +/- 8 min and reduced the slow waves spikes by about 25%. Pancreatic secretion showed significant increase to about 20%. CCK maximum. Similar but transient effects were observed when glyceryl trinitrate (GTN) (a donor of NO) (1 mg/kg-h) was administered. After ingestion of meal, the MMC cycles were replaced by irregular spike activity with an average of about 35% slow waves with spikes and pancreatic secretion rose to about 70% of CCK maximum. Infusion of L-Arg (10 mg/kg-h) reduced by about 90% the postprandial spike activity but failed to affect significantly the pancreatic secretion. Also, injection of GTN (1 mg/kg-h) reduced the spike activity but did not influence pancreatic secretion. L-NNA in fed dogs caused an initial increase in spike activity followed by phase III and about 60% inhibition of pancreatic secretion. L-NNA added to L-Arg infusion reversed in part both intestinal motility and pancreatic secretory effects of L-Arg infusion. We conclude that NO system exerts a tonic inhibitory influence on intestinal myoelectric activity by reducing the frequency of MMC pacesetter and by suppressing the postprandial activity but stimulates pancreatic secretion.

Animals↗
PubMed1993

Microcirculatory and motor effects of endogenous nitric oxide in the rat gut.

The aim of the study was to determine the role of endogenous nitric oxide (NO) as the mediator of intestinal blood flow and motility. Experiments were performed on anesthetized rats. Blood flow in the jejunum was determined by Laser-Doppler flowmeter. Motility was monitored on the basis of changes in intrajejunal pressure. Systemic arterial pressure was also recorded. To investigate the potential role of nitric oxide in the regulation of basal intestinal blood flow and motility the NO synthase inhibitor NG-nitro-L-arginine (L-NNA) was given systemically. Intravenous bolus of L-NNA (15 mg/kg) reduced basal intestinal blood flow and increased both intestinal motility and arterial pressure in the dose-dependent manner. To test the specificity of the NO synthase blockade we administered L-arginine alone or in combination with L-NNA. Pretreatment with L-arginine (100.0 mg/kg i.v.) alone had no major influence but when combined with L-NNA it reversed the intestinal circulatory and motor effects of L-NNA. The results of these studies suggest that endogenous NO exerts a tonic relaxatory influence on the smooth muscle of the intestinal vessels and intestinal wall.

Animals↗
PubMed1993

Nitric oxide inhibits the myoelectric activity of the small intestine in dogs.

Intestinal motility in fasted animals shows cyclic changes (MMC) that are interrupted by feeding. The aim of this study was to determine the possible implication of nitric oxide (NO) (that was proposed as nonadrenergic noncholinergic neurotransmitter) in the motor components of MMC in 5 conscious dogs equipped with monopolar electrodes implanted along the small bowel. In fasted dogs with typical MMCs, L-NNA (an inhibitor of NO synthase) (5 mg/kg-h i.v.) decreased the MMC interval from control 80 +/- 7 to 60 +/- 4 min and increased significantly the spike activity. Infusion of L-arginine (L-Arg) (a substrate of NO synthase) (10 mg/kg-h i.v.) increased the MMC interval from control 79 +/- 7 to 96 +/- 8 min and reduced the slow waves with spikes by about 25%. Similar but transient effects were observed when glycerin trinitrate (GTN) (a donor of NO) (1 mg/kg-h) was administered. After ingestion of meal, the MMC cycles were replaced by irregular spike activity with an average of about 35% slow waves with spikes. Infusion of L-Arg (10 mg/kg-h) reduced by about 90% the postprandial spike activity. Also, infusion of GTN (1 mg/kg-h) strongly reduced the postprandial spike activity. L-NNA in fed dogs caused an initial increase in spike activity followed by phase III-like activity. Similar effects were obtained when L-NNA was infused in dogs with fed-like motility patterns induced by i.v. infusion of caerulein (75 pmol/kg-h). L-NNA added to L-Arg infusion reversed in part the changes of intestinal motility patterns induced by L-Arg. We conclude that NO system exerts a tonic inhibitory influence on intestinal myoelectric activity by reducing the frequency of MMC pacesetter and by suppressing the postprandial spike activity.

Animals↗
PubMed1991

Role of cholecystokinin in postprandial and vagally stimulated duodenal and gallbladder motility in dogs.

This study was designed to determine the role of cholecystokinin (CCK) in postprandial motility pattern of the duodenum and gallbladder (GB) in conscious dogs provided with chronic duodenal electrodes for recording of myoelectric activity and GB fistulas for measurement of intraluminal pressure and volume of GB and to calculate the GB motility index (MI) and GB emptying rate. During naturally occurring activity front (phase III MMC) in the duodenum there was significant increase in the MI of GB accompanied by about 20-30% reduction in the GB volume. These changes in duodenal and GB motility pattern could be duplicated by i.v. motilin. Feeding abolished the appearance of spontaneous activity front in the duodenum and greatly increased motility of GB while reducing its volume. Administration of CCK receptor antagonists in fed dogs failed to affect the motility changes induced by meal in the duodenum but abolished these of the GB. Vagal cholinergic stimulation with insulin, 2DG or urecholine caused similar effects to that induced by food i.e. increased duodenal spike activity, abolished phase III of the MMC, decreased GB volume and increased GB motility. Pretreatment with CCK antagonists did not affect significantly duodenal spike activity or GB motility but significantly increased the GB volume. Atropine 125 micrograms/kg) blocked almost completely spontaneous activity front in the duodenum and accompanying alterations in the motility and volume of GB. We conclude that CCK contributes to the MMC related alterations in the GB motor activity and is essential in cholinergic stimulation induced of the GB emptying but not in vagally induced duodenal and GB motility.

Animals↗
PubMed1988

Cholecystokinin in the regulation of intestinal motility and pancreatic secretion in dogs.

Peptidal (CR-1409) and nonpeptidal (L-364,718) cholecystokinin (CCK) receptor antagonists were used to determine the possible involvement of CCK in the fasted and fed intestinal motility patterns and the related alterations in pancreatic secretion. Dogs were implanted with electrodes along the small bowel and with chronic pancreatic fistulas. In fasted dogs, the typical migrating motor complex (MMC) cycles and accompanying fluctuations in pancreatic secretion were recorded. Neither of the CCK antagonists affected these motor and secretory components of the MMC. Feeding interrupted the MMC and increased spike activity at all levels of the small bowel, and this was accompanied by a significant increase in pancreatic secretion and in plasma hormone [gastrin, CCK, and pancreatic polypeptide (PP)] levels. Both CCK antagonists significantly reduced the postprandial spike activity but failed to restore the fasted pattern. Exogenous gastrin and CCK, as well as bombesin, induced fedlike motility patterns accompanied by marked pancreatic protein secretion. These effects were completely reversed to the fasted patterns during intravenous infusion of CCK antagonists. In contrast, cholinergic stimulation (bethanechol) induced a fedlike pattern that was more resistant to CCK antagonists. We conclude that CCK does not play a major role in the fasted motility pattern and related fluctuations in pancreatic secretion but may be partly involved (by itself and by released PP) in the induction of the fed motility pattern and the postprandial stimulation of the exocrine pancreas.

Animals↗
PubMed1987

Vagal cholinergic control of gastric alkaline secretion in normal subjects and duodenal ulcer patients.

Gastric alkaline secretion was determined in ranitidine treated healthy subjects and duodenal ulcer (DU) patients using gastric perfusion aspiration system and back titration of gastric perfusate to original pH 6.0. Basal alkaline secretion showed periodic fluctuations reaching peaks at phase III of the migrating motor complex (MMC) in the stomach. Mean basal alkaline secretion in healthy normals and DU patients averaged 1120 +/- 124 and 880 +/- 72 mumol/h, respectively and no correlation was found between basal and maximally stimulated gastric acid and alkaline secretion. Modified sham feeding in normal subjects and in DU patients increased this secretion to the peaks of about 28 and 36% of the maximal alkaline response to intragastric application of 16,16 dimethyl-PGE2 in these subjects. Vagotomy did not affect significantly basal alkaline secretion but prevented the rise in alkaline secretion induced by modified sham feeding. Atropine (5-20 micrograms/kg) decreased dose dependently basal, and prevented the modified sham feeding induced alkaline secretion, while pirenzepine (5-20 micrograms/kg) had little influence on basal, and did not affect the modified sham feeding induced, alkaline secretion. This study shows that basal gastric alkaline secretion fluctuates in phase with gastric motor activity, and is similar in normal and DU patients. Vagal stimulation strongly increases alkaline secretion, the effect being abolished by vagotomy and atropine, but not by pirenzepine, suggesting the involvement of M2 rather than M1 subtypes of muscarinic receptors in this stimulation.

Adult↗
PubMed1987

Role of GIP and insulin in glucose-induced changes in intestinal motility patterns.

This study was designed to correlate the intestinal motility patterns with duodenal glucose loads and the increments in plasma gastric inhibitory peptide (GIP) and insulin levels after these loads or after the administration of exogenous hormones in conscious dogs. Isotonic glucose instilled intraduodenally at lower loads (5.2-42.4 mmol/h) only caused a moderate increase in spike activity, but at higher loads (84.8 mmol/h) it disrupted migrating myoelectric complexes (MMC), being accompanied by marked increases in plasma GIP and insulin levels. Duodenal loads of isotonic mannitol resulted in similar motility changes but without alteration in plasma GIP or insulin. Hypertonic glucose (20%) in the duodenum also caused an increase in spike activity, and at higher loads (72 mmol/h or higher) it disrupted MMCs and resulted in significant increments in plasma GIP and insulin levels. Physiological doses of exogenous GIP (25-400 pmol X kg-1 X h-1) or insulin (12-24 mU X kg-1 X h-1) did not affect the motility pattern, but at higher doses, raising plasma hormone over the levels occurring after a mixed meal, GIP (400 pmol X kg-1 X h-1) increased significantly the MMC interval, whereas insulin (48-96 pmol X kg-1 X h-1) induced a fed-like motility pattern. Intravenous 20% glucose (72 mmol/h) caused a marked rise in plasma insulin (but not GIP) levels but failed to affect the intestinal motility as did 20% mannitol infused intravenously in the same dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Cephalic phase of gastroduodenal alkaline secretion.

Alkaline secretion measured under basal conditions in the intact stomach of conscious dogs averaged 47 mumol/30 min and was about twice lower than that recorded in the proximal (approximately 7 cm long) portion of the duodenum. Vagal excitation elicited by sham feeding and insulin resulted in a marked stimulation of alkaline secretion both from the stomach and the duodenum. Atropine significantly reduced gastric and duodenal alkaline secretion under basal state. It abolished gastric and diminished duodenal alkaline response to sham feeding and insulin hypoglycemia, while propranolol was without significant influence. Indomethacin reduced by approximately 75% basal duodenal alkaline secretion but did not prevent the increment in alkaline response to vagal stimulation. We postulate the existence of the cephalic phase of gastroduodenal alkaline secretion, which seems to be cholinergically dependent in the stomach and partly of noncholinergic and nonadrenergic character but prostaglandin dependent in the duodenum.

Animals↗
PubMed1986

Relation between duodenal alkaline secretion and motility in fasted and sham-fed dogs.

A relation between duodenal myoelectric and motor activity and alkaline secretion has been investigated in conscious dogs under basal conditions and following vagal excitation with and without pretreatment with atropine or indomethacin. It was found that duodenal alkaline secretion shows typical periodicity in phase with the myoelectric or motor activity of the duodenum, reaching a peak during phase III and a nadir during phase I of the migrating motor complex (MMC). Sham feeding interrupted the motor and secretory MMC cycle and caused a prolonged increase in duodenal myoelectric or motor activity as well as a sudden and marked rise in duodenal alkaline secretion accompanied by a significant elevation in plasma gastrin and pancreatic polypeptide. Atropine and indomethacin abolished the motor and secretory duodenal cycles and reduced basal alkaline secretion significantly. Atropine abolished, whereas indomethacin increased duodenal myoelectric or motor activity during basal conditions and after vagal stimulation. Neither atropine nor indomethacin abolished sham feeding-induced duodenal alkaline secretion. We conclude that duodenal alkaline secretion fluctuates cyclically in phase with duodenal motility, vagal excitation results in a potent stimulation of duodenal motor and secretory activity, and the mechanism of vagally induced duodenal alkaline secretion is only partly cholinergic and does not involve endogenous generation of prostaglandins.

Action Potentials↗
PubMed1986

Cephalic phase of gastroduodenal alkaline secretion.

This study was designed to determine gastric alkaline secretion (GAS) and duodenal alkaline secretion (DAS) and their relation to the duodenal motility pattern in conscious dogs under basal conditions and after vagal stimulation by sham-feeding and insulin hypoglycaemia. GAS was measured in the gastric perfusate and DAS was determined in the perfusate of the upper duodenum (7 cm in length between occluding balloons). Resting GAS and DAS showed typical periodicity in phase with myoelectric and motor activity, reaching peaks during phases II and III, respectively, and nadir during phase I of the migrating motor cycle (MMC). Vagal excitation by sham-feeding or insulin hypoglycaemia resulted in an immediate rise in GAS and DAS, accompanied by a suppression of MMC. Atropine (25 micrograms/kg) reduced basal GAS and DAS by about 50% and abolished GAS but not DAS in response to vagal stimulation, being accompanied by complete suppression of MMC for several hours. Following injection of indomethacin (2.5 mg/kg) to suppress the generation of endogenous prostaglandins, a prolonged reduction in basal GAS and DAS and an increase in the myoelectric activity and the disruption of the MMC occurred. Neither GAS nor DAS responses to vagal stimulation were affected by indomethacin. We conclude that resting GAS and DAS fluctuate cyclically in phase with gastroduodenal motor activity, and that vagal excitation results in a potent stimulation of alkaline secretion and myoelectric activity which are, in part, cholinergic and do not depend upon the generation of endogenous prostaglandins.

Animals↗
PubMed1985

Gastrointestinal secretory, motor and circulatory effects of corticotropin releasing factor (CRF).

This study was designed to determine the effects of CRF on the gastrointestinal functions such as secretion, motility and circulation in dogs. CRF was found to inhibit dose-dependently gastric acid response to pentagastrin but not to histamine. CRF stimulated pancreatic bicarbonate and protein secretion under basal conditions and in response to secretin or cholecystokinin (CCK). This stimulation was accompanied by an increase in plasma levels of pancreatic polypeptide (PP), but not of secretin or gastrin. CRF caused a partial inhibition of the migrating motor complexes in fasted dogs and increased spike activity of the small bowel. These motor effects of CRF probably resulted from the action of the released PP on the intestinal smooth muscle. CRF is also a potent and selective stimulant of the mesenteric blood flow. This effect may be secondary to the stimulation of intestinal motility and metabolism.

Action Potentials↗
PubMed1985

Role of prostaglandins in control of intestinal motility.

Intestinal myoelectric activity was measured in four conscious dogs with implanted monopolar electrodes after administration of prostaglandins (PG) and indomethacin (Indo), a potent inhibitor of PG biosynthesis. PGE2 and PGI2 given intravenously caused a dose-dependent decrease in the frequency of the migrating myoelectric complex (MMC) in fasted dogs and in postprandial spike activity in fed animals. In contrast, PGF2 alpha interrupted the MMC and caused a fedlike pattern in fasted dogs and did not affect the postprandial spike activity. Similar effects were observed after intra-arterial infusion of PGs. PGE2 and PGI2 infused into the superior mesenteric artery caused a dose-dependent inhibition of the fasted and postprandial pattern of myoelectric activity of the small bowel, whereas PGF2 alpha blocked the MMC and increased spike activity. Indo injected in a single intravenous dose caused a significant reduction in the MMC interval, and Indo infused intravenously in a constant dose induced fedlike motility pattern in fasted dogs but had little effect on the postprandial activity in these animals. This study demonstrates that exogenous PGs of E and I series administered intravenously or intra-arterially inhibit intestinal motility, whereas PGF2 alpha has opposite effects. The finding that Indo increases intestinal motility indicates that endogenous PGs are important in the physiological control of intestinal motility.

Animals↗
PubMed1980

Influence of methionine-enkephalin and morphine on myoelectric activity of small bowel.

Enkephalins, naturally occurring peptides with powerful opiatelike effects, have recently been detected throughout the tissues of the alimentary tract, but their role is unknown. This study was designed to compare the effects of methionine-enkephalin (met-enkephalin) and morphine on the myoelectrical pattern of the small bowel. Five conscious dogs were prepared with electrodes spaced 25 cm apart along the entire small intestine. Spike activity and slow waves were recorded with a Beckman Dynograph. Records were obtained in fasted conditions and following a meat meal or intravenous infusion of caerulein while animals received intravenous infusion of either met-enkephalin or morphine in various doses (range 10-160 microgram/kg . h). Met-enkephalin at a dose of 40 microgram/kg . h caused a significant decrease in spike activity and in the frequency of bursts of the interdigestive myoelectric complexes (IMC), whereas morphine almost doubled the frequency of the IMC. Met-enkephalin in dogs given food or infused with caerulein significantly decreased the fed-type spike activity of the small bowel, whereas morphine did not affect it. The effects of met-enkephalin and morphine on the intestinal myoelectrical pattern can be reversed by naloxone, an opioid antagonist, suggesting that they are mediated by separate opioid receptors.

Action Potentials↗
PubMed1978

Effect of somatostatin on myoelectrical activity of small bowel.

Somatostatin, a growth hormone-release inhibiting hormone, has been found to be a powerful inhibitor of gastric and pancreatic secretion as well as of hormone release in the digestive system. This study was undertaken to determine the influence of somatostatin on the myoelectrical activity pattern of the small bowel. Three conscious dogs were prepared with electrodes spaced 25 cm apart along the entire small intestine. Intravenous infusions of somatostatin were administered in various doses (0.6--5.0 microgram/kg.h) while spike activity and slow waves were recorded under fasting conditions, after a meat meal, or during intravenous infusion of gastrin, caerulein, or insulin. Somatostatin at a dose of 0.6 microgram/kg.h almost doubled the frequency of the interdigestive myoelectric complex. Somatostatin in fed dogs caused a dose-dependent decrease of the normal fed spike activity, and at higher doses it induced a pattern like that seen in fasting animals. The slow-wave frequency in both fasted and fed conditions was not changed significantly. We conclude that somatostatin given under basal conditions increases the frequency of the interdigestive complex and, when administered after feeding, converts the fed-type pattern to the fasted-type pattern. It may therefore play a promoting role in initiating the interdigestive myoelectric complex.

Action Potentials↗