Influence of intrinsic nerves on electromyogram of cat colon in vitro.

1978 ◽  
Vol 234 (6) ◽  
pp. E641 ◽  
Author(s):  
J Christensen ◽  
S Anuras ◽  
C Arthur
Keyword(s):  
Local Anesthetic ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Slow Waves ◽  
Adrenergic Agonists ◽  
Spike Burst ◽  
Intrinsic Nerves ◽  
Alpha Antagonist ◽  
Spike Bursts

The electromyogram of the circular muscle layer of the cat colon was studied in vitro in superfused strips of muscle. Records exhibited electrical slow waves and migrating spike bursts, as described previously. Both the neurotoxin, tetrodotoxin, and the local anesthetic lidocaine, (P less than 0.05) prolonged the duration of migrating spike bursts, but migrating spike bursts were not affected by the adrenergic alpha-antagonist, phenoxybenzamine, nor by the adrenergic beta-antagonist, propranolol. Also, physostigmine and atropine did not affect them. Large concentrations of catecholamines did abolish them. This suggests that the migrating spike burst represents periodic release of the muscle from the tonic influence of nonadrenergic inhibitory nerves in the intramural plexuses. Slow-wave frequency and the congruence of slow waves were not affected (P greater than 0.05) by the antagonists listed above, nor by cholinergic and adrenergic agonists. This suggests that the slow waves are not importantly controlled by intrinsic nerves.

Longitudinal contractions in the duodenum: their fluid-mechanical function

1975 ◽  
Vol 228 (6) ◽  
pp. 1887-1892 ◽  
Author(s):  
J Melville ◽  
E Macagno ◽  
J Christensen
Keyword(s):  
Longitudinal Muscle ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Slow Waves ◽  
Longitudinal Muscle Layer ◽  
Circular Muscle Layer ◽  
Model Flow ◽  
Displacement Wave ◽  
Marked Points

The hypothesis examined was that contractions of the longitudinal muscle layer occurin the duodenum which are independent of those of the circular muscle layer and that they induce flow of duodenal contents. A segment of opossum duodenum isolated in vitro was marked and photographed during periods of longitudinal muscle contraction, when the circular muscle layer appeared inactive. The prequency of longitudinal oscillation of the marked points was 20.5 cycles/min. The longitudinal displacement wave spread caudad with an average velocity of 3.27 cm/s. Frequency and velocity of electrical slow waves were determined in similiar duodenal segments. Slow-wave frquencywas 18.9 cycles/min. In a two-dimensional mechanical model, flow induced by simulatedlongitudinal muscle layer appear to be driven by the electrical slow waves of the duodenum. They are capable of inducing a pattern of flow in which ocntents flow betweenthe core and the periphery of the intestinal conduit.

Phase lock of electrical slow waves and spike bursts in cat duodenum

1975 ◽  
Vol 229 (3) ◽  
pp. 608-612 ◽  
Author(s):  
AR Sancholuz ◽  
Croley TE ◽  
J Christensen ◽  
EO Macagno ◽  
Glover
Keyword(s):  
Slow Wave ◽  
Delay Time ◽  
Phase Relationship ◽  
Slow Waves ◽  
Electrode Position ◽  
Spike Burst ◽  
Phase Lock ◽  
Wave Cycle ◽  
Spike Bursts

The phase relationship between slow waves and spike bursts was studied in vitro in the cat duodenum. Electrodes were arranged radially about the duodenum. Records were read for T1, the time between the slow-wave "valley" and the first spike, and T2, the time between successive valleys. The distributions of the ratio T1/T2 showed very small differences, not uniquely attributable to radial electrode position. The distribution of T1/T2 indicated that spike bursts began 58.8% of the way through a slow-wave cycle, measured from the valley. Also, electrodes were arranged longitudinally and records were read to determine deltaSW, the slow-wave delay time between adjacent electrode positions, and deltaS, the spike burst delay time between adjacent electrode positions. The correlation of deltaS and deltaSW suggested a linear relation, and a regression resulted in a good linear description. These results are consistent with an assumed phase lock of spike bursts to slow waves.

HCl-induced inflammatory mediators in cat esophageal mucosa and inflammatory mediators in esophageal circular muscle in an in vitro model of esophagitis

2006 ◽  
Vol 290 (6) ◽  
pp. G1307-G1317 ◽  
Author(s):  
Ling Cheng ◽  
Weibiao Cao ◽  
Claudio Fiocchi ◽  
Jose Behar ◽  
Piero Biancani ◽  
...  
Keyword(s):  
Inflammatory Mediators ◽  
Platelet Activating Factor ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Normal Mucosa ◽  
Esophageal Mucosa ◽  
Mrna Levels ◽  
Physiol Gastrointest Liver ◽  
Krebs Buffer

Platelet-activating factor (PAF) and interleukin-6 (IL-6) are produced in the esophagus in response to HCl and affect ACh release, causing changes in esophageal motor function similar to esophagitis (Cheng L, Cao W, Fiocchi C, Behar J, Biancani P, and Harnett KM. Am J Physiol Gastrointest Liver Physiol 289: G418–G428, 2005). We therefore examined HCl-activated mechanisms for production of PAF and IL-6 in cat esophageal mucosa and circular muscle. A segment of normal mucosa was tied at both ends, forming a mucosal sac (Cheng L, Cao W, Fiocchi C, Behar J, Biancani P, and Harnett KM. Am J Physiol Gastrointest Liver Physiol 289: G860–G869, 2005) that was filled with acidic Krebs buffer (pH 5.8) or normal Krebs buffer (pH 7.0) as control and kept in oxygenated Krebs buffer for 3 h. The supernatant of the acidic sac (MS-HCl) abolished contraction of normal muscle strips in response to electric field stimulation. The inhibition was reversed by the PAF antagonist CV3988 and by IL-6 antibodies. PAF and IL-6 levels in MS-HCl and mucosa were significantly elevated over control. IL-6 levels in mucosa and supernatant were reduced by CV3988, suggesting that formation of IL-6 depends on PAF. PAF-receptor mRNA levels were not detected by RT-PCR in normal mucosa, but were significantly elevated after exposure to HCl, indicating that HCl causes production of PAF and expression of PAF receptors in esophageal mucosa and that PAF causes production of IL-6. PAF and IL-6, produced in the mucosa, are released to affect the circular muscle layer. In the circular muscle, PAF causes production of additional IL-6 that activates NADPH oxidase to induce production of H2O2. H2O2 causes formation of IL-1β that may induce production of PAF in the muscle, possibly closing a self-sustaining cycle of production of inflammatory mediators.

Circumferential, not longitudinal, colonic stretch increases synaptic input to mouse prevertebral ganglion neurons

2003 ◽  
Vol 285 (6) ◽  
pp. G1129-G1138 ◽  
Author(s):  
Steven M. Miller ◽  
J. H. Szurszewski
Keyword(s):  
Synaptic Input ◽  
Muscle Tension ◽  
Circular Muscle ◽  
Longitudinal Axis ◽  
Muscle Layer ◽  
Intraluminal Pressure ◽  
Colon Wall ◽  
Mesenteric Ganglion ◽  
Ganglion Neurons

The relationship between longitudinal and circular muscle tension in the mouse colon and mechanosensory excitatory synaptic input to neurons in the superior mesenteric ganglion (SMG) was investigated in vitro. Electrical activity was recorded intracellularly from SMG neurons, and muscle tension was simultaneously monitored in the longitudinal, circumferential, or both axes. Colonic intraluminal pressure and volume changes were also monitored simultaneously with muscle tension changes. The results showed that the frequency of fast excitatory postsynaptic potentials (fEPSPs) in SMG neurons increased when colonic muscle tension decreased, when the colon relaxed and refilled with fluid after contraction, and during receptive relaxation preceding spontaneous colonic contractions. In contrast, fEPSP frequency decreased when colonic muscle tension increased during spontaneous colonic contraction and emptying. Manual stretch of the colon wall to 10-15% beyond resting length in the circumferential axis of flat sheet preparations increased fEPSP frequency in SMG neurons, but stretch in the longitudinal axis to 15% beyond resting length in the same preparations did not. There was no increase in synaptic input when tubular colon segments were stretched in their long axes up to 20% beyond their resting length. The circumferential stretch-sensitive increase in the frequency of synaptic input to SMG neurons persisted when the colonic muscles were relaxed pharmacologically by nifedipine (2 μM) or nicardipine (3 μM). These results suggest that colonic mechanosensory afferent nerves projecting to the SMG function as length or stretch detectors in parallel to the circular muscle layer.

Myogenic mechanism for peristalsis in the cat esophagus

1999 ◽  
Vol 277 (2) ◽  
pp. G306-G313 ◽  
Author(s):  
Harold G. Preiksaitis ◽  
Nicholas E. Diamant
Keyword(s):  
Muscle Contraction ◽  
Slow Wave ◽  
Circular Muscle ◽  
Smooth Muscle Contraction ◽  
Slow Waves ◽  
Mechanical Activity ◽  
Control Mechanisms ◽  
Slow Wave Oscillations

A myogenic control system (MCS) is a fundamental determinant of peristalsis in the stomach, small bowel, and colon. In the esophagus, attention has focused on neuronal control, the potential for a MCS receiving less attention. The myogenic properties of the cat esophagus were studied in vitro with and without nerves blocked by 1 μM TTX. Muscle contraction was recorded, while electrical activity was monitored by suction electrodes. Spontaneous, nonperistaltic, electrical, and mechanical activity was seen in the longitudinal muscle and persisted after TTX. Spontaneous circular muscle activity was minimal, and peristalsis was not observed without pharmacological activation. Direct electrical stimulation (ES) in the presence of bethanechol or tetraethylammonium chloride (TEA) produced slow-wave oscillations and spike potentials accompanying smooth muscle contraction that progressed along the esophagus. Increased concentrations of either drug in the presence of TTX produced slow waves and spike discharges, accompanied by peristalsis in 5 of 8 TEA- and 2 of 11 bethanechol-stimulated preparations without ES. Depolarization of the muscle by increasing K+ concentration also produced slow waves but no peristalsis. We conclude that the MCS in the esophagus requires specific activation and is manifest by slow-wave oscillations of the membrane potential, which appear to be necessary, but are not sufficient for myogenic peristalsis. In vivo, additional control mechanisms are likely supplied by nerves.

Origin of Motion in the Human Ureter: Mechanics, Energetics and Kinetics of the Myosin Molecular Motors

2012 ◽  
Vol 79 (2) ◽  
pp. 123-129 ◽  
Author(s):  
Romina Vargiu ◽  
Anna Perinu ◽  
Antonello De Lisa ◽  
Frank Tintrup ◽  
Francesco Manca ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Molecular Motors ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Shortening Velocity ◽  
Smooth Muscle Layer ◽  
Circular Smooth Muscle ◽  
Longitudinal Smooth Muscle ◽  
Human Ureter

Background Ureteral peristalsis is the result of coordinated mechanical motor performance of longitudinal and circular smooth muscle layer of the ureter wall. The main aim of this study was to characterize in smooth muscle of proximal segments of human ureter, the mechanical properties at level of muscle tissue and at level of myosin molecular motors. Methods Ureteral samples were collected from 15 patients, who underwent nephrectomy for renal cancer. Smooth muscle strips longitudinally and circularly oriented from proximal segments of human ureter were used for the in vitro experiments. Mechanical indices including the maximum unloaded shortening velocity (Vmax), and the maximum isometric tension (P0) normalized per cross-sectional area, were determined in vitro determined in electrically evoked contractions of longitudinal and circular smooth muscle strips. Myosin cross-bridge (CB) number per mm2 (Ψ) the elementary force per single CB (Ψ) and kinetic parameters were calculated in muscle strips, using Huxley's equations adapted to nonsarcomeric muscles. Results Longitudinal smooth muscle strips exhibited a significantly (p<0.05) faster Vmax (63%) and a higher P0 (40%), if compared to circular strips. Moreover, longitudinal muscle strips showed a significantly higher unitary force (Ψ) per CB. However, no significant differences were observed in CB number, the attachment (f1) and the detachment (g2) rate constants between longitudinal and circular muscle strips. Conclusions The main result obtained in the present work documents that the mechanical, energetic and unitary forces per CB of longitudinal layer of proximal ureter are better compared to the circular one; these preliminary findings suggested, unlike intestinal smooth muscle, a major role of longitudinal smooth muscle layer in the ureter peristalsis.

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

2007 ◽  
Vol 292 (4) ◽  
pp. G1162-G1172 ◽  
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.

Excitatory and inhibitory neural regulation of canine pyloric smooth muscle

1990 ◽  
Vol 259 (1) ◽  
pp. G125-G133 ◽  
Author(s):  
F. Vogalis ◽  
K. M. Sanders
Keyword(s):  
Action Potentials ◽  
Slow Component ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Slow Waves ◽  
Cross Sectional ◽  
Intrinsic Innervation ◽  
Circular Layer ◽  
Neuromuscular Apparatus ◽  
Excitatory Junction Potentials

Studies were performed to characterize the intrinsic innervation of the circular muscle layer of the canine pylorus. Cross-sectional strips of muscle were studied with intracellular recording techniques, and junction potentials were elicited with transmural nerve stimulation. Neurally mediated responses were recorded from cells at several points through the thickness of the circular layer. Excitatory junction potentials (EJPs) increased and inhibitory junction potentials (IJPs) decreased in amplitude with distance from the myenteric border of the circular muscle. Atropine blocked EJPs throughout the circular layer, demonstrating that excitatory inputs are primarily cholinergic. The gradient in IJP amplitude persisted after blockade of EJPs. Three components of IJPs were identified: 1) a fast, apamin-sensitive component that reached a peak and decayed within approximately 1 s; 2) a slower, apamin-insensitive component that reached a peak within 800 ms but decayed slowly over 5 s; and 3) a very slow component that reached a maximum in 7-10 s. Junctional potentials affected the pattern of myogenic electrical activity. Transmural stimulation could evoke premature slow waves in the myenteric portion of the circular layer but when excitatory inputs were blocked, IJPs greatly reduced the amplitude of slow waves. EJPs elicited action potentials in submucosal portion of circular muscles, and IJPs hyperpolarized these cells. The influence of intrinsic nerves on contractile patterns of pyloric muscles was also characterized. These data demonstrate that a neuromuscular apparatus exists within the gastroduodenal junction for 1) local regulation of slow waves and 2) independent control of the myenteric and submucosal regions of the circular layer.

Electrical slow-wave activity from the circular layer of cat terminal antrum

1991 ◽  
Vol 261 (1) ◽  
pp. G78-G82
Author(s):  
L. M. Renzetti ◽  
M. B. Wang ◽  
J. P. Ryan
Keyword(s):  
Slow Wave ◽  
Circular Muscle ◽  
Muscle Cells ◽  
Muscle Layer ◽  
Wave Activity ◽  
Slow Waves ◽  
Slow Wave Activity ◽  
Plateau Phase ◽  
Circular Layer ◽  
Upstroke Velocity

Intracellular recording techniques were used to characterize the electrical slow-wave activity through the thickness of the circular muscle layer of the cat terminal antrum. Muscle strips were pinned out in cross section to the floor of a recording chamber perfused with Krebs buffer. Circular muscle cells from the myenteric to the submucosal border then were impaled with 20- to 40-M omega glass microelectrodes, and slow-wave activity was recorded. Slow waves from the myenteric side of the circular layer consisted of an upstroke depolarization, a prominent plateau phase, and a downstroke repolarization. Slow-wave characteristics for cells along the myenteric border were Em, -74.2 +/- 1.3 mV; duration, 5.3 +/- 0.5 s; upstroke amplitude, 29.4 +/- 3.4 mV; upstroke velocity, 0.20 +/- 0.03 V/s; and frequency, 5.8 +/- 0.5/min. Slow waves from muscle cells along the submucosal side of the preparation lacked a discernible plateau phase. Slow waves from submucosal border cells had the following characteristics: Em, -80.4 +/- 1.4 mV (P less than 0.01); duration, 3.5 +/- 0.4 s (P less than 0.01); upstroke amplitude, 44.0 +/- 2.4 mV (P less than 0.01); upstroke velocity, 0.56 +/- 0.06 V/s (P less than 0.01); and frequency, 4.2 +/- 0.4/min (P less than 0.05). Slow waves were not affected by 10(-7)M tetrodotoxin and 10(-6)M atropine or by removal of the longitudinal muscle layer. Slow-wave activity within each region was maintained after dissecting the circular layer into submucosal and myenteric segments. The results suggest that two distinct slow waves exist within the circular muscle layer of the cat terminal antrum.(ABSTRACT TRUNCATED AT 250 WORDS)

Pylorectomy reduces the satiety action of cholecystokinin

1988 ◽  
Vol 255 (6) ◽  
pp. R1059-R1063 ◽  
Author(s):  
T. H. Moran ◽  
L. Shnayder ◽  
A. M. Hostetler ◽  
P. R. McHugh
Keyword(s):  
Binding Sites ◽  
Contractile Response ◽  
Behavioral Responses ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Pyloric Sphincter ◽  
Cck Receptors ◽  
Physiological Assessment ◽  
Significant Attenuation

Rat gastric cholecystokinin (CCK) receptors are localized to the circular muscle layer of the pyloric sphincter, and a role for these receptors in the mediation of CCK satiety has been proposed. To directly assess the contribution of this receptor population in CCK satiety, the area of the pyloric sphincter containing these receptors was surgically removed, and the behavioral responses to CCK were compared pre- and postpylorectomy. The presence of CCK receptors in the gastroduodenal junction was assessed by either in vitro CCK receptor autoradiography or in vitro contractile response to CCK. The results depended on the time after pylorectomy during which testing occurred. Two to 3 wk after pylorectomy rats demonstrated a significant attenuation of CCK satiety such that while the response to 1 and 2 micrograms/kg was intact, any additional inhibition by 4 and 8 micrograms/kg was eliminated. At this time, no evidence of CCK receptors around the gastroduodenal junction was found. In contrast, 2-3 mo after pylorectomy, the normal dose-response inhibition to CCK was intact. Evidence for the presence of CCK binding sites at the gastroduodenal junction was found by both autoradiography and physiological assessment. These results indicate a role for pyloric CCK receptors in the mediation of CCK satiety.

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