Muscarinic and 5-HT4 receptors participate in the regulation of the frequency of spontaneous contractions of the longitudinal muscle in rat distal colon

Spontaneous contractions of the intestine are thought to play an important role in the gastrointestinal motility, including peristalsis. In the present study, we investigated mechanisms for regulation of the frequency of spontaneous contractions, using longitudinal muscle strips in rat distal colon. Atropine significantly decreased the frequency of spontaneous contractions, indicating that neuromuscular transmission via muscarinic receptors increases the frequency of spontaneous contractions. SB-204070, 5-HT4 receptor antagonist also significantly decreased the frequency of spontaneous contractions, indicating that the activation of 5-HT4 receptors also increases the frequency of spontaneous contractions. In conclusion, it is suggested that muscarinic and 5-HT4 receptors participate in the regulation of the frequency of spontaneous contractions in the longitudinal muscle in rat distal colon, and that the frequency of spontaneous contraction is controlled by the enteric neurons.     

Propionate modulates spontaneous contractions via enteric nerves and prostaglandin release in the rat distal colon

Short-chain fatty acids, such as propionate and acetate, are produced by a bacterial fermentation of carbohydrates in the colonic lumen. We examined the effects of propionate on the frequency and mean amplitude of spontaneous giant contractions (GCs) in circular muscle strips of the rat distal colon with the mucosa attached. An addition of propionate increased the frequency of GCs for about 20 min (> or =1 mm), but the mean amplitude was decreased (> or =0.1 mm). The propionate-induced increase in the frequency of GCs was blocked by the muscarinic acetylcholine receptor antagonist, atropine. In contrast, the nicotinic receptor antagonist, hexamethonium, augmented the response. The propionate-induced decrease in the mean amplitude of GCs was prevented by the cyclooxygenase inhibitor, piroxicam. A pretreatment of the tissues with acetate prevented the propionate-induced modulations of the frequency and amplitude of GCs. These results suggest that propionate increases the frequency of GCs by an activation of cholinergic motor neurons and decreases the mean amplitude by a prostaglandin release. Propionate as well as acetate may be involved in the regulation of spontaneous circular muscle activity in the rat distal colon.     

Motor responses elicited by local electrical stimulation of the distal colon in the anaesthetized rat

A method to study electrically induced distal colonic motility in the rat in vivo is reported. The animals were anaesthetized with methohexital and chloralose and were artificially ventilated. Motility of a segment (2 cm) of the distal colon was monitored as volume changes of an intraluminal balloon, introduced via the anus. Local electrical stimulation of the wall of the segment was achieved by means of a bipolar electrode folded around the gut. Stimulations produced reproducible contractile responses in a frequency dependent fashion. Stimulation characteristics resembled those of other autonomic neuro-effector systems. The adrenergic neuron-blocker, guanethidine, significantly lowered colonic tone, but had no other effects on spontaneous or electrically induced motility. Atropine significantly lowered colonic tone. After the administration of this compound the electrically induced contractions were significantly smaller with a shorter duration and, furthermore, appeared upon the cessation of stimulation ('off' or 'rebound' contraction). Following the administration of tetrodotoxin (TTX, given close i.a. via a cannula with its tip in distal aorta) basal colonic tone and the number of spontaneously occurring contractions increased. The amplitude and duration of the electrically induced responses were significantly attenuated and, furthermore, appeared as 'rebound' contractions which were preceded by a relaxation. Such TTX-resistant responses may be myogenic, but a neurogenic origin cannot be excluded. The present study showed that local electrical stimulation of the distal colon elicits cholinergic contractions, but also atropine- and TTX-resistant motor responses.     

Atropine and naloxone block the colonic contraction elicited by cholecystokinin and pentagastrin

The effects of cholecystokinin (CCK) and gastrin on proximal and distal colonic motility were investigated because of the possible role of these peptides in feeding-induced colonic motility. Experiments were performed using 22 chloralose-urethane anaesthetized cats in which the colon was acutely denervated. The volume changes of the proximal and distal colon were recorded with water-filled flaccid balloons. The venous effluxes from the proximal and distal colon were recorded separately using drop recorder units. CCK-8, I-200 pmol X min-I close i.a., and pentagastrin, I-200 pmol X min-I close i.a., evoked dose-dependent contractions of the colon without altering systemic arterial blood pressure and colonic blood flow. The CCK peptides -8, -33 and -39 produced contractions of similar magnitude in the proximal and distal colon. The stimulatory effect of CCK-8 and pentagastrin on colonic motility was blocked by tetrodotoxin (I microgram X kg-I i.a.) and hexamethonium (I0 mg X kg-I i.v.). Atropine (0.5 mg X kg-I i.v.) completely blocked the responses to CCK-8 and pentagastrin in the distal colon but only partially in the proximal colon. Additional administration of naloxone (I mg X kg-I i.a.) abolished the remaining contractile response to the peptides in the proximal colon. The present results support the idea that CCK and pentagastrin have a stimulatory effect on distal colonic motility mediated via preganglionic and postganglionic cholinergic pathways. The possible role of opioid peptides and cholinergic mechanisms in the proximal colon is discussed.     

Intraluminal administration of zingerol, a non-pungent analogue of zingerone, inhibits colonic motility in rats

Zingerone, a pungent component of ginger, may exert beneficial therapeutic effects on hypermotility-induced diarrhea because it has the ability to inhibit contractions of colonic smooth muscles. However, the pungency is undesirable for possible therapeutic use. The purpose of this study was to examine effects of zingerol, a non-pungent analogue of zingerone, in rats. Colonic motility in vivo was evaluated by measuring intraluminal pressure changes and expelled fluid volume from the colon in anesthetized rats. Mechanical contractile activities of isolated colonic segments were also recorded. Intracolonic administration of zingerol attenuated colonic motility in vivo without affecting blood pressure and heart rate in a manner similar to that of zingerone. Zingerol also inhibited spontaneous contractile movements in isolated colonic segments, suggesting that zingerol directly acts on the colon. Zingerol had no effect on jejunal motility, although zingerone showed an inhibitory effect to the jejunum. These findings suggest that zingerol can inhibit colonic motility without adverse effects on small intestinal motility and the cardiovascular system. The non-pungent property of zingerol will be useful as an oral or suppository medicine for treating diarrhea and other gastrointestinal disorders.     

Effects of neurotensin, substance P and methionine-enkephalin on colonic motility

The influence of neurotensin, substance P and methionine-enkephalin (met-enkephaline) on proximal and distal colonic motility was studied in anesthetized cats. When administered i.v, at a dose of 14 pmol x kg-1 x min-1, neurotensin increased basal smooth muscle tone and antiperistaltic activity in the proximal colon. After higher doses of neurotensin the basal muscle tone also increased in the distal colon. Substance P at a dose of 17 pmol x kg-1 x min-1 selectively and powerfully stimulated the distal colon, thus causing a mass contraction pattern with a concomitant decrease in peristaltic amplitude. In the proximal part of the colon 17 pmol x kg -1 x min-1 of substance P exerted an inhibitory action on the peristaltic amplitude in animals with a high level of spontaneous activity. In addition, the basal muscle tone was slightly decreased. In animals with sluggish spontaneous activity, however, no effects were detected in the proximal colon. With increasing doses of substance P forceful contractions of the proximal colon were also registered. Met-enkephalin at a dose of 40 pmol x kg-1 x min-1 increased the smooth muscle basal tone with no effect on the peristaltic activity in the proximal or distal segments. The effect on basal tone was blocked by naloxone. Thus, neurotensin, substance P and met-enkephalin have distinct motor actions on the colon. At low doses neurotensin may stimulate the churning and mixing functions of the proximal colon. Substance P exerts its major effects on the distal part with a mass contraction response and met-enkepahlin increases the basal muscle tone equally in the proximal and distal parts of the colon.     

Non-nicotinic, non-adrenergic excitatory motor fibres in the preganglionic sympathetic supply to the feline colon. An axon reflex arrangement associated to thin sensory neurons, involving substance P?

Experiments were performed on chloralosed cats with ligated adrenals. The peripheral ends of the preganglionic sympathetic nerves to the colon were stimulated and colonic motility was monitored by a volumetric method. Electric nerve stimulation with various intensities elicited inhibitory motor responses and occasionally contractions. Hexamethonium and/or guanethidine blocked all inhibitory actions and revealed pure excitatory responses at high stimulation intensities. These colonic contractions were inhibited by atropine. However, atropine-resistant contractions were sometimes observed, predominantly in the colorectal region. Thoracic sympathetic nerves affected the motility in the proximal colon only, while lumbar sympathetic nerves acted on both proximal and distal parts. Strength-duration relationships and sensitivity to local heating suggest that the excitatory responses are due to an antidromic activation of thin, possibly afferent nerve fibres. Small doses of substance P injected close i.a. induced colonic contractions unchanged by hexamethonium and/or guanethidine but sensitive to atropine. The neurally-induced colonic contractions are suggested to be due to an antidromic activation of thin sensory neurons which in the periphery release substance P, in turn activating cholinergic motor neurons, thus constituting an axon reflex arrangement. The possibility of a similar axon reflex mechanism, associated to thin afferents, activating adrenergic inhibitory neurons at the prevertebral ganglionic level is discussed.     

Nitric oxide regenerates the normal colonic peristaltic activity in mdx dystrophic mouse

We demonstrated in vitro that the colonic peristaltic activity is modified in dystrophin-deficient mdx mouse indicating a defect in the enteric nervous system (ENS). Since nitric oxide (NO) has been proposed as a putative inhibitory mediator of ENS, here we have examined the effects of both L-Arginine (L-Arg) and Nomega-nitro-L-arginine methyl ester (L-NAME) on the peristaltic activity of mdx mouse distal colon. The motor pattern of colonic segment showed irregular peristaltic waves. L-Arg (10(-7) - 10(-5) M) induced the peristaltic activity to slow down. At a concentration of 10(-5) M, L-Arg produced hypomotility, characterised by a decrease in amplitude, frequency and ejected fluid volume. Conversely, L-NAME elicited hypermotility, this effect being reversed once again by the subsequent addition of L-Arg. Interestingly the addition of 10(-5) M L-Arg to the organ bath led to the normal progression, in an oral to aboral direction, of 90% of the peristaltic waves. This last result strongly suggests that exogenous application of L-Arg restores the integrative circuits of the ENS responsible for programming and co-ordinating peristaltic activity in the distal colon of mdx mouse.     

On the transmission of sacral parasympathetic nervous influence on distal colonic and rectal motility in the cat

Experiments were performed on cats anaesthetized with chloralose and treated with adrenoceptor blocking agents. Distal colonic and rectal motility were selectively recorded by a volumetric method. The effects of muscarinic and ganglionic nicotine receptor blockade on motor responses induced by graded efferent electrical pelvic nerve stimulation (PNS) were studied. Stimulation at low current strength evoked contractions in both the colon and the rectum, which were sensitive to atropine and to hexamethonium. High intensity stimulation elicited distal colonic contractions resistant to both atropine and hexamethonium. Similar excitatory responses to high strength PNS were also observed in the rectum, though not in all experiments. Stimulation at intermediate intensities evoked distal colonic and rectal relaxations which were resistant to atropine but blocked by hexamethonium. The results indicate that PNS influences colonic and rectal motility by activation of at least three discrete non-adrenergic nervous pathways: (1) low-threshold excitatory fibres involving nicotinic and muscarinic transmission, (2) high-threshold excitatory fibres with a non-muscarinic, non-nicotinic transmission mechanism, (3) inhibitory fibres with an intermediate stimulus intensity threshold, exerting their effect by a non-muscarinic mechanism involving a nicotinic step.     

Colonic Motility in the Cat

Rostad Colonic motility in the cat. 1. Extraluminal strain gage technique. Influence of anesthesia and temperature. Acta physiol. scand. 1973. 89. 79- 90. A technique for recording colonic motility in vivo with extraluminal strain gage transducers is described. This technique allowed segmental recording of the motility and proved more sensitive than intraluminal pressure devices. The transducers did not appear to interfere with the spontaneous colonic activity. Immediately after laparotomy considerable activity was observed in all parts of the colon. The degree of spontaneous motility varied from animal to animal, and from time to time in the same animal. The colon was seldom quiet unless the anesthesia was deep. Two main types of spontaneous contraction waves were observed: (i) slow waves of 0.5-2.0 min duration, and (ii) rhythmic waves of a frequency of 4–7 per min. Cooling of the abdominal wall resulted in augmented colonic motility, warming caused relaxation and reduced activity. Variation in body temperature between 3G and 39^o did not influence the motility.     

外源性硫化氢及K_(ATP)通道对大鼠慢性应激结肠高动力的调节

目的:研究外源性硫化氢(hydrogen sulfide,H2S)及ATP敏感性钾通道(ATP-sensitive potassium channels,KATP)在慢性应激结肠高动力中的作用。方法:制作慢性避水应激(water avoidance stress,WAS)和假避水应激(sham water avoidance stress,SWAS)大鼠模型,观察2组大鼠结肠肌条的收缩活性以及硫氢化钠(Na HS)和格列本脲预处理后对2组大鼠结肠肌条收缩影响并计算Na HS的半数抑制浓度(half maximal inhibitory concentration,IC50),使用免疫荧光及Western blotting法观察KATP通道各亚基在结肠中的分布及表达。结果:WAS组结肠肌条收缩活性明显高于SWAS组;Na HS浓度依赖性抑制2组大鼠纵行肌(longitudinal muscle,LM)和环形肌(circular muscle,CM)的收缩;WAS组LM和CM的Na HS IC50分别为0.2033 mmol/L和0.1438 mmol/L,均明显低于SWAS组(P0.01);格列本脲明显增加2组大鼠肌条Na HS IC50(P0.01);Kir6.1、Kir6.2和SUR-2B在2组大鼠结肠固有肌细胞膜均有分布;WAS组(去除黏膜及黏膜下层后)Kir6.1和SUR2B蛋白表达高于SWAS组(P0.01)。结论:H2S外源性供体Na HS对慢性应激结肠高动力具有潜在的治疗作用。KATP通道亚基Kir6.1/SUR2B表达增加可能是慢性应激结肠动力紊乱的一种适应性反应。     

Impairment and restoration of spontaneous contractile activity of longitudinal smooth muscles in the TNBS-inflamed hamster distal colon

In the present study, we aimed to determine how inflammation affects spontaneous motility in the longitudinal direction of a hamster colon preparation. Trinitrobenzene sulfonic acid (TNBS) injected into the distal colon caused diarrhea 4-7 days after the treatment, but diarrhea was not observed in hamsters kept for 4 weeks. At 1 week after induction of colitis, spontaneous motility in the longitudinal direction was strongly suppressed. Contraction of longitudinal smooth muscles induced by electrical field stimulation was impaired, but not that induced by exogenously applied acetylcholine, indicating that acute inflammation preferentially impairs neurotransmissions with a minor effect on contractility of the longitudinal smooth muscle itself. The spontaneous motility reappeared in the colonic preparation isolated from the hamster maintained for 4 weeks after induction of colitis. The reappearance of the motility accompanied cholinergic and nitrergic regulations of contractile activity. These results demonstrated that impairment and following restoration of spontaneous contractile activity of longitudinal smooth muscles in the TNBS-inflamed distal colon of the hamster may depend on the damage and recovery of neural factors, rather than alteration of muscle contractility.     

Neuropeptide Y may mediate effects of sympathetic nerve stimulations on colonic motility and blood flow in the cat

The present study investigated sympathetic mechanisms involved in the regulation of colonic motility and blood flow in the cat. Infusion of neuropeptide Y (NPY) close i.a. produced an inhibition of colonic motility and a vasoconstriction of long duration but no post-infusion vasodilatation. In contrast to NPY, porcine pancreatic polypeptide did not evoke any vascular or motility response. On a molar basis, NPY was 25 times more potent than noradrenaline in producing 50% reduction of the colonic blood flow. These vascular and motility effects of NPY were resistant to guanethidine, phentolamine, phenoxybenzamine and propranolol. Thus, the action of NPY on vascular and colonic smooth muscle did not seem to be mediated via adrenergic receptors. Noradrenaline administered close i.a. produced inhibition of colonic motility, and vasoconstriction followed by a rapid vasodilatation. These effects were completely blocked by combined alpha- and beta-adrenoceptor blockade. Electrical stimulation of the splanchnic and lumbar colonic nerves produced an overall inhibition of colonic motility, and vasoconstriction of the proximal and distal colon, respectively, with a rapid post-stimulatory vasodilatation. After combined alpha- and beta-adrenoceptor blockade the inhibitory effect of the nerve stimulations on colonic motility partly remained together with a marked vasoconstriction, which was most pronounced upon lumbar colonic nerve stimulation. All vascular effects of sympathetic nerve stimulation were eradicated by guanethidine, which also abolished the inhibitory motility response to splanchnic nerve stimulation. However, lumbar colonic nerve stimulation elicited a colonic contraction, possibly due to stimulation of afferent C-fibres. The present findings indicate the existence of a sympathetic nonadrenergic neuronal mechanism mediating vasoconstriction and inhibition of colonic motility in the cat. Thus, NPY may be released from noradrenergic neurons to act on colonic smooth muscle and vessels.     

Prolonged ambulatory monitoring of colonic motor activity in the pig.

The aim of this study was to develop a chronic model suitable for repeated, long-term studies of the interaction of behavior and colonic function in unrestrained pigs. Cecostomies were created in three 20-30 kg micropigs under general anesthesia. Fistulas were created by suturing the bowel to the abdominal wall. Recordings were made by passing a small (8F) solid-state pressure transducer through the fistula into the proximal bowel and connecting it to a battery-operated data logger worn in a vest on the pig's back. Cecostomies have remained patent and trouble-free for over 18 months. No serious infections have occurred. Preliminary data from a total of thirteen 24-h recording sessions showed 54% of all contractile activity to be in the 2-4 cpm frequency range. Increased motility was seen following meals and upon morning awakening. Motility was minimal during the night. Infrequent (10.31 +/- 2.05/24 h; mean +/- SD) propagated contractions were also noted. These contractions were generally of low amplitude (33.24 +/- 3.81 mmHg). These techniques allow prolonged, intraluminal recordings to be made from the colon of the unrestrained pig.     

The effects of 5-hydroxytryptamine on large intestinal motility and blood flow in the cat

The effects of 5-HT on proximal colonic and rectal motility and total colonic blood flow were studied in anaesthetized cats and compared with those evoked by pelvic nerve stimulation. Vasodilator responses, consistently elicited by low doses (5-10 micrograms/min close i.a.) and intermediate doses (10-50 micrograms/min) of 5-HT were invariably abolished by hexamethonium indicating a nerve mediated response. Simultaneously to the vasodilator response both cholinergic and non-cholinergic hexamethonium sensitive non-adrenergic motility responses were evoked in the proximal colon. Furthermore non-cholinergic, non-adrenergic inhibitory neurons were excited. In the rectum excitation of such inhibitory neurons was the most consistent finding. The mechanisms behind the nerve mediated vascular and motility responses seem to differ as only the vascular effects were blocked by dihydroergotamine. The nerve mediated responses were in many respects similar to those evoked by pelvic nerve stimulation indicating that 5-HT exerts its effects on the same instrinsic neurons as the pelvic nerves. At intermediate and high doses (50-100 micrograms/min) the effects exerted on the instrinsic reflex arcs were modulated by direct effects on the smooth muscle.     

Comparison of proximal and distal colonic muscle of the rabbit.

Mechanical length-tension properties and response to neurohumoral agents were compared for proximal and distal colonic muscle. Resting tension during stretch, acetylcholine-stimulated tension, and the total tension were determined. Proximal circular muscle developed a maximum total tension of 0.96 +/- 0.18 kg/cm2 (mean +/- SE) compared to 0.86 +/- 0.06 kg/cm2 for the distal colon (P greater than 0.05). Resting tension was 0.33 +/- 0.03 kg/cm2 for the proximal colon and 0.05 +/- 0.01 kg/cm2 for the distal colon at the length of optimal acetylcholine-stimulated tension (Lo) (P less than 0.01). Longitudinal muscle showed a similar difference for the proximal and distal colon. The high resting tension in the proximal colonic muscle was reduced by nitroprusside or calcium-free Krebs with EGTA. Dose-response curves to acetylcholine, histamine, phenylephrine, and isoproterenol were similar for the muscle of either part of the colon. Gastrin or cholecystokinin had no effect on the muscle. In summary, the circular or longitudinal muscles of the proximal and distal colon have different length-tension properties but only minimal differences in response to neurohumoral agents.     

Chronic restraint stress has no more stimulatory effects on colonic motility in rats

Previous studies have shown that acute stress stimulates colonic motor function via a central corticotropin releasing factor (CRF) in rodents. However, little is known whether colonic motility is altered following chronic stress. We studied the changes of colonic motor function in response to chronic stress or daily administration of CRF in rats. Rats were subjected to restraint stress for 90 min for 5 consecutive days (chronic stress). Another group of rats received intracisternal (IC)-injection of CRF (1 μg) for 5 consecutive days. At the 1st day of restraint stress, calculated motility index was significantly increased by over 200% of basal in the proximal and distal colon. Similar results were obtained in response to the 2nd and 3rd day of restraint stress. In contrast, at the 5th day, restraint stress caused no more significant increase of colonic motility. Similarly, accelerated colonic transit induced by acute stress was no more observed following chronic stress. Increased, colonic motility and accelerated colonic transit induced by CRF were not attenuated at the 5th day. It is suggested that adaptation mechanism is developed following chronic stress. The decrease in colonic motor function in chronic stress is not due to reduced sensitivity to central CRF.     

Study of the functional activity of the cecocolonic junction with identification of a "physiologic sphincter", "cecocolonic inhibitory reflex" and "colocecal excitatory reflex"

Radiologic, endoscopic and histomorphologic studies have suggested the presence of a sphincter at the cecocolonic junction (CCJ), while some investigators have denied its existence. To investigate the physiologic activity at the CCJ, the right colon was exposed during right hemicolectomy for early colonic cancer in 11 patients (mean age 43.6+/-12.3 years; 8 men). Three manometric catheters were introduced through colotomy to be separately located in the cecum, CCJ and ascending colon. We determined the CCJ pressure response to cecal and colonic distension by means of a balloon filled with saline in increments of 10 ml. The test was repeated after individual anesthetization of cecum, CCJ and ascending colon. The CCJ measured 1.6+/-0.6 cm in length and had a higher pressure ( p<0.05) than the cecum or colon. Large-volume cecal distension effected a significant CCJ pressure reduction which was augmented as the distension increased. Latency decreased upon increase of the distending volume. In contrast, the CCJ responded to large-volume colonic distension by pressure elevation which increased upon increase of the distending volume. Latency diminished with increased distension. Small-volume cecal or colonic distension effected no CCJ pressure response. The anesthetized CCJ did not respond to distension of the cecum or colon. Likewise, the CCJ did not exhibit a pressure response to distension of the anesthetized cecum or colon. The CCJ is a high-pressure zone which reacts to cecal or colonic distension by dilatation or narrowing, respectively. These data presumably denote the existence of a physiologic sphincter at the CCJ. We suggest that the CCJ pressure response to cecal or colonic distension is reflex and mediated through the cecocolonic inhibitory and colocecal excitatory reflexes, respectively. The role of the CCJ and related reflexes in colonic motility disorders needs to be studied.     

Effects of nicotinic receptor blockade on the colonic mucosal response to luminal bile acids in anaesthetized rats

AIM: To test the hypothesis that nicotinic receptor mechanisms mediate the effects of bile acids on the colonic mucosa. METHODS: The epithelial transport response to 4 mm deoxycholic acid (DCA) was studied in vitro and in vivo, in rat colon. In vitro, epithelial resistance was measured by square pulse analysis, and net membrane current was calculated from the transmucosal potential difference (PD) and resistance. In vivo, we measured PD and net fluid transport. RESULTS: In vitro, DCA significantly increased membrane current and induced a progressive decrease in epithelial resistance, which in the distal colon eventually resulted in a significant PD reduction. This response was not significantly affected by hexamethonium. In vivo, DCA reduced PD with a significantly larger response in distal colon, but had no consistent effect on net fluid absorption. Nicotinic receptor blockade per se increased net fluid absorption and slightly reduced PD in proximal colon, and inhibited spontaneous net fluid secretion and markedly reduced PD in distal colon. Nicotinic receptor blockade significantly attenuated the bile-acid induced PD response. CONCLUSION: The data do not support the theory that a bile acid-activated secretory reflex exists in rat colon. The reduced PD response after hexamethonium suggests that a mechanism involving nicotinic receptors may potentiate the permeability response to luminal bile acids.     

Stability of Myoelectric Slow Waves and Contractions Recorded from the Distal Colon

The stability of physiological activity in the distal colon was investigated by recording 5-6 hours in each of 6 healthy adults. Contractions and myoelectric slow waves were recorded from the sigmoid colon (25-30 cm from the skin surface) and rectum (10-15 cm), and pressure waves were recorded from the proximal small intestine. The activity index (sum of areas of all waves divided by recording time) varied by 200% to 800% across 4-min samples for all motility and myoelectric slow wave recordings. Spectral analysis indicated that contractile activity waxed and waned in a cycle with a period of 40-55 min in the colon and 64-80 min in the small intestine. Myoelectric slow wave activity in the colon cycled with a period of 30-40 min. Contractile activity in the sigmoid colon was correlated with similar activity in the rectum, but myoelectric slow wave activity in the colon was not correlated with myoelectric slow waves in the rectum. The frequency composition of contractions and slow waves was unstable over time.