Excitatory and inhibitory enteric neural input to intestinal muscle acting on ongoing myogenic activity determines the rich repertoire of motor patterns involved in digestive function. The enteric neural activity cannot yet be established during movement of intact intestine in vivo or in vitro. We propose the hypothesis that is possible to deduce indirectly, but reliably, the state of activation of the enteric neural input to the muscle from measurements of the mechanical state of the intestinal muscle. The fundamental biomechanical model on which our hypothesis is based is the “three-element model” proposed by Hill. Our strategy is based on simultaneous video recording of changes in diameters and intraluminal pressure with a fiber-optic manometry in isolated segments of rabbit colon. We created a composite spatiotemporal map (DPMap) from diameter (DMap) and pressure changes (PMaps). In this composite map rhythmic myogenic motor patterns can readily be distinguished from the distension induced neural peristaltic contractions. Plotting the diameter changes against corresponding pressure changes at each location of the segment, generates “orbits” that represent the state of the muscle according to its ability to contract or relax actively or undergoing passive changes. With a software developed in MatLab, we identified twelve possible discrete mechanical states and plotted them showing where the intestine actively contracted and relaxed isometrically, auxotonically or isotonically, as well as where passive changes occurred or was quiescent. Clustering all discrete active contractions and relaxations states generated for the first time a spatio-temporal map of where enteric excitatory and inhibitory neural input to the muscle occurs during physiological movements. Recording internal diameter by an impedance probe proved equivalent to measuring external diameter, making possible to further develop similar strategy in vivo and humans.

The effects of enteric nerve stimuli were investigated on spontaneously occurring colonic migrating motor complexes (CMMCs) in isolated mouse colon. Changes in circular smooth muscle tension were recorded simultaneously from the proximal, mid and distal regions of an in vitro preparation of whole mouse colon at 36 +/- 1 degrees C. The CMMCs were recorded from all preparations with a mean interval between contractions ranging from 135.2 +/- 9.3 to 163.3 +/- 22.4 s. The CMMCs migrated spontaneously from the proximal to distal colon and were abolished by tetrodotoxin (1 micromol L-1). In approximately half of all trials (57 of 103, n = 31), trains of stimuli (20 Hz, 2-5 s, 1 ms, 40-70 V) delivered to the mid or distal regions of colon, during the intervals between CMMCs, elicited a premature CMMC. However, similar trains of stimuli delivered to the proximal colon were without similar effects (33 trials, n = 13). It is suggested that in isolated whole mouse colon, CMMCs can be evoked prematurely by trains of electrical stimuli applied to the enteric nerves. The observation that nerve stimuli failed to evoke a premature CMMC from the proximal colon suggests that selective activation of functional ascending pathways may be required to initiate a premature CMMC.

We investigated the involvement of muscle tone and circular muscle (CM) contraction in peristalsis in isolated guinea‐pig small intestine. A segment of jejunum (≈13 cm) was mounted into a three chambered partitioned bath. Peristaltic waves were initiated in the oral chamber eitherby: (1) infusing fluid into the oral end of the jejunum; the ejected fluid was diverted via a cannula from reaching the intermediate and anal chambers, or by (2) intraluminal balloon distension of the empty oral segment. Tension of the circular muscle was measured in all three chambers. Peristaltic waves elicited by fluid infusion were evoked at an abrupt threshold. In contrast, peristaltic waves elicited by distension could be graded in amplitude according to stimulus intensity. Peristaltic waves evoked in an empty intestine exhibited similar propagation velocities to peristaltic waves associated with fluid propulsion. Nifedipine (200‐400 nM) added to the intermediate chamber to block muscle contraction did not prevent peristaltic waves elicited by either stimulus from propagating into the anal chamber, although their amplitude was attenuated. Nifedipine to the site of stimulation (oral chamber) abolished peristaltic waves generated by either stimulus. Tetrodotoxin (1‐2 μM), or a low Ca2+‐high Mg2+ solution to the intermediate chamber abolished the propagation of peristalsis from the oral to anal chambers. In conclusion, graded peristaltic waves can occur in an empty intestine. Therefore peristalsis is not necessarily an ‘all‐or‐none’ phenomenon. Peristalsis depends on the spread of nervous activity along the bowel, rather than the reactivation of neural circuits caused by displacement of fluid in the lumen. However, local muscle tone and contraction are important for the initiation and maintenance of peristaltic propagation.

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