Peristalsis in the Guinea Pig Small Intestine In Vitro Is Impaired by Acetaminophen but Not Aspirin and Dipyrone

Sacs of everted small intestine from a variety of animals were incubated in bicarbonate-saline containing vitamin B12 with and without intrinsic factor (IF). B12 uptake by rat intestine was stimulated only by its own intrinsic factor. Guinea pig ileum responded to all intrinsic factors tested (guinea pig, rat, hog, hamster, human being and rabbit). The intestines of hamster and rabbit were intermediate in specificity, responding to some, but not all, of the IF preparations. Species differences occur in both the intestine and intrinsic factor preparations. The guinea pig ileum was suggested as a possible assay for both hog and human IF.

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Factors controlling B12 uptake by intestinal sacs in vitro

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1960.198.1.103 ◽

1960 ◽

Vol 198 (1) ◽

pp. 103-107 ◽

Cited By ~ 16

Author(s):

Elliott W. Strauss ◽

T. Hastings Wilson

Keyword(s):

Small Intestine ◽

Low Temperature ◽

Guinea Pig ◽

Calcium Ion ◽

Intrinsic Factor ◽

Intestinal Wall ◽

Vitamin B ◽

Anaerobic Conditions ◽

Intestinal Uptake

Sacs of everted small intestine were incubated in bicarbonate-saline containing radioactive vitamin B12 with or without a source of gastric intrinsic factor (IF). In both the hamster and guinea pig the lowest ileum was most active in B12 uptake in the presence of intrinsic factor, the upper jejunum showing little or no uptake. Low temperature and anaerobic conditions completely abolished the stimulatory effect of IF on B12 uptake. Intrinsic factor did not bind to the intestinal wall in the absence of B12 (even in the presence of calcium ion) as the IF activity could be completely removed by gentle washing of the tissue. The vitamin and intrinsic factor must be present together to cause intestinal uptake of B12.

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Mechanisms underlying nutrient-induced segmentation in isolated guinea pig small intestine

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00441.2006 ◽

2007 ◽

Vol 292 (4) ◽

pp. G1162-G1172 ◽

Cited By ~ 34

Author(s):

R. M. Gwynne ◽

J. C. Bornstein

Keyword(s):

Small Intestine ◽

Guinea Pig ◽

Motor Neurons ◽

Slow Wave ◽

Neural Circuit ◽

Circular Muscle ◽

Decanoic Acid ◽

Slow Waves ◽

Longitudinal Position

Mechanisms underlying nutrient-induced segmentation within the gut are not well understood. We have shown that decanoic acid and some amino acids induce neurally dependent segmentation in guinea pig small intestine in vitro. This study examined the neural mechanisms underlying segmentation in the circular muscle and whether the timing of segmentation contractions also depends on slow waves. Decanoic acid (1 mM) was infused into the lumen of guinea pig duodenum and jejunum. Video imaging was used to monitor intestinal diameter as a function of both longitudinal position and time. Circular muscle electrical activity was recorded by using suction electrodes. Recordings from sites of segmenting contractions showed they are always associated with excitatory junction potentials leading to action potentials. Recordings from sites oral and anal to segmenting contractions revealed inhibitory junction potentials that were time locked to those contractions. Slow waves were never observed underlying segmenting contractions. In paralyzed preparations, intracellular recording revealed that slow-wave frequency was highly consistent at 19.5 (SD 1.4) cycles per minute (c/min) in duodenum and 16.6 (SD 1.1) c/min in jejunum. By contrast, the frequencies of segmenting contractions varied widely (duodenum: 3.6–28.8 c/min, median 10.8 c/min; jejunum: 3.0–27.0 c/min, median 7.8 c/min) and sometimes exceeded slow-wave frequencies for that region. Thus nutrient-induced segmentation contractions in guinea pig small intestine do not depend on slow-wave activity. Rather they result from a neural circuit producing rhythmic localized activity in excitatory motor neurons, while simultaneously activating surrounding inhibitory motor neurons.

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Interaction of enkephalin and caerulein on guinea pig small intestine

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1983.244.1.g65 ◽

1983 ◽

Vol 244 (1) ◽

pp. G65-G70

Author(s):

W. M. Yau ◽

P. F. Lingle ◽

M. L. Youther

Keyword(s):

Small Intestine ◽

Guinea Pig ◽

Muscarinic Receptors ◽

Dose Response ◽

Response Curve ◽

Acetylcholine Release ◽

Control Level ◽

Release Studies ◽

Release Of Acetylcholine

This is a report on the effect of caerulein and methionine-enkephalin interaction on mechanical contraction and acetylcholine release in vitro. The ability of enkephalin to relax caerulein-induced contractions and the manner in which the caerulein dose-response curve was shifted in the presence of enkephalin strongly suggest that enkephalin and caerulein are functional antagonists in this system. The failure of enkephalin to alter the action of exogenous acetylcholine implies that such an antagonism is not mediated through a competition with postsynaptic muscarinic receptors on the muscle. Data from acetylcholine-release studies indicate that caerulein stimulation was dose related. As with the mechanical contractions, the release of acetylcholine in response to caerulein was inhibited by enkephalin. However, naloxone was capable of blocking this inhibition and restoring the release to its control level without interfering with caerulein stimulation. These data provide evidence for the modulatory roles of neuronal peptides in the cholinergic control of gut motility.

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Characterization of leukotriene actions on enteric neurons in the guinea-pig small intestine in vitro

Gastroenterology ◽

10.1016/s0016-5085(01)82657-3 ◽

2001 ◽

Vol 120 (5) ◽

pp. A535-A535

Author(s):

S LIU ◽

H HU ◽

C GAO ◽

N GAO ◽

J WOOD

Keyword(s):

Small Intestine ◽

Guinea Pig ◽

Enteric Neurons

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NALOXONE ENHANCES PERISTALSIS IN THE GUINEA PIG SMALL INTESTINE IN VITRO. INFLUENCE ON DIFFERENT PARAMETERS OF PERISTALSIS

Opiate Receptors and the Neurochemical Correlates of Pain ◽

10.1016/b978-0-08-026390-8.50019-4 ◽

1980 ◽

pp. 129-132

Author(s):

W. Kromer ◽

W. Pretzlaff

Keyword(s):

Small Intestine ◽

Guinea Pig

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The myogenic component in distention-induced peristalsis in the guinea pig small intestine

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.2001.280.3.g491 ◽

2001 ◽

Vol 280 (3) ◽

pp. G491-G500 ◽

Cited By ~ 16

Author(s):

Graeme Donnelly ◽

Timothy D. Jackson ◽

Krista Ambrous ◽

Jing Ye ◽

Adeel Safdar ◽

...

Keyword(s):

Small Intestine ◽

Guinea Pig ◽

Slow Wave ◽

Action Potentials ◽

Slow Waves ◽

Intraluminal Pressure ◽

Control Activity ◽

Potential Oscillations ◽

Frequency Gradient

In an in vitro model for distention-induced peristalsis in the guinea pig small intestine, the electrical activity, intraluminal pressure, and outflow of contents were studied simultaneously to search for evidence of myogenic control activity. Intraluminal distention induced periods of nifedipine-sensitive slow wave activity with superimposed action potentials, alternating with periods of quiescence. Slow waves and associated high intraluminal pressure transients propagated aborally, causing outflow of content. In the proximal small intestine, a frequency gradient of distention-induced slow waves was observed, with a frequency of 19 cycles/min in the first 1 cm and 11 cycles/min 10 cm distally. Intracellular recording revealed that the guinea pig small intestinal musculature, in response to carbachol, generated slow waves with superimposed action potentials, both sensitive to nifedipine. These slow waves also exhibited a frequency gradient. In addition, distention and cholinergic stimulation induced high-frequency membrane potential oscillations (∼55 cycles/min) that were not associated with distention-induced peristalsis. Continuous distention produced excitation of the musculature, in part neurally mediated, that resulted in periodic occurrence of bursts of distally propagating nifedipine-sensitive slow waves with superimposed action potentials associated with propagating intraluminal pressure waves that caused pulsatile outflow of content at the slow wave frequency.

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Receptors for vasoactive intestinal peptide and secretin on small intestinal epithelial cells

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1980.238.3.g190 ◽

1980 ◽

Vol 238 (3) ◽

pp. G190-G196

Author(s):

H. J. Binder ◽

G. F. Lemp ◽

J. D. Gardner

Keyword(s):

Small Intestine ◽

Guinea Pig ◽

Vasoactive Intestinal Peptide ◽

Binding Sites ◽

Prostaglandin E1 ◽

Short Circuit ◽

Short Circuit Current ◽

Maximal Effect ◽

Single Class

Binding of 125I-labeled vasoactive intestinal peptide (VIP) to dispersed enterocytes prepared from guinea pig small intestine was saturable, temperature dependent, and reversible, and reflected interaction of the labeled peptide with a single class of binding sites. Each enterocyte possessed approximately 60,000 binding sites and binding of the tracer to these sites could be inhibited by VIP [concentration for half-maximal effect (Kd), 12 nM] and by secretin (Kd greater than 1 micro M), but not by glucagon, gastrin, cholecystokinin, calcitonin, bombesin, litorin, physalaemin, substance P, eledoisin, serotonin, carbamylcholine, or histamine. With VIP and secretin, there was a close correlation between the relative potency for inhibition of binding of 125I-VIP and that for increasing cellular cAMP. For a given peptide, however, a 10-fold higher concentration was required for half-maximal inhibition of binding than for half-maximal stimulation of cellular cAMP. In addition to inhibiting binding of 125I-VIP and increasing cellular cAMP in enterocytes, secretin caused an increase in short-circuit current across guinea pig small intestine in vitro. Prostaglandin E1 increased cellular cAMP, but did not alter binding of 125I-VIP and the increase in cAMP caused by prostaglandin E1 plus VIP or secretin was equal to the sum of the increase caused by each agent alone.

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