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Keywords:

  • bacterial overgrowth;
  • coloileal reflux;
  • ICS motility;
  • ICS tone;
  • vagal afferents

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. ICS motility patterns
  5. The ileocaecocolonic segment: a functional entity
  6. Functional correlates of ICS motility
  7. Reflexes affecting ICS motility
  8. Neuronal control of the ICS
  9. Humoral control of the ICS
  10. Role of ICS in preventing bacterial overgrowth
  11. Conclusion
  12. References

Abstract  The human ileocolonic sphincter (ICS) develops a sustained tone mainly due to propagated and not propagated phasic motor activity. The ileocaecocolonic segment is also able to behave, yet uncommonly, as a synchronized segment involving propagated contractions originating from the ileum and migrating to the proximal colon. The ICS motor activity alone has a limited role towards forward flow. On the contrary, the functional entity corresponding to the distal ileum and the ICS provides a clearance mechanism for reflux of colonic contents into the small intestine. The presence of short chain fatty acids (SCFA) in the distal ileum, sensed either by endocrine cells or chemo-sensitive vagal afferents, is an important actor in triggering this clearance mechanism. The ICS tone is in part myogenic but a neuronal nitrergic component is also involved. Reflex excitatory and inhibitory responses of the ICS originating from ileal or colonic distension involve primarily spinal nitrergic and adrenergic pathways.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. ICS motility patterns
  5. The ileocaecocolonic segment: a functional entity
  6. Functional correlates of ICS motility
  7. Reflexes affecting ICS motility
  8. Neuronal control of the ICS
  9. Humoral control of the ICS
  10. Role of ICS in preventing bacterial overgrowth
  11. Conclusion
  12. References

The ileocolonic sphincter (ICS) was historically referred to as the ‘apothecary barrier’ because of its putative role towards a reinforcement of water absorption by the colon. Nowadays, improved recording methods together with sophisticated surgical models allowing an easy access to the ileocolonic junction in animals and humans have allowed demonstrating the complex properties of ICS towards the regulation of retrograde and anterograde flow. This is achieved through (i) sphincter properties of the ICS and (ii) tight integration of its motor activity with that of more proximal and distal parts of the gastrointestinal tract.

ICS motility patterns

  1. Top of page
  2. Abstract
  3. Introduction
  4. ICS motility patterns
  5. The ileocaecocolonic segment: a functional entity
  6. Functional correlates of ICS motility
  7. Reflexes affecting ICS motility
  8. Neuronal control of the ICS
  9. Humoral control of the ICS
  10. Role of ICS in preventing bacterial overgrowth
  11. Conclusion
  12. References

Numerous in vitro experimental data suggest that a sphincter zone is present at the ileocolonic junction in animals. The ICS circular muscle cells from the guinea-pig have a resting membrane potential lower than those located either in the ileum or in the caecum.1 In addition, muscle strips from the ileocolonic junction show isometric tone of myogenic origin.2,3 In conscious dog, using an elegant surgical preparation allowing an easy access to the ICS, a high-pressure zone of 26 mmHg over a distance of about 3 cm is recorded during the pioneer studies of Quigley et al.4–6 Later, a high-pressure zone has been found in other mammals by various research teams. In horse, a species with an extended caecocolonic segment the high-pressure zone is only 6 mmHg over a distance of 5 cm.7 In pig, a species also with a large caecocolonic segment, the high-pressure zone is slightly larger yet less than that recorded in dog with a mean pressure of 15 mmHg over 3 cm length.8 Manometric studies of the human ICS have yielded conflicting observations, with some investigators demonstrating a sustained high-pressure zone9,10 and others not demonstrating this.11–14 These discrepancies might relate to the difficulty to maintain and to assess the position of the manometric sensor astride the ICS. Indeed, unlike the pyloric sphincter that could be located non-invasively, in real time and with millimetre accuracy by double transmucosal membrane potential difference recording, the only alternative for the ICS is based on radiology methods. Dinning et al.15 using temporary, side diverting, defunctioning ileostomies, have been able to record ICS pressure in a configuration close to that surgically produced by Quigley et al. in dogs,16 hence allowing precise positioning of the manometric assembly across the ICS for prolonged periods. In these patients, a sustained pressure of about 10 mmHg is observed either using pull-through or sleeve recording over a 4.8 cm distance.

While the resting tone differs in amplitude from human to animal, a somewhat constant feature, specific to the ICS, is the interrelation between intrinsic tone and phasic pressure waves. Both motor patterns contribute to build a significant pressure barrier at the ICS. In fasted humans, phasic activity of the ICS, unrelated to motor activity of more oral or aboral zones, is observed for 35% of the recording time.15 During these waves that occur at about four to eight waves per minute, the basal tone is doubled (Fig. 1). Aside from contractions restricted to the ICS, another mechanism involving propagated phasic contractions is also responsible for increase in tone. This one coexists with the aforementioned one in humans and it is the only one found in dogs and horses. In fasted dogs, phase III of the migrating motor complex causes a sustained and prolonged rise in ICS tone.16 An increased ICS tone is also observed during the migration of discrete clustered contractions (DCC) along the distal ileum.4 On the contrary, ICS tone is reduced in humans and in dogs while prolonged propagated contractions (PPC) are observed on the distal ileum.4,15 This pattern appears to be the only one able to trigger relaxation of the ICS as spontaneous relaxations are observed only in dogs and in extremely rare occasions for limited periods lasting about 10 s each (Fig. 2). Surprisingly, whereas in human and in dogs most of the propagated contractions recorded at the ICS originate from the ileum, the opposite is observed in horse for which about two-third of the ICS contractions originate from the extended caecum. Such contractions are followed by a drop in ileal pH indicating a reflux of acidic caecal contents in the distal ileum.7

image

Figure 1. Phasic pressure waves specific to the ileocolonic sphincter (ICS) recorded on the sleeve placed astride the human ICS. Such activity limited to the ICS was recorded for 35% of fasting recording time. Reprinted with permission from Dinning et al. (1999).15

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image

Figure 2. Two main motor propagated patterns observed on the ileocolonic segment in humans. (A) Ileal propagating sequences that transversed the ileocolonic sphincter (ICS) into the caecum occurring during periods of quiescence within the ICS. (B) Ileal propagating pressure waves that did not extend into the caecum invariably inhibited the ICS tone and ICS phasic waves. All distances are referenced to the midsleeve. Reprinted with permission from Dinning et al. (1999).15

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The ileocaecocolonic segment: a functional entity

  1. Top of page
  2. Abstract
  3. Introduction
  4. ICS motility patterns
  5. The ileocaecocolonic segment: a functional entity
  6. Functional correlates of ICS motility
  7. Reflexes affecting ICS motility
  8. Neuronal control of the ICS
  9. Humoral control of the ICS
  10. Role of ICS in preventing bacterial overgrowth
  11. Conclusion
  12. References

In a way similar to antropyloroduodenal coordination, the ileocaecocolonic segment is able to behave as a synchronized segment. Indeed, in dogs and to a lesser extent in humans, ileal motor events propagate across the ICS into the colon. For instance, Quigley et al. show that 50% of ileal DCCs and 76% of ileal prolonged propagating contractions continued propagating in the proximal canine colon.4 In humans,17 there is a 30% association between ileal and caecal propagating events with, as in the canine model, a greater proportion of ileal prolonged propagating contractions associated with caecal propagating sequences. There are two equally possible explanations to account for this ileocaecocolonic coordination. Caecal filling as a consequence of ileal propagating activity18 may secondarily initiate caecal propagated sequences. Alternatively, the phenomenon may represent an extension of the peristaltic reflex across the ICS such as the one already described at the antropyloroduodenal area.19,20 Nevertheless, while the ileocaecocolonic segment is able to work as a functional entity, this propagated motor pattern is rare in humans as ileal propagated events occur at a frequency of only 0.2 events per hour.17

Functional correlates of ICS motility

  1. Top of page
  2. Abstract
  3. Introduction
  4. ICS motility patterns
  5. The ileocaecocolonic segment: a functional entity
  6. Functional correlates of ICS motility
  7. Reflexes affecting ICS motility
  8. Neuronal control of the ICS
  9. Humoral control of the ICS
  10. Role of ICS in preventing bacterial overgrowth
  11. Conclusion
  12. References

The role of ICS motility towards a control of oral and aboral flow is still controversial but unlike the flow pattern occurring at the pyloric level,21 backflow does not follow immediately a forward flow episode.22 Therefore, it is necessary to present both flow patterns independently.

Forward flow from the ileum to the caecum is episodic23,24 leading to the early concept of the ICS as an ‘intestinal stomach’25 which stores residue and then empties in the colon26 (Fig. 3). This is achieved, in dogs only, by the passage of phase III through the ileum.24 As most of the MMC do not reach the terminal ileum in humans, ileal emptying is performed using a separate mechanism that could not be associated with a specific motor pattern. Indeed, Spiller et al., who measured caecal filling scintigraphically, could not relate ileal or ICS motor patterns to episodes of caecal filling.23 The participation of ICS tone or phasic motor activity to control forward flow is difficult to assess due to our incapacity to measure physical resistance21 of the ICS to flow over extended recording sessions. To date, the only available data originate from surgical preparations with or without anatomical or functional ICS. Surgical ablation of the ICS in rat27 and in dog18 results in a slight retardation or no retardation in transit. Using a canine model of sphincterotomy to weaken the ICS, the Mayo group28 has demonstrated that ICS has little effect on transit. Indeed, (i) ileal flow displays the same fluctuations before and after sphincterotomy, (ii) progression of the meal to the terminal ileum are unaltered by sphincterotomy and (iii) transit times of boluses are the same before and after sphincterotomy. Therefore, the control of forward ileocolonic flow resides at an integrated level involving functions of the distal ileum and the proximal colon.

image

Figure 3. Simultaneous recording of ileal motor events, ileocolonic sphincter (ICS) motility and ileal flow in colectomized dog. The onset of discrete clustered contractions (left panel) or prolonged propagated contraction (right panel) is associated with ileal flow. Reprinted with permission from Kruis et al. (1987).18

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Backward flow from the caecocolon to the ileum is also episodic. In dog, the volume of the refluxate is low accounting for about 7% of the total radioactivity injected to the caecocolon.29 This minimal reflux rate might be explained by the competence of the canine ICS towards reflux. Indeed, surgical section of the ileo-caecal ligament in dog, a procedure that suppresses the ileocolonic angle and reduces sphincter competence,30 increases the amount of caecoileal reflux to 44% of the total radioactivity.29 Furthermore, surgical removal of the ICS maximizes reflux ultimately leading to bacterial overgrowth.31 Accurate timing between reflux episodes and motor events can be achieved using the pig as an animal model.32 Indeed, due to the vast fermentation reservoir producing large amount of short chain fatty acids (SCFA), the pH of the colonic contents refluxate is low and pH drops in the ileum7 correspond to reflux episodes in a similar manner as those recorded in the distal oesophagus in humans. Using this animal model, we have demonstrated that (i) reflux episodes are frequently occurring events six to eight times per hour; (ii) these reflux events are temporally related to motility patterns of the terminal ileum.33 Some ileal motor patterns facilitate reflux as they occur before the onset of the pH drop whereas others are a consequence of the reflux as they occur either simultaneously or after the pH drop. About one-half of the reflux episodes are preceded by retrograde propagated contraction. On the contrary, anterograde propagated contractions resembling either PPCs or DCCs described in dogs are observed during or immediately after reflux episodes. Therefore, at least in pigs, PPC and DCC might provide a clearance mechanism for the distal ileum (Fig. 4).

image

Figure 4. Concomitant recording of ileal motility and distal ileal pH as an indicator of coloileal reflux episode in conscious pig. A retrograde ileal contraction (heavy dotted line) occurred before the onset of the pH dip. A delay of about 2 s was observed between the onset of pH dip and the onset of the contraction on the most distal strain gauge. Unclassified anterograde propagated contractions (light dotted lines) occurred frequently during reflux event and served to clear the ileum from colonic refluxate. Reprinted with permission from Cuche and Malbert (1998).33

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Reflexes affecting ICS motility

  1. Top of page
  2. Abstract
  3. Introduction
  4. ICS motility patterns
  5. The ileocaecocolonic segment: a functional entity
  6. Functional correlates of ICS motility
  7. Reflexes affecting ICS motility
  8. Neuronal control of the ICS
  9. Humoral control of the ICS
  10. Role of ICS in preventing bacterial overgrowth
  11. Conclusion
  12. References

ICS motility after a meal

In dogs and humans, the percentage of time that phasic activity is present increases at the ICS after food intake.4,14 This is reminiscent of the ‘gastroileal’ reflex describing an increased motor activity of the distal ileum after a meal.34,35 Unlike the former consensus, conflicting data exist about changes in ICS tone after a meal. In dogs, after food intake, tonic pressure at the ICS is about one-third lower than in the interdigestive state.5 Furthermore, fluctuation of tone due to superimposed DCC is dampened. On the contrary, in humans, ICS tone is higher immediately after a meal and afterwards lower than during the interdigestive period.15 A striking phenomenon does occur in the canine ileum in the late-postprandial period, i.e. when residue of a meal reaches the distal small bowel.36 This consists in a unique pattern of motility of pressure waves at a frequency (20–24 per min) much greater than that of the ileal slow wave. These pressure waves coincide with contractions of the circular muscle layer.

Influence of ileal and colonic distensions

Colonic distension is followed consistently by contraction of the ICS in dogs and in humans (Fig. 5). This enhanced motility of the ICS comprises simultaneously an increase in tone together with larger amplitude ICS phasic pressure waves15 while the ileal contractions are unaffected.16 An earlier study has reported inhibition of such contractions but this result is questionable due to the available recording method.13 In a porcine model,8 a more complex pattern of response was observed depending on the degree of distension. For low distending pressure, about one-third of the responses were inhibitory whereas the remaining were excitatory. Nevertheless, similar to what was observed in dogs and in humans, high distending pressures triggered excitatory responses.

image

Figure 5. Increase in ileocolonic sphincter (ICS) tone recorded during distension of the proximal colon in conscious dog. This tetrodotoxin (TTX)-sensitive reflex might involve extrinsic spinal neural pathway. Reprinted with permission from Quigley et al. (1985).16

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Ileal distension induces variable responses for ICS motility irrespective of the species. For distension performed at the vicinity of ICS, both inhibitory and excitatory responses are observed in humans, the nature of the response being dependent mainly on the tone present in the ICS at time of the distension. Similar inhibitory/excitatory responses have been described in animal models.8,16,37 Hence, it is likely that there are descending excitatory and inhibitory pathways both of which are activated by ileal distension. These pathways do not extend over long distances as distension of the proximal ileum (i.e. 10 cm oral to the ICS) was not able to elicit ICS response.

Influence of ileal or colonic contents

In dogs, colonic administration of acetic acid increases ICS tone.38 Conversely, 100 mmol L−1 acetic acid infused into the distal ileum, does not alter the basal pressure of the ICS. Nevertheless, because of the intricate relationship between ICS tone and phasic contractions, the overall pressure of the sphincter rises as a consequence of more frequent DCCs. These excitatory responses were described in dogs,38–40 rats,41 pigs33 and in humans42 after the administration of SCFA. The local motor effects of SCFA towards ileal motility might involve the release of PYY because administration of SCFA in the ileum releases this hormone43–46 and exogenous administration of peptide YY (PYY) triggers motor activity in the ileum.47 However, to date we are unaware of studies directly demonstrating an effect of PYY on the ICS. In addition to this putative humoral pathway, direct activation of vagal afferents sensitive to SCFA may be involved. Indeed, local anaesthesia of the ileum abolishes the effect of SCFA.40,48 Furthermore, vagal mechano-sensitive neurones inhibited by SCFA have been identified in the ileal mucosa of the pig49 (Fig. 6). The SCFA might interact with vagal units by two putative mechanisms. The SCFA induced contractions in isolated ileal muscle cells by means of an acid-sensitive Ca-dependent mechanism41 that could also occur at the terminal ending of vagal afferents. Similarly, the large PYY response induced by SCFA might also activate vagal afferents.50

image

Figure 6. Reduced mechanical sensitivity of an ileal vagal afferent (conduction velocity 5.6 m s−1) to distension before and after mucosal contact with short chain fatty acids (SCFA) 1.4 mol L−1. Distension (300 mL) of the ileum was less efficient to generate afferent activity after infusion of SCFA (1.4 mol L−1) than after isotonic saline infusion indicating a reduced sensitivity to mechanical distension elicited by SCFA. Top right insert corresponds to the discriminator template for the ileal unit. Reprinted with permission from Chen et al. (1997).50

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Neuronal control of the ICS

  1. Top of page
  2. Abstract
  3. Introduction
  4. ICS motility patterns
  5. The ileocaecocolonic segment: a functional entity
  6. Functional correlates of ICS motility
  7. Reflexes affecting ICS motility
  8. Neuronal control of the ICS
  9. Humoral control of the ICS
  10. Role of ICS in preventing bacterial overgrowth
  11. Conclusion
  12. References

Tetrodotoxin (TTX)-resistant myogenic tone is observed in vivo in cat,51,52 pigs8 and in an in vitro canine model.53–55 The origin of this myogenic tone might result from a relatively positive resting muscle cell membrane potential coupled with small, spontaneous oscillations in resting membrane potential. While ICS tone might be in part myogenic, local neuronal nitrergic control of the ICS has been also demonstrated. Nitric oxide synthase (NOS) inhibition increases ICS tone in denervated and innervated canine intestinal loops.56 Similarly, the NO donor sodium nitroprusside reduces ICS tone in pigs while NOS inhibition by N-nitro-l-arginine methyl ester (l-NAME) increases tone.8 Furthermore, in vitro, both exogenous NO and non-adrenergic non-cholinergic (NANC) nerve stimulation by field stimulation causes hyperpolarization or inhibitory junction potentials.53,57

Using an elegant extrinsically denervated ileocolonic preparation in conscious dogs, the Mayo group has recently demonstrated an absence of change in ICS tone before and after extrinsic denervation.56 The persistent ICS pressure contrasts with the increased ileal phasic activity observed after denervation. This might relate to diminished tonic sympathetic input because ileal tissue levels of catecholamines are markedly low or absent after denervation. The former result is consistent with earlier observations in cat demonstrating that ICS persists after vagal and splanchnic nerve sections.58,59 In several species, stimulation of the splanchnic nerve causes an increase in ICS tone.60 This is reminiscent of the demonstration of α-1 and -2 excitatory adrenergic pathways to the ICS.58,61,62 Recently, in pigs, an inhibitory β-adrenergic pathway has also been demonstrated because isoproterenol reduces ICS pressure by about 30%.8 Furthermore, an adrenergic spinal neural excitatory pathway has been implicated in reflex contraction of the feline ICS in vivo.52 Vagal efferent stimulation is also likely to modify the ICS resistance as during vagal stimulation the trans-sphincteric flow is reduced while the motor activity of the ileum increased.63 Furthermore, excitatory muscarinic64 and inhibitory nicotinic57,61 influences on ICS tone have been demonstrated in a variety of species.

Improvements in sphincter recording technology have made possible to distinguish the impact of ileal and colonic distensions on ICS motility without cross-recording between distending and ICS pressures. The next logical step has been to understand the neural pathways involved in reflexes originating from the colon or the ileum and directed towards the ICS. Indeed, all these reflexes were TTX-sensitive.8,64 Colonic distension in anaesthetized cat causes ICS to contract, a reflex that is mediated by an extrinsic spinal neural pathway involving both tachykinin and catecholamines as neurotransmitters.52 In anaesthetized pig, the same excitatory response was observed. In the presence of l-NAME, colonic distension triggered inhibition of ICS tone.8 However, neither NG-nitro-l-arginine (l-NNA) nor l-arginine modified the ICS response to colonic distension in canine innervated loops.56 It is possible that the different levels of colonic distension used in these studies were at the origin of this discrepancy as ICS pressure induced by colonic distension was related inversely to distension volume.16 One possible pathway for this excitatory colonic reflex could involve colonic mechanosensory afferent input to neurones in the superior mesenteric ganglion.65 In dogs, the relaxation of the ICS induced by ileal distension is abolished after extrinsic denervation but not after l-NNA indicating that ileal distension activates extrinsic pathways not solely dependent on NO.56 Conversely, in pigs, ICS responses to ileal distension are abolished in the presence of both l-NAME and propranolol8 indicating that this inhibitory pathway involves both nitrergic and β-adrenergic postganglionic neurones.

Humoral control of the ICS

  1. Top of page
  2. Abstract
  3. Introduction
  4. ICS motility patterns
  5. The ileocaecocolonic segment: a functional entity
  6. Functional correlates of ICS motility
  7. Reflexes affecting ICS motility
  8. Neuronal control of the ICS
  9. Humoral control of the ICS
  10. Role of ICS in preventing bacterial overgrowth
  11. Conclusion
  12. References

Whereas the distal ileum synthesizes a number of hormones that act on the upper part of the gut such as PYY, glucagon-like peptide-1 (GLP-1),66 neurotensin,67 a limited number of these have been demonstrated to alter ICS function. Cholecystokinin (CCK) and gastrin induce a contraction of pig ileum smooth muscle by a direct myogenic effect depending on the interaction of these peptides with distinct receptor sites.68 However, in vivo, relaxation,9 stimulation69 or an absence2 of effect are reported. Neurotensin, a hormone and a neurotransmitter acts as an hormone in the rat distal ileum.70 Close intra-arterial administration of neurotensin in dogs71 and systemically in pigs72 inhibit ileal smooth muscle activity. In the anaesthetized cat, the effect of local administration of neurotensin on the ICS is more complex.73 At low dose, neurotensin induces a dose-dependent contraction of the sphincter while at high dose (1 μg kg−1) a relaxation of the ICS is observed. The dose-dependent contraction of the ICS is partially abolished by α-2 receptor blockade. Such dose-dependent action of neurotensin on the ICS might explain the decrease in luminal content transit observed fluoroscopically in conscious dogs after 10 pmol kg−1 min−1 neurotensin.74 In conscious rabbit, somatostatin increases the pressure necessary to pass fluid through the ICS.75 This potential increase in tone is in accordance with the depolarizing effect of somatostatin on ileal circular muscle through the inhibition of the release of NO-related compound.76

Role of ICS in preventing bacterial overgrowth

  1. Top of page
  2. Abstract
  3. Introduction
  4. ICS motility patterns
  5. The ileocaecocolonic segment: a functional entity
  6. Functional correlates of ICS motility
  7. Reflexes affecting ICS motility
  8. Neuronal control of the ICS
  9. Humoral control of the ICS
  10. Role of ICS in preventing bacterial overgrowth
  11. Conclusion
  12. References

The potential role of the ICS in limiting coloileal reflux has deserved further interest77 as the ICS separates two regions of the gut that differ ecologically and is supposed to be involved in the prevention of colonization of the ileum by colonic microflora. The operative loss of the ICS can enhance the retrograde bacterial ascension and, under certain circumstances, can lead to a severe bacterial overgrowth.78 This disturbance is a common finding in the terminal ileum of intestinal allograft recipients.79–81 However, the sole responsibility of ICS removal in such surgical outcome is difficult to establish. Indeed, additional factors such as manipulation of the transplanted bowel, lymphatic disruption, abnormal colonic motility, high steroid doses, postoperative need for temporary i.v. nutrition could be involved. This might explain why a clinical study in children fails to report an association between bacterial overgrowth and the lack of ICS.82 Furthermore, bacterial colonization and overgrowth occurred, in rats, after removal of the ileum with or without ICS preservation.83 Surprisingly, there were lower bacteria counts when the ICS was resected compared with ICS preservation. At present, no convincing explanation could support such result.

Conclusion

  1. Top of page
  2. Abstract
  3. Introduction
  4. ICS motility patterns
  5. The ileocaecocolonic segment: a functional entity
  6. Functional correlates of ICS motility
  7. Reflexes affecting ICS motility
  8. Neuronal control of the ICS
  9. Humoral control of the ICS
  10. Role of ICS in preventing bacterial overgrowth
  11. Conclusion
  12. References

In their extensive review of ICS motility, Phillips et al.84 highlighted the sphincteric properties of the ileocolonic junction based on their pioneering work in dogs and then in humans. Using the same adequate recording methods, an ICS has now been recognized by numerous research teams in dogs, pigs, horse and humans. However, we now understand that, unlike the pylorus, the ICS controls forward and backward flow through the integration of its motility with that of the distal ileum and proximal colon. Such combined activity explains the recent emphasis on local ileo-sphincteric and caeco-sphincteric reflexes. Some of the questions asked in the late 1980s as ‘might the generation of PPCs be related to coloileal reflux’ have now found the beginning of an answer. Indeed, in some species, PPCs are acting as clearance mechanism for SCFA-containing colonic reflux. Nevertheless, some of the questions, may be the most important towards the clinical significance of the ICS motility patterns, are still unanswered. For instance, the processes that achieve forward flow through the ICS are largely putative. The report in humans of a motor pattern localized to the ICS85 and resembling isolated pyloric pressure waves might bring further insights for a better understanding of the ICS role.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. ICS motility patterns
  5. The ileocaecocolonic segment: a functional entity
  6. Functional correlates of ICS motility
  7. Reflexes affecting ICS motility
  8. Neuronal control of the ICS
  9. Humoral control of the ICS
  10. Role of ICS in preventing bacterial overgrowth
  11. Conclusion
  12. References
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    Quigley EM, Phillips SF, Dent J. Distinctive patterns of interdigestive motility at the canine ileocolonic junction. Gastroenterology 1984; 87: 83644.
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    Dinning PG, Bampton PA, Kennedy ML, Cook IJ. Relationship between terminal ileal pressure waves and propagating proximal colonic pressure waves. Am J Physiol 1999; 277: G98392.
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    Allescher HD, Dent J, Daniel EE, Kostolanska F, Fox JET. Extrinsic and intrinsic neural control of pyloric sphincter pressure in the dog. J Physiol (Lond) 1988; 401: 1738.
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    Malbert CH. Passage of chyme, resistance and flow sensitive receptors at the antro-pyloro-duodenal junction. In: HolleGE, WoodJD, eds. Advances in the Innervation of the Gastrointestinal Tract. Amsterdam, The Netherlands: Elsevier Science Publishers B.V., 1992: 50112.
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    Malbert CH, Ruckebusch Y. Relationships between pressure and flow across the gastroduodenal junction in dogs. Am J Physiol 1991; 260(4 Pt 1): G6537.
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    Malbert CH, Roger T. The visualization of the pony caecocolic junction by the process of echotomography and its pharmacological reactions. Rev Med Vet 1989; 140: 85762.
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    Spiller RC, Brown ML, Phillips SF. Emptying of the terminal ileum in intact humans. Influence of meal residue and ileal motility. Gastroenterology 1987; 92: 7249.
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    Spiller RC, Brown ML, Phillips SF, Azpiroz F. Scintigraphic measurements of canine ileocolonic transit. Direct and indirect effects of eating. Gastroenterology 1986; 91: 121320.
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