Manometric patterns of rat colonic motor activity and defecation

Croci, Tiziano; Basilisco, Guido; Bassani, Alessandro; Manara, L.

doi:10.1007/bf02088133

Cited by 10 publications

(11 citation statements)

References 20 publications

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“…Luminal pressure was raised by clamping luminal effluent and clamp was released when pressure reached 10 cmH 2O. We used the 10-cmH2O pressure increment, because most of physiological pressure of rat proximal colon is not more than 10 mmHg (8).…”

Section: Methodssupporting

confidence: 39%

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Luminally released serotonin stimulates colonic motility and accelerates colonic transit in rats

Tsukamoto

Ariga²,

Mantyh³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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(EC) cells of the epithelial cells release 5-HT into the lumen, as well as basolateral border. However, the physiological role of released 5-HT into the lumen is poorly understood. Concentrations of 5-HT in the colonic mucosa, colonic lumen, and feces were measured by HPLC in rats. To investigate whether intraluminal 5-HT accelerates colonic transit, 5-HT and 51 Cr were administered into the lumen of the proximal colon, and colonic transit was measured. To investigate whether 5-HT is released into the lumen, we used an ex vivo model of isolated vascularly and luminally perfused rat proximal colon. To investigate whether luminal 5-HT is involved in regulating stressinduced colonic motility, the distal colonic motility was recorded under the stress loading, and a 5-HT3 receptor antagonist (ondansetron, 10 Ϫ6 M, 0.5 ml) was administered intraluminally of the distal colon. Tissue content of 5-HT in the proximal colon (15.2 Ϯ 4.3 ng/mg wet tissue) was significantly higher than that in the distal colon (3.3 Ϯ 0.7 ng/mg wet tissue), while fecal content and luminal concentration of 5-HT was almost the same between the proximal and distal colon. Luminal administration of 5-HT (10 Ϫ6 -10 Ϫ5 M) significantly accelerated colonic transit. Elevation of intraluminal pressure by 10 cmH2O significantly increased the luminal concentration of 5-HT but not the vascular concentration of 5-HT. Stress-induced stimulation of the distal colonic motility was significantly attenuated by the luminal administration of ondansetron. These results suggest that luminally released 5-HT from EC cells plays an important role in regulating colonic motility in rats. enterochromaffin cells; distal colon; luminal pressure; restraint stress SEROTONIN (5-HT) IN THE GASTROINTESTINAL (GI) tract is involved in regulating GI motility. While 5-HT acts as a neurotransmitter of the enteric nervous system (15), the majority of 5-HT is stored in enterochromaffin (EC) cells of epithelial cells.EC cells have been considered to release 5-HT mainly into the blood vessels and/or intrinsic nerve terminal via a basolateral border (14). In contrast, others showed that 5-HT is also released into the intestinal lumen in response to vagal nerve stimulation (1,20), luminal acidification (25), and food intake (10). Immunoelectron microscopic study showed the anatomical evidence that 5-HT is released from EC cells in response to an increase of luminal pressure of the rat duodenum (12). However, the physiological role of released 5-HT into the GI lumen is poorly understood.In this study, we hypothesize that luminally released 5-HT from EC cells of the proximal colon is transferred distally with feces and stimulates motility of the distal colon, resulting in acceleration of colonic transit in rats. We also investigated the mechanism of luminal release of 5-HT of the rat proximal colon.There is accumulated evidence that a variety of stress stimulates colonic motility, colonic transit, and fecal pellet output (9,21,35,38,47). Stress-induced acceleration of colonic motor function...

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Section: Methodssupporting

confidence: 39%

“…In our study, we used the rat proximal colon. Pressure was raised to 10 cmH 2 O, because the majority of the wave amplitude of normal peristaltic in the proximal colon is less than 10 mmHg (7.6 cmH 2 O) in rats (8). The mechanism of luminal release of 5-HT may depend on the degree of luminal pressure and/or organs.…”

Section: Discussionmentioning

confidence: 41%

Luminally released serotonin stimulates colonic motility and accelerates colonic transit in rats

Tsukamoto

Ariga²,

Mantyh³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The first 20 min of contractions were compared with the 20-to 60-min time period. In rats, the high-amplitude migrating distal colon contractions have pressure rise over 15 mmHg (10). Since in the present study we could not reliably attribute pressures below the 10 mmHg level to colonic contractile pressures, we took the 10 mmHg as the detectable threshold and added the 15 mmHg rise, as defined by Croci et al (10), and considered pressures over 25 mmHg as the threshold for defining an excursion in the pressure trace as a GMC.…”

Section: Assessment Of Colonic Motor Functionmentioning

confidence: 40%

“…In rats, the high-amplitude migrating distal colon contractions have pressure rise over 15 mmHg (10). Since in the present study we could not reliably attribute pressures below the 10 mmHg level to colonic contractile pressures, we took the 10 mmHg as the detectable threshold and added the 15 mmHg rise, as defined by Croci et al (10), and considered pressures over 25 mmHg as the threshold for defining an excursion in the pressure trace as a GMC. Although several studies identified and described CMMC as the main contractile pattern in isolated mouse colon (12,47), there is so far only one study that reported colonic contractility in awake mice (40).…”

Section: Assessment Of Colonic Motor Functionmentioning

confidence: 40%

Cholinergic giant migrating contractions in conscious mouse colon assessed by using a novel noninvasive solid-state manometry method: modulation by stressors

Gourcerol¹,

Wang²,

Adelson³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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Gourcerol G, Wang L, Adelson DW, Larauche M, Taché Y, Million M. Cholinergic giant migrating contractions in conscious mouse colon assessed by using a novel noninvasive solid-state manometry method: modulation by stressors. Am J Physiol Gastrointest Liver Physiol 296: G992-G1002, 2009. First published March 19, 2009 doi:10.1152/ajpgi.90436.2008.-There is a glaring lack of knowledge on mouse colonic motility in vivo, primarily due to unavailability of adequate recording methods. Using a noninvasive miniature catheter pressure transducer inserted into the distal colon, we assessed changes in colonic motility in conscious mice induced by various acute or chronic stressors and determined the neurotransmitters mediating these changes. Mice exposed to restraint stress (RS) for 60 min displayed distal colonic phasic contractions including highamplitude giant migrating contractions (GMCs), which had peak amplitudes Ͼ25 mmHg and occurred at a rate of 15-25 h Ϫ1 of which over 50% were aborally propagative. Responses during the first 20-min of RS were characterized by high-frequency and high-amplitude contractions that were correlated with defecation. RS-induced GMCs and fecal pellet output were blocked by atropine (0.5 mg/kg ip) or the corticotrophin releasing factor (CRF) receptor antagonist astressin-B (100 g/kg ip). RS activated colonic myenteric neurons as shown by Fos immunoreactivity. In mice previously exposed to repeated RS (60 min/day, 14 days), or in transgenic mice that overexpress CRF, the duration of stimulation of phasic colonic contractions was significantly shorter (10 vs. 20 min). In contrast to RS, abdominal surgery abolished colonic contractions including GMCs. These findings provide the first evidence for the presence of frequent cholinergic-dependent GMCs in the distal colon of conscious mice and their modulation by acute and chronic stressors. Noninvasive colonic manometry opens new venues to investigate colonic motor function in genetically modified mice relevant to diseases that involve colonic motility alterations.

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“…Before surgery and at the end of each recording session, catheters were filled with distilled water and closed by heating at the proximal ends. Rats were allowed to recover from surgery for five to six days, then intraluminal intestinal pressure was recorded as previously described (Croci et al , 1994a) by use of a hydraulic capillary infusion system. A low‐compliance perfusion apparatus (Sensor Medics, Milan, Italy), consisting of a tank of bidistilled water, was subjected to a nitrogen pressure of 418 mmHg from a gas cylinder connected in series through a regulator.…”

Section: Methodsmentioning

confidence: 99%

Role of tachykinins in castor oil diarrhoea in rats

Croci

Landi

Emonds‐Alt

et al. 1997

British J Pharmacology

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104

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1 We set out to ascertain the role of tachykinins, neurokinin A and substance P, in castor oil-induced diarrhoea in rats as disclosed by the inhibitory e ect of the non-peptide NK 1 -and NK 2 -receptor antagonists, SR 140333 and SR 48968, respectively. 2 SR 48968 (0.02 to 20 mg kg 71 , s.c. or p.o.), and the opioid receptor agonist loperamide (1 ± 10 mg kg 71 , p.o.), dose-dependently prevented castor oil e ects: % inhibition vs castor oil, diarrhoea 0 to 100, increase in faecal mass 7 to 90 and water content 16 to 90. SR 140333 (0.02 to 20 mg kg 71 , s.c.) and the platelet activating factor antagonist SR 27417 (5 to 500 mg kg 71 , p.o.) did not prevent the increase in faecal water content, but reduced faecal mass (35 to 66%) and diarrhoea (0 to 57%). 3 The R-enantiomers of tachykinin NK 1 and NK 2 receptor antagonists, SR 140603 and SR 48605 (both at 2 or 20 mg kg 71 , s.c.) had no e ect other than reducing faecal mass at the highest dose tested. 4 SR 48968 (20 mg kg 71 , p.o.) but not loperamide (10 mg kg 71 , p.o.) given 24 h before castor oil, still slightly but signi®cantly reduced by 30% the increase of faecal mass output; both treatments signi®cantly reduced (30 to 70%) the e ect of castor oil on faecal water content, although the incidence of diarrhoea was only slightly less than in controls. 5 In castor oil-treated rats, naloxone (2 mg kg 71 , s.c.) completely blocked the antidiarrhoeal action of loperamide (10 mg kg 71 , p.o.) but not of SR 48968 (20 mg kg 71 , p.o.); a similar result was obtained on faecal mass and water content. 6 Castor oil strongly increased the occurrence of manometrically recorded propulsive giant contractions (500 to 1000% over control values) of transverse and distal colon, this e ect being signi®cantly prevented (80 to 100%) by SR 48968 and loperamide and partially by SR 140333 (35% distal colon, 70% transverse colon). 7 In castor oil free rats, loperamide but not SR 48968 or SR 140333 signi®cantly reduced by 50% the gastrointestinal transit of a charcoal test meal, as well as 24 h faecal mass output. Consistently, loperamide, unlike the tachykinin receptor antagonists, had a dramatic e ect on manometric recordings of intestinal motility, reducing all kinds of colonic contractions. 8 Our ®ndings suggest that castor oil diarrhoea in rats entails activation of NK 1 and NK 2 receptors by endogenous tachykinins, whose antagonists may have a potential as antidiarrhoeal agents free from the constipating action of opioids.

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Manometric patterns of rat colonic motor activity and defecation

Cited by 10 publications

References 20 publications

Luminally released serotonin stimulates colonic motility and accelerates colonic transit in rats

Luminally released serotonin stimulates colonic motility and accelerates colonic transit in rats

Cholinergic giant migrating contractions in conscious mouse colon assessed by using a novel noninvasive solid-state manometry method: modulation by stressors

Role of tachykinins in castor oil diarrhoea in rats

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