EFFECTS OF MASH DIET AND PELLETS UPON DIGESTIVE MOTOR FUNCTIONS IN DOMESTIC HENS AND GUINEA HENS

1983 ◽  
Vol 63 (3) ◽  
pp. 663-669 ◽  
Author(s):  
M. ROCHE ◽  
F. ACHARD ◽  
Y. RUCKEBUSCH
Keyword(s):  
Smooth Muscle ◽  
Intestinal Motility ◽  
Food Habits ◽  
Food Restriction ◽  
Environmental Changes ◽  
Diurnal Cycles ◽  
Intestinal Activity ◽  
Key Words Birds ◽  
Spike Bursts ◽  
Smooth Muscle Electrical Activity

The changes of gastric and intestinal motilities induced by food restriction and refeeding with pellets instead of an all-mash diet were compared in hens and guinea hens. Smooth muscle electrical activity was recorded in both species, which differed by their degree of domestication and food habits. Six-day fasting reduced gastric activity in both species, a phenomenon paralleled by an increase in intestinal motility and the disappearance of the diurnal cycles of gastro-intestinal activity. Refeeding increased gastric activity and reduced the intestinal activity in hens. By contrast with hens, pellets failed to induce major changes in the guinea hens, despite an increased frequency of gastric spike bursts and inhibition of the orad propagation of the intestinal spike bursts. The results suggest that hens, despite a lower responsiveness to environmental changes, are more sensitive than guinea hens to changes in diet. Key words: Birds, digestive electromyography, diet, physiological rhythms

Inhibition by Barbiturates of Barium-Stimulated Intestinal Motility

1956 ◽  
Vol 185 (3) ◽  
pp. 624-626 ◽  
Author(s):  
L. Walker ◽  
H. Necheles
Keyword(s):  
Smooth Muscle ◽  
Intravenous Injection ◽  
Large Intestine ◽  
Intestinal Motility ◽  
Normal Male ◽  
Male And Female ◽  
Intestinal Activity ◽  
Small And Large Intestine ◽  
Cholinergic Effects

Following our demonstration that barium-stimulated intestinal activity could be depressed or inhibited with atropine, we have found that barbiturates had similar effects. In normal male and female mongrel dogs, anesthetized with chloralose-urethane, intestinal motility was stimulated by constant intravenous injection of BaCl2, and motility was registered by a balloon kymograph system. Nembutal, barbital and Amytal sodium, given intravenously, depressed motility of the small and large intestine in most instances, but the effects of the different barbiturates varied. It is concluded that barbiturates may depress cholinergic effects of barium, but also that they may depress smooth muscle directly.

A basic relationship between gastric and duodenal motilities in chickens.

1978 ◽  
Vol 235 (6) ◽  
pp. E670
Author(s):  
M Roche ◽  
Y Ruckebusch
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Electrical Activity ◽  
Circadian Variation ◽  
Dark Light ◽  
Daily Frequency ◽  
Basic Relationship ◽  
Spike Bursts ◽  
Smooth Muscle Electrical Activity

Chickens were chronically fitted with a duodenal cannula and pairs of electrodes implanted in the wall of the muscular stomach, duodenum and ileum. Smooth muscle electrical activity was recorded in both fed and fasted conditions under a 12--12 h dark-light schedule. Two major patterns of activity were identified. The first consisted of spike bursts that propagated rapidly either aborally from the stomach or orally from the ileum. Aborad-propagated spike bursts were most frequent during the daytime; this circadian variation was abolished by vagotomy, which also increased the frequency of orad-propagated spike bursts. The second pattern was characterized by periods of repetitive spike bursts lasting 3--10 min and spreading aborally at a slower rate. In the fasted chicken, the daily frequency was increased and the period of repetitive spike bursts resembled the prolonged bursts of spike potentials recorded in the feline small intestine. The results suggest that the propulsion of digesta might depend on the ratio of spike bursts moving aborally from the stomach to those moving orally from the ileum. Both factors were influenced by the level of stomach activity.

Stimulation of duodenal motility by hyperosmolar mannitol depends on local osmoreceptor control

1994 ◽  
Vol 266 (5) ◽  
pp. G940-G943 ◽  
Author(s):  
H. C. Lin ◽  
J. D. Elashoff ◽  
G. M. Kwok ◽  
Y. G. Gu ◽  
J. H. Meyer
Keyword(s):  
Intestinal Motility ◽  
Control Mechanism ◽  
Experimental Methods ◽  
Dose Effect ◽  
Duodenal Motility ◽  
Significant Difference ◽  
Intestinal Distension ◽  
Osmotic Equilibration ◽  
Spike Bursts ◽  
Stimulation Of

Duodenal motility is stimulated by hyperosmolar solution. Since intestinal distension also stimulates intestinal motility, this increase in the motility response may be due to either stimulation of duodenal local osmoreceptor control or intestinal distension resulting from osmotic equilibration. To test which mechanism is primarily responsible for this osmotically sensitive effect, we compared the number of duodenal spike bursts in five dogs equipped with duodenal fistulas that allowed for the preservation or removal of intestinal distension. The response to 300 vs. 1,200 mosM mannitol was compared under three experimental perfusion methods: 1) distension was preserved both proximal and distal to the fistula (DD); 2) distension proximal to the fistula was removed (rD); and 3) distension both proximal and distal to the fistula was removed (rr). The test solutions had access to either the whole gut (DD and rD) or only the first 10 cm of the duodenum (rr). We found that 1) there were more spike bursts after the hyperosmolar solution (dose effect, P < 0.05, analysis of variance); 2) there was no significant difference between the three experimental methods; and 3) the stimulating effect of hyperosmolar solution depended on the first 10 cm of the duodenum. Thus, since hyperosmolar solution increased duodenal motility regardless of whether intestinal distension was preserved or removed, the stimulating effect of hyperosmolar solution on duodenal motility was primarily the result of a local osmoreceptor control mechanism located in the first 10 cm of the duodenum.

scholarly journals Improving Small Intestinal Motility in Experimental Acute Necrotising Pancreatitis by Modulating the CPI-17/MLCP Pathway Using Chaiqin Chengqi Decoction

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Ziqi Lin ◽  
Chenlong Zhang ◽  
Xiaoxin Zhang ◽  
Na Shi ◽  
Yongjian Wen ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Intestinal Motility ◽  
Contractile Function ◽  
Specific Inhibitor ◽  
Intestinal Smooth Muscle ◽  
Fatty Acid Binding ◽  
Treatment Groups ◽  
Necrotising Pancreatitis ◽  
Acute Necrotising Pancreatitis ◽  
Small Intestinal

Protein kinase C-potentiated inhibitor protein of 17 kDa (CPI-17), a specific inhibitor of myosin light-chain phosphatase (MLCP) regulated by proinflammatory cytokines, is central for calcium sensitisation. We investigated the effects of chaiqin chengqi decoction (CQCQD) on the CPI-17/MLCP pathway in the small intestinal smooth muscle cells (SMCs) and strips (SMS) in an AP model. Necrotising AP was induced in rats by intraperitoneal injections (IPI) of L-ornithine (3.0 g/kg, pH 7.0; hourly × 2) at 1 hour apart; controls received saline. In treatment groups, carbachol (CCh; 60 μg/kg, IPI) or CQCQD (20 g/kg; 2-hourly × 3, intragastric) was administered. The necrotising AP model was associated with systemic inflammation (serum IL-1β and TNF-α) and worsened jejunum histopathology and motility (serum vasoactive intestinal peptide and intestinal fatty acid-binding protein) as the disease progressed. There was decreased intracellular calcium concentration ([Ca2+]i) SMCs. Contractile function of isolated SMCs was reduced and associated with down-regulated expression of key mRNAs and proteins of the CPI-17/MLCP pathway as well as increased IL-1β and TNF-α. CQCQD and CCh significantly reversed these changes and the disease severity. These data suggest that CQCQD can improve intestinal motility by modulating the CPI-17/MLCP pathway in small intestinal smooth muscle during AP.

Relations among canine intestinal motility, blood flow, and oxygenation

1986 ◽  
Vol 251 (1) ◽  
pp. G25-G33
Author(s):  
P. R. Kvietys ◽  
J. A. Barrowman ◽  
S. L. Harper ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Oxygen Uptake ◽  
Linear Relationship ◽  
Intestinal Motility ◽  
Intestinal Smooth Muscle ◽  
Arterial Infusion ◽  
Motility Index ◽  
Dose Dependent Fashion ◽  
Dose Dependent

Blood flow, arteriovenous O2 difference, and lumen pressure were measured in isolated loops of canine ileum. Ileal pressure was increased by an intra-arterial infusion of either Met-enkephalin or acetylcholine. Pressures were quantitated using a motility index (MI = mean of the pressure peaks divided by number of contractions per minute). Both Met-enkephalin and acetylcholine increased MI in a dose-dependent fashion. The highest MI achieved with acetylcholine was 37.9 mmHg, while Met-enkephalin produced a maximal MI of 8.1 mmHg. Ileal oxygen uptake increased when MI reached values greater than 6. There was a direct linear relationship between oxygen uptake and MI. Distension of the lumen in the absence of motility resulted in a decrease in oxygen uptake when lumen pressure reached 15–20 mmHg. The results of these studies indicate that contractions of intestinal smooth muscle can increase intestinal oxygen uptake and may contribute to the overall oxygen demands of the gut under conditions of fasting and feeding. Furthermore, large (greater than 20 mmHg) increments in lumen pressure during enhanced motility may compromise intestinal oxygenation.

PACAP and nitric oxide inhibit contractions in the proximal intestine of the atlantic cod, Gadus morhua

2000 ◽  
Vol 203 (3) ◽  
pp. 575-583 ◽  
Author(s):  
C. Olsson ◽  
S. Holmgren
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Intestinal Motility ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Inhibitory Response ◽  
Nitric Oxide Donor ◽  
The Mean ◽  
Proximal Intestine ◽  
Spontaneous Contractions

The possible inhibitory roles of pituitary adenylate cyclase-activating polypeptide (PACAP), vasoactive intestinal polypeptide (VIP) and nitric oxide in the control of intestinal motility were investigated in the Atlantic cod, Gadus morhua. Circular and longitudinal smooth muscle preparations developed spontaneous contractions that were inhibited by atropine (10(−)(5)mol l(−)(1)). PACAP 27 and PACAP 38 (10(−)(7)mol l(−)(1)) reduced the amplitude of the contractions but did not usually affect the resting tension. In the circular preparations, the mean active force developed (above resting level; +/− s.e.m.) was reduced from 0. 62+/−0.18 mN to 0.03+/−0.03 mN (N=10) by PACAP 27 and from 0.53+/−0. 20 mN to 0.31+/−0.13 mN (N=7) by PACAP 38, while neither cod nor mammalian VIP (10(−)(10)-10(−)(6)mol l(−)(1)) had any effect. In the longitudinal preparations, PACAP 27 reduced the force developed from 1.58+/−0.22 mN to 0.44+/−0.25 mN (N=8) and PACAP 38 reduced it from 1.61+/−0.47 mN to 0.75+/−0.28 mN (N=5). The nitric oxide donor sodium nitroprusside (NaNP) almost abolished the contractions in the circular preparations, reducing the mean force developed from 0. 47+/−0.05 mN to 0.02+/−0.06 mN (10(−)(6)mol l(−)(1); N=9) and 0+/−0. 07 mN (10(−)(5)mol l(−)(1); N=8). In the longitudinal preparations, NaNP reduced the force developed from 2.03+/−0.36 mN to 0.33+/−0.22 mN (10(−)(6)mol l(−)(1); N=8) and 0.19+/−0.30 mN (10(−)(5)mol l(−)(1); N=8). The L-arginine analogue N(G)-nitro-L-arginine methyl ester (L-NAME; 3×10(−)(4)mol l(−)(1)) enhanced the contractions in both circular and longitudinal preparations, increasing the mean force developed from 0.51+/−0.12 mN to 0.94+/−0.21 mN (N=8) and from 1.49+/−0.36 mN to 3.34+/−0.67 mN (N=7), respectively. However, preincubation with L-NAME before a second addition of PACAP 27 (10(−)(7)mol l(−)(1)) did not affect the response to PACAP, neither did preincubation with the guanylate cyclase inhibitor 6-anilinoquinoline-5,8-quinone (LY83583; 10(−)(5)mol l(−)(1)), while the inhibitory response to NaNP (3×10(−)(7)mol l(−)(1)) was abolished by LY83583. The PACAP analogue PACAP 6–27 (3×10(−)(7)mol l(−)(1)) had no effect on the response to either NaNP (3×10(−)(7)mol l(−)(1)) or PACAP 27 (10(−)(8)mol l(−)(1)) in the circular preparations. These findings indicate the presence of both a cholinergic and a nitrergic tonus in the smooth muscle preparations of the cod. Although PACAP and NaNP both inhibit contractions, there is no evidence of any interactions between the two substances. In addition, NaNP, but not PACAP, probably acts via stimulating the production of cyclic GMP. In conclusion, both PACAP and nitric oxide may act as inhibitory transmitters, using distinct signalling pathways, in the control of intestinal motility in the Atlantic cod.

Longitudinal and circumferential spread of spike bursts in canine jejunum in vivo

1980 ◽  
Vol 239 (4) ◽  
pp. G311-G318 ◽  
Author(s):  
N. S. Dusdieker ◽  
R. W. Summers
Keyword(s):  
Phase Ii ◽  
Slow Wave ◽  
Intestinal Motility ◽  
New Method ◽  
Phase Iii ◽  
Cross Sectional ◽  
Spike Burst ◽  
Healthy Dogs ◽  
Spike Bursts

This study demonstrates a new method for quantitatively analyzing individual intestinal spike bursts and establishes the distribution of spike burst spread under conditions of fasting and feeding in conscious healthy dogs. The dimensions and propagation lengths of individual jejunal spike bursts were determined by studying spike burst spread within slow-wave cycles. Electromyograms were recorded simultaneously from multiple closely spaced serosal electrodes in the jejunum (4 equally distant around the circumference and 16 along the long axis at 3-cm intervals). At least 75% of the time, spike bursts involved the entire cross-sectional circumference simultaneously. Greater than 50% of spike bursts during fasting or feeding spread distally 3-30 cm. The remainder were isolated or segmental spike bursts involving < 3 cm of jejunum. The lengths of propagative spike bursts increased with the time during phase II and reached a maximum of 30-40 cm during phase III. Fed activity showed a mixture of segmental and longer propagative spike bursts that varied little with time after feeding. Propagative spike bursts > 3 cm in length produced at least 85% of the total myoelectric burst activity regardless of the state of fasting or feeding and constitute the major form of intestinal motility in the canine jejunum.

scholarly journals Maternal food restriction modulates cerebrovascular structure and contractility in adult rat offspring: effects of metyrapone

2014 ◽  
Vol 306 (6) ◽  
pp. R401-R410 ◽  
Author(s):  
Lara M. Durrant ◽  
Omid Khorram ◽  
John N. Buchholz ◽  
William J. Pearce
Keyword(s):  
Smooth Muscle ◽  
Food Restriction ◽  
Cardiovascular Health ◽  
Synthesis Inhibitor ◽  
Adult Rat ◽  
Rat Offspring ◽  
Artery Stiffness ◽  
Prenatal Undernutrition ◽  
And Function ◽  
Ad Libitum Feeding

Although the effects of prenatal undernutrition on adult cardiovascular health have been well studied, its effects on the cerebrovascular structure and function remain unknown. We used a pair-fed rat model of 50% caloric restriction from day 11 of gestation to term, with ad libitum feeding after birth. We validated that maternal food restriction (MFR) stress is mediated by glucocorticoids by administering metyrapone, a corticosterone synthesis inhibitor, to MFR mothers at day 11 of gestation. At age 8 mo, offspring from Control, MFR, and MFR + Metyrapone groups were killed, and middle cerebral artery (MCA) segments were studied using vessel-bath myography and confocal microscopy. Colocalization of smooth muscle α-actin (SMαA) with nonmuscle (NM), SM1 and SM2 myosin heavy-chain (MHC) isoforms was used to assess smooth muscle phenotype. Our results indicate that artery stiffness and wall thickness were increased, pressure-evoked myogenic reactivity was depressed, and myofilament Ca2+ sensitivity was decreased in offspring of MFR compared with Control rats. MCA from MFR offspring exhibited a significantly greater SMαA/NM colocalization, suggesting that the smooth muscle cells had been altered toward a noncontractile phenotype. MET significantly reversed the effects of MFR on stiffness but not myogenic reactivity, lowered SMαA/NM colocalization, and increased SMαA/SM2 colocalization. Together, our data suggest that MFR alters cerebrovascular contractility via both glucocorticoid-dependent and glucocorticoid-independent mechanisms.

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