Variations in plasma motilin, somatostatin, and pancreatic polypeptide concentrations and the interdigestive myoelectric complex in dog

1985 ◽  
Vol 63 (12) ◽  
pp. 1495-1500 ◽  
Author(s):  
P. Poitras ◽  
M. Lemoyne ◽  
D. Tasse ◽  
L. Trudel ◽  
T. Y. Yamda ◽  
...  
Keyword(s):  
Pancreatic Polypeptide ◽  
Plasma Levels ◽  
Intestinal Motility ◽  
Plasma Concentrations ◽  
Statistical Correlation ◽  
Significant Rise ◽  
Phase Iii ◽  
Blood Levels ◽  
Plasma Motilin ◽  
Related Increase

We have looked at the plasma concentrations of motilin, pancreatic polypeptide (PP), and somatostatin (STS) during the various phases of the interdigestive motor complex (IDMC) in dogs. As expected, motilin cyclical increase was always associated with the phase III of the IDMC. Statistical analysis of PP variations revealed a significant rise 10 min before duodenal phase III; however, in individual animals, this relationship was inconsistent. Although a dose-related increase in PP blood levels was induced by administration of synthetic canine motilin (0–200 ng kg−1 iv), fasting plasma levels of PP were not correlated with the concentrations of circulating endogenous motilin. After truncal vagotomy, while motilin release and the intestinal motility pattern remained unaltered, the phase III associated cyclical increases of PP disappeared. Infusion of physiological amounts of PP (1 μg kg−1 h−1 for 3 h) mimicking the postprandial release failed to reproduce a fed pattern type of intestinal motility and of motilin secretion. No statistical correlation could be established between STS plasma levels and the motor activity of the intestine. STS plasma levels were not correlated with circulating concentrations of motilin and the exogenous administration of physiological doses of synthetic canine motilin failed to modify STS plasma levels. Morphine (200 μg kg−1 iv) stimulated only the release of motilin. These data suggest that the role played by circulating concentrations of PP and STS in the control of the IDMC in dog is at most minimal.

Relationship of postprandial motilin, gastrin, and pancreatic polypeptide release to intestinal motility during vagal interruption

1992 ◽  
Vol 70 (8) ◽  
pp. 1148-1153 ◽  
Author(s):  
S. A. Chung ◽  
G. R. Greenberg ◽  
N. E. Diamant
Keyword(s):  
Pancreatic Polypeptide ◽  
Intestinal Motility ◽  
Plasma Concentrations ◽  
Phase Iii ◽  
Fed State ◽  
Vagal Blockade ◽  
Small Intestinal ◽  
Relationship Of ◽  
Vagal Cooling ◽  
Sustained Increase

Experiments were performed to determine how postprandial motilin, gastrin, and pancreatic polypeptide plasma concentrations measured during vagal blockade relate to coincident small intestinal motility patterns. Feeding produced a postprandial pattern of intestinal motility coincident with a sustained increase in gastrin and pancreatic polypeptide and a decline in motilin plasma concentrations. Vagal blockade replaced the fed pattern with one similar to migrating motor complex (MMC) activity. Highest motilin plasma concentrations were observed during phase III of this MMC-like activity, as occurs in the fasted state. Vagal blockade reduced but did not abolish the postprandial increase in plasma gastrin and pancreatic polypeptide concentrations. Termination of vagal cooling produced a decline in motilin and an elevation in gastrin and pancreatic polypeptide concentrations, coincident with the return of the fed pattern. In conclusion, during vagal blockade in the fed state (i) motilin, but not gastrin or pancreatic polypeptide plasma concentrations, fluctuate with the MMC-like activity, and any measurement of motilin concentrations under these circumstances must be interpreted on the basis of gut motility patterns, and (ii) gastrin and pancreatic polypeptide concentrations are marginally elevated, but these changes are not enough to disrupt the MMC or have any motor effect. Lastly, the fed pattern and the postprandial changes in motilin, gastrin, and pancreatic polypeptide concentrations are in part dependent upon intact vagal pathways.Key words: gastrointestinal motility, vagus, motilin, gastrin, pancreatic polypeptide.

Relationship of plasma motilin concentration to fat ingestion, duodenal acidification and alkalinization, and migrating motor complexes in dogs

1981 ◽  
Vol 59 (2) ◽  
pp. 180-187 ◽  
Author(s):  
J. E. T. Fox ◽  
N. S. Track ◽  
E. E. Daniel
Keyword(s):  
Species Difference ◽  
Maximal Activity ◽  
Significant Rise ◽  
Migrating Motor Complex ◽  
Phase Iii ◽  
Complex Activity ◽  
Duodenal Motility ◽  
Motor Complex ◽  
Duodenal Acidification ◽  
Plasma Motilin

Plasma motilin concentrations were measured in dogs following duodenal acidification and alkalinization and gastric instillation of fat. Antral and duodenal motility were recorded concurrently using intraluminal manometry. Alkalinization of the duodenum produced an increase in antral and duodenal motility and a significant rise in plasma motilin. Alkaline infusions at 5 mL/min into the duodenum initiated phase III of a migrating motor complex both in the antrum and in the duodenum. Duodenal acid infusions produced no change in plasma motilin concentrations while inhibiting antral motility and stimulating duodenal motility for the duration of the infusion. Gastric instillation of 60 g fat produced a 25% increase above basal motilin levels at 50 min after instillation. Motilin levels monitored during spontaneous migrating motor complexes showed peak motilin levels occurring during maximal activity of the antral duodenal region in seven out of nine motor complexes examined but motilin peaks also occurred without migrating complexes being present in this area and, as well, complexes occurred when motilin was undetectable. These results taken together with our other studies in man confirm that a true species difference exists between man and dog in the hormonal motor response to duodenal alkalinization. Although a relationship appears to exist between the appearance of maximal migrating motor complex activity in the gastroduodenal area and plasma motilin concentrations in dogs as in humans, the motilin peaks are probably neither necessary nor sufficient to induce phase III activity.

Five-year administration of fenretinide: pharmacokinetics and effects on plasma retinol concentrations.

1993 ◽  
Vol 11 (10) ◽  
pp. 2036-2042 ◽  
Author(s):  
F Formelli ◽  
M Clerici ◽  
T Campa ◽  
M G Di Mauro ◽  
A Magni ◽  
...  
Keyword(s):  
Plasma Levels ◽  
High Performance ◽  
Plasma Concentrations ◽  
Nipple Discharge ◽  
Treatment Interruption ◽  
Phase Iii ◽  
Breast Cancer Patients ◽  
Plasma Retinol ◽  
Drug Plasma Levels ◽  
Level Reduction

PURPOSE Monitoring of fenretinide (4HPR) levels, kinetics, and effects on retinal was performed in patients who participated in a phase I trial and who continued to be treated for 5 years as phase III trial patients. Accumulation of 4HPR in the breast was also assessed. PATIENTS AND METHODS Plasma concentrations of 4HPR, of its main metabolite N-(4-methoxyphenyl)retinamide (4MPR), and of retinol were assayed by high-performance liquid chromatography (HPLC) in breast cancer patients treated orally with 4HPR 200 mg/d for 5 years with a 3-day drug interruption at the end of each month. RESULTS 4HPR, at 200 mg/d, resulted in average 4HPR plasma levels of approximately 1 mumol/L, which remained steady and caused steady retinol level reduction; 4MPR levels, similar to those of 4HPR, slightly but significantly increased during the first 35 months, but at 5 years they were similar to those at 5 months. During daily treatment, baseline retinol concentrations were reduced by 71%; after a 3-day drug interruption, all patients recovered and the mean reduction was 38%. After discontinuation of 5-year treatment, 4HPR and 4MPR half-lives (t1/2 beta) were 27 and 54 hours, respectively, similar to those reported after 28 daily treatments. After 6 and 12 months, the concentrations of 4HPR were at the limit of detectability (0.01 mumol/L), whereas those of 4MPR were five times higher. Baseline retinol concentrations were already recovered after 1 month. Accumulation of this retinoid in the breast was evidenced by concentrations of 4HPR and 4MPR in nipple discharge and in breast biopsies that were 10 and 20 times higher, respectively, than those found in plasma. CONCLUSION 4HPR, at 200 mg/d for 5 years, resulted in constant drug plasma levels and constant retinol level reduction. After treatment interruption, 4HPR plasma concentrations decreased at the limit of detectability at 6 months and baseline retinol plasma concentrations were recovered after 1 month.

Effect of adrenalectomy on the regulation of the secretion of gonadotrophins and prolactin in the lactating rat

1983 ◽  
Vol 98 (2) ◽  
pp. 227-232 ◽  
Author(s):  
P. van der Schoot ◽  
W. J. de Greef
Keyword(s):  
Plasma Levels ◽  
Inhibitory Action ◽  
Adrenal Glands ◽  
Marked Effect ◽  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Blood Levels ◽  
Adrenal Hormones ◽  
Adrenocortical Hormones ◽  
Adrenalectomized Rats

The suckling stimulus exerts an inhibitory action on the release of gonadotrophins during lactation. The possible involvement of the adrenal glands in this process was examined by studying the plasma levels of gonadotrophins in lactating rats ovariectomized on the day after parturition. It appeared that the suppression, throughout suckling, of the rise in levels of gonadotrophins in blood after ovariectomy occurred to the same extent in adrenalectomized and in sham-operated animals. It thus seems unlikely that adrenocortical hormones, albeit secreted in larger quantities during lactation, exert an inhibitory effect on the release of gonadotrophins. Adrenalectomy had a marked effect on the plasma concentrations of prolactin during the second half of lactation. Whereas plasma concentrations of prolactin in the first half of lactation were similar in adrenalectomized and sham-operated rats, the concentrations in adrenalectomized rats did not undergo the reduction found in sham-operated rats. Adrenal hormones may thus be involved in the reduction of blood levels of prolactin observed in rats and in other mammals as lactation progresses.

Motilin and the postprandial motility of the antrum

1992 ◽  
Vol 70 (11) ◽  
pp. 1491-1495 ◽  
Author(s):  
M. Boivin ◽  
M. Riberdy ◽  
M. -C. Raymond ◽  
L. Trudel ◽  
P. Poitras
Keyword(s):  
Contractile Response ◽  
Plasma Concentrations ◽  
Phase Iii ◽  
Gastrointestinal Hormone ◽  
Postprandial Period ◽  
Postprandial Motility ◽  
Smooth Muscle Function ◽  
Plasma Motilin ◽  
Erythromycin Lactobionate ◽  
Motilin Receptor

This study was designed to establish whether the rise in plasma motilin observed after a meal in humans can influence the postprandial motor activity of the antrum. Antroduodenal postprandial motility profiles and indices obtained from 5 controls and 5 subjects infused with exogenous synthetic motilin (0.1 μg∙kg−1) or with the motilin receptor agonist erythromycin lactobionate (200 mg) were compared. Motilin infusion increased plasma motilin concentrations about 5 times above the physiological range but failed to modify the normal postprandial contractile response. On the other hand, in 4 of the 5 subjects, erythromycin induced an intense motor response that mimicked phase III of the migrating motor complex. Our study demonstrates that, during the postprandial period, motilin antral receptors can be stimulated only with doses of motilin exceeding the physiological plasma concentrations, and that the motor effect obtained did not mimic the usual postprandial motility pattern. Our results, therefore, do not support the proposal that the postprandial motility of the antrum is regulated by the plasma levels of motilin.Key words: antral motility, gastrointestinal hormone, gastrointestinal motility, motilin, regulatory peptide, smooth muscle function.

ANNUAL VARIATIONS IN PLASMA LEVELS OF TESTOSTERONE AND LUTEINIZING HORMONE IN THE LABORATORY MALE MONGREL DOG

1980 ◽  
Vol 86 (3) ◽  
pp. 425-430 ◽  
Author(s):  
R. E. FALVO ◽  
L. R. DEPALATIS ◽  
J. MOORE ◽  
T. A. KEPIC ◽  
J. MILLER
Keyword(s):  
Plasma Levels ◽  
Plasma Concentrations ◽  
Significant Rise ◽  
Release Mechanism ◽  
Cyclic Pattern ◽  
Blood Samples ◽  
Annual Variations ◽  
Mongrel Dog ◽  
The Mean ◽  
Cyclic Changes

Blood samples, drawn every 15 days (September 1975–September 1976) from four laboratory-housed male mongrel dogs, were assayed by radioimmunoassay for levels of testosterone and LH in the plasma. The mean plasma concentrations of testosterone remained relatively constant for most of the year with the exception of a significant rise in late August and early September. Mean plasma levels of LH showed a cyclic pattern throughout the year which could be represented by a cosine function curve. However, this cyclic pattern of LH was not accompanied by cyclic changes in plasma levels of testosterone and there was no relationship between these two hormones during the period of 1 year. As the cyclic pattern of LH was altered, the plasma level of testosterone began to rise and reached its highest concentration. Since this alteration of the LH cycle occurred before the increased concentrations of testosterone, and since there was no relationship between these two hormones for the period of a year, we have concluded that there may be another hormone(s) involved which either alters the sensitivity of the canine testis to LH or alters the LH synthesis/release mechanism of the pituitary gland.

CORRELATION OF REVERSE-T3 AND 3,3′-T2 (T2′) PLASMA CONCENTRATIONS UNDER PHYSIOLOGICAL AND EXPERIMENTAL CONDITIONS IN MAN

1978 ◽  
Vol 89 (4) ◽  
pp. 679-686 ◽  
Author(s):  
M. Hüfner ◽  
M. Grussendorf
Keyword(s):  
Plasma Levels ◽  
Plasma Concentrations ◽  
Blood Levels ◽  
Experimental Conditions ◽  
Reverse T3 ◽  
Physiological Conditions ◽  
Minor Degree ◽  
A Minor ◽  
Therapeutic Doses ◽  
Normal Adults

ABSTRACT T2′ plasma levels are measured under different conditions and correlated to the respective rT3 concentrations. Specific RIAs for T2′ and rT3 are used. Pharmacological doses of T3 cause an increase of plasma T2′; if T3 or T4 doses are administered to an athyroid patient which cause a similar level of plasma T3 the increase of T2′ is much larger during T4 treatment. Cord blood levels of T2′ are 2–3-fold higher than in normal adults whereas rT3 concentrations are about 10 times higher than normal. After birth rT3 and T2′ levels decrease in about a parallel manner. After a bolus iv injection of 500 μg rT3, T2′ starts to increase as early as 2 min after injection. PTU in therapeutic doses causes a rapid increase of plasma rT3 with a maximum 4 h after ingestion. A dose of 150 mg PTU causes a maximum of about 100% above baseline. T2′ also increases but to a lesser degree (about 50 % above baseline). We conclude that rT3 is the most important precursor of T2′ whereas T3 contributes only to a minor degree to the total T2′ production under physiological conditions.

Effect of trimebutine on intestinal motility and plasma motilin in the dog

1986 ◽  
Vol 251 (3) ◽  
pp. G349-G353 ◽  
Author(s):  
P. Poitras ◽  
C. Honde ◽  
J. Havrankova ◽  
R. G. Lahaie ◽  
L. Trudel ◽  
...  
Keyword(s):  
Small Intestine ◽  
Spontaneous Activity ◽  
Intestinal Motility ◽  
Short Interval ◽  
Blood Sampling ◽  
Phase Iii ◽  
Postprandial Period ◽  
Proximal Duodenum ◽  
Plasma Motilin

In a previous report, trimebutine was shown to induce premature periods of phase III activity in fasting dogs, and its action was blocked by naloxone. In this study, we observed that trimebutine (5 mg X kg-1 iv) could induce premature phase IIIs in canine small intestine during interdigestive and digestive periods; trimebutine-induced phase IIIs were migrating along the small intestine faster than spontaneous activity fronts and; trimebutine-induced phase IIIs were accompanied by sharp rises in concentrations of plasma motilin. To further elucidate the trimebutine-stimulatory mechanism, we verified its effects on the release of various circulating peptides that influence intestinal motility: short-interval blood sampling during trimebutine infusion revealed that plasma motilin increases induced by trimebutine preceded the beginning of phase III in proximal duodenum; and gastrin and insulin postprandial releases were abolished by trimebutine. Therefore, trimebutine, by its simultaneous but opposite effects on various peptides that individually carry positive (e.g., motilin) or negative (e.g., gastrin and insulin) influences on the generation of activity fronts, could alter the equilibrium between stimulatory and inhibitory forces in such a way that, in some circumstances (e.g., postprandial period), stimulatory mechanisms become predominant.

Vagal control of migrating motor complex-related peaks in canine plasma motilin, pancreatic polypeptide, and gastrin

1983 ◽  
Vol 61 (11) ◽  
pp. 1289-1298 ◽  
Author(s):  
K. E. Hall ◽  
G. R. Greenberg ◽  
T. Y. El-Sharkawy ◽  
N. E. Diamant
Keyword(s):  
Pancreatic Polypeptide ◽  
Time Course ◽  
Late Phase ◽  
Migrating Motor Complex ◽  
Phase Iii ◽  
Motor Complex ◽  
Vagal Blockade ◽  
Excitatory Pathways ◽  
Plasma Motilin ◽  
Canine Plasma

The role of the vagus nerve in the control of fasting plasma pancreatic polypeptide (PP), gastrin, and motilin levels was investigated in conscious dogs. Lowest plasma levels of motilin (81 ± 8 pmol/L), PP (19 ± 1 pmol/L) and gastrin (5 ± 1 pmol/L) were observed during phase I of the migrating motor complex (MMC). Significant peaks in plasma motilin (127 ± 11 pmol/L, P < 0.005), PP (26 ± 2 pmol/L, P < 0.005), and gastrin (14 ± 2 pmol/L, P < 0.005) were seen, coinciding with the appearance of phase II (PP and gastrin) or phase III (motilin) of the migrating motor complex in the upper gut. Whereas bilateral vagal blockade abolished the peaks in PP and gastrin, a significant (P < 0.025) increment in plasma motilin remained, which correlated with the late phase III equivalent of the vagally independent complex (VIC) in the duodenum. This VIC-related motilin peak (170 ± 20 pmol/L) was significantly higher (P < 0.025) and the time course (9 ± 2 min) significantly shorter (P < 0.01) than the peak (127 ± 11 pmol/L) and duration (31 ± 9 min) observed without vagal blockade. Thus, in fasting, the cyclical increments of PP and gastrin are both dependent on excitatory vagal innervation, whereas excitatory pathways controlling phase III associated peak motilin release are nonvagal. In addition, the pattern of fasting motilin release and the amplitude of peak motilin secretion may be affected by vagal inhibition.

Do motilin and pancreatic polypeptide regulate duodenal bile acid delivery?

1988 ◽  
Vol 66 (12) ◽  
pp. 1499-1504
Author(s):  
R. B. Scott ◽  
S. C. Diamant ◽  
G. R. Greenberg
Keyword(s):  
Bile Acid ◽  
Pancreatic Polypeptide ◽  
Plasma Levels ◽  
Sphincter Of Oddi ◽  
Gallbladder Motility ◽  
Gallbladder Contraction ◽  
Postprandial Period ◽  
Standard Meal ◽  
Duodenal Motility ◽  
Plasma Motilin

The plasma levels of the enteric hormones, motilin and pancreatic polypeptide, cycle in association with fasting intestinal motility and are altered by feeding. Intravenous administration of motilin causes gallbladder contraction and increased sphincter of Oddi phasic motor activity, whereas pancreatic polypeptide causes gallbladder relaxation. To determine if endogenous plasma levels of motilin and pancreatic polypeptide control sphincter of Oddi and gallbladder motility, and regulate duodenal bile acid delivery, we measured during fasting and after feeding the correlation between (a) changes in plasma motilin or pancreatic polypeptide, and (b) the duodenal delivery of a steady-state hepatic output of radiolabelled bile acid. Four dogs were prepared with duodenal cannulas. Duodenal motility was recorded manometrically. Plasma levels of pancreatic polypeptide and motilin were determined during a full cycle of the migrating myoelectric complex for 20 min before and 40 min after ingestion of a standard meal. To assess the effect of the sphincter of Oddi and the gallbladder together, or the gallbladder alone on duodenal bile acid delivery, the dogs received a continuous i.v. infusion of [14C]taurocholic acid (TCA); duodenal delivery of TCA was quantitated with the sphincter of Oddi intact using duodenal marker perfusion, or with the sphincter of Oddi cannulated and zero outflow resistance. In the interdigestive period with the sphincter of Oddi intact, only 0.1 (r2) of the variance of duodenal bile acid delivery can be predicted from the variance of motilin, and the correlation of plasma pancreatic polypeptide with duodenal TCA delivery is opposite that expected if pancreatic polypeptide caused gallbladder relaxation. In the interdigestive period with the sphincter of Oddi cannulated, or in the postprandial period with the sphincter of Oddi intact or cannulated, the correlations of plasma motilin and pancreatic polypeptide with duodenal TCA delivery are opposite those expected if motilin induces gallbladder contraction, and pancreatic polypeptide induces gallbladder relaxation. Assuming these mechanisms, a causal association between variation in plasma motilin or pancreatic polypeptide and interdigestive or postprandial duodenal bile acid delivery is unlikely.

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