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Journal articles on the topic 'Distension'
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1
Bouhassira, Didier, Jean-Marc Sabaté, Benoit Coffin, Daniel Le Bars, Jean-Claude Willer, and Raymond Jian. "Effects of rectal distensions on nociceptive flexion reflexes in humans." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 3 (September 1, 1998): G410—G417. http://dx.doi.org/10.1152/ajpgi.1998.275.3.g410.
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We previously showed that gastric distension inhibits the somatic nociceptive flexion RIII reflex. To explore further the viscerosomatic interactions, we tested in the present study the effects of rectal distensions on RIII reflexes. Rapid and slow-ramp rectal distensions were performed in 10 healthy volunteers with an electronic barostat. The RIII reflex was continuously recorded from the lower limb during both types of distension and from the upper limb during rapid distensions. The visceral sensations were scored on a graded questionnaire. Rapid distensions facilitated the RIII reflex recorded from the lower limb, but at the highest distension level, facilitation was followed by inhibition. Slow-ramp distension induced gradual inhibition of the RIII reflex, which correlated with both distension volume and visceral sensation. RIII reflex recorded from the upper limb was also inhibited by rapid rectal distensions. Reflex inhibitions were probably related to the activation of pain modulation systems. One plausible explanation for the facilitatory effects, observed only at the lower limb, is the convergence of rectal and reflex afferents at the same levels of the spinal cord. The differential effects of rapid and slow-ramp distensions suggest the activation of two distinct populations of mechanoreceptors by these two modes of distension.
2
Coffin, Benoit, Robert Chollet, Bernard Flourié, Marc Lémann, Claire Franchisseur, Jean-Claude Rambaud, and Raymond Jian. "Intraluminal modulation of gastric sensitivity to distension: effects of hydrochloric acid and meal." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 5 (May 1, 2001): G904—G909. http://dx.doi.org/10.1152/ajpgi.2001.280.5.g904.
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Conscious sensations in response to gut distensions may be modulated by temporospatial interactions among different stimuli. This study investigated whether symptoms induced by gastric distension may be modified by hydrochloric acid (HCl) gastric infusion and meal ingestion. In nine healthy subjects, fixed pressure (isobaric) and fixed volume (isovolumetric) distensions were performed during continuous (4 ml/min) intragastric saline or HCl infusion, during fasting and after meal ingestion, until the maximal distension step defined as discomfort or a predefined maximal volume. During fasting isobaric distensions, the maximal distension step was significantly decreased during HCl compared with saline. The intragastric volumes were not significantly different, but the wall tension was significantly lower during HCl than saline. HCl increased gastric compliance. Meal ingestion relaxed the stomach and decreased the pressure at the maximal distension step during saline, but HCl did not further decrease it compared with fasting. During isovolumetric distensions, HCl also increased gastric compliance, but in both fasted and fed states it did not modify the maximal distension steps. In conclusion, sensations in response to gastric isobaric distensions, but not to isovolumetric distensions, are influenced by gastric acid infusion and meal ingestion. The effects of HCl might be related to a sensitization of mucosal mechanoreceptors.
3
Law, Ngai-Moh, Adil E. Bharucha, and Alan R. Zinsmeister. "Rectal and colonic distension elicit viscerovisceral reflexes in humans." American Journal of Physiology-Gastrointestinal and Liver Physiology 283, no. 2 (August 1, 2002): G384—G389. http://dx.doi.org/10.1152/ajpgi.00359.2001.
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Colonic transit is slowed in patients with disordered rectal evacuation, but the mechanism of this phenomenon is unclear. Our objective was to investigate rectocolonic inhibitory reflexes in humans to provide potential insight into patients with obstructed defecation. In 30 healthy subjects, a barostat-manometric assembly recorded colonic tone and phasic activity in the descending colon during rectal distension and recorded rectal tone during colonic distension. Phasic distensions were 8, 16, and 32 mmHg above balloon operating pressure, and staircase inflations were comprised of balloon inflation then deflation in 2-mmHg increments at 30-s intervals from 0 to 36 mmHg. Colonic balloon volumes increased to a similar extent during phasic rectal distensions 8, 16, and 32 mmHg above operating pressure, reflecting reduced colonic tone; balloon volumes also increased and phasic pressure activity decreased during staircase rectal distensions. In contrast, rectal balloon volume declined, reflecting increased tone during phasic and staircase colonic distensions. Thus rectal distension inhibited colonic motor activity, indicative of a viscerovisceral inhibitory reflex.
4
Paterson, W. G., S. Rattan, and R. K. Goyal. "Esophageal responses to transient and sustained esophageal distension." American Journal of Physiology-Gastrointestinal and Liver Physiology 255, no. 5 (November 1, 1988): G587—G595. http://dx.doi.org/10.1152/ajpgi.1988.255.5.g587.
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With the use of intraluminal manometry in alpha-chloralose-anesthetized opossums, distal esophageal and lower esophageal sphincter responses to prolonged midesophageal balloon distension were compared with those evoked by single transient distensions, vagal efferent stimulation, and swallowing. Balloon inflation caused sphincteric relaxation that recovered during small volume but persisted during large volume-prolonged distension. The esophageal body was either quiescent or exhibited nonperistaltic contractions during prolonged distension. Balloon deflation induced non-peristaltic esophageal and sphincteric contractions as well as further sphincter relaxation. Responses to prolonged large and small volume balloon distension resembled those evoked by high- and low-frequency vagal efferent stimulation, respectively. However, vagal-stimulated "on" contractions were not seen with balloon distension, and atropine did not modify excitatory responses occurring during or after prolonged distension. Although transient distension induced peristaltic esophageal contractions, the peristaltic velocity was faster than swallow-induced peristalsis. With transient distension, atropine prolonged the latency to contraction in the mid but not the distal smooth muscle segment and thus increased peristaltic velocity. These studies demonstrate that 1) esophageal distension evokes a wide spectrum of lower esophageal sphincter and esophageal body response, and 2) cholinergic neurons play a minimal role in distension-induced responses of the distal esophageal circular muscle below the distending balloon.
5
Sabate, Jean-Marc, Benoit Coffin, Raymond Jian, Daniel Le Bars, and Didier Bouhassira. "Rectal sensitivity assessed by a reflexologic technique: further evidence for two types of mechanoreceptors." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 4 (October 1, 2000): G692—G699. http://dx.doi.org/10.1152/ajpgi.2000.279.4.g692.
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We previously showed that slow-ramp rectal distensions induce graded inhibitions of the somatic nociceptive RIII reflex recorded from the lower limb, which correlated with both distension volume and visceral sensation. In contrast, rapid phasic rectal distensions induced facilitatory or biphasic effects (i.e., facilitations followed by inhibitions) depending on the level of distension. To examine the role of mucosal and serosal rectal mechanoreceptors in these viscerosomatic interactions, we analyzed, in six healthy volunteers, the effects of both types of rectal distension on the RIII reflex after topical application of lidocaine or placebo administered in a double-blind and crossover fashion. Inhibitions of the RIII reflex induced by both slow-ramp and rapid distensions were strongly reduced after administration of lidocaine but not after placebo. In contrast, facilitations of the RIII reflex observed during the initial phase of rapid distensions were not modified after lidocaine or placebo applications. These results suggest that inhibitions, but not facilitations, of the nociceptive RIII reflex triggered by rectal distensions depend preferentially on the activation of superficial mucosal receptors. This reflexologic technique might thus represent an interesting tool for studying the role of the different rectal mechanoreceptors involved in visceral sensations.
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Mittal, R. K., D. F. Rochester, and R. W. McCallum. "Sphincteric action of the diaphragm during a relaxed lower esophageal sphincter in humans." American Journal of Physiology-Gastrointestinal and Liver Physiology 256, no. 1 (January 1, 1989): G139—G144. http://dx.doi.org/10.1152/ajpgi.1989.256.1.g139.
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We studied the effects of involuntary and voluntary contraction of the diaphragm on esophagogastric junction (EGJ) pressure during esophageal distension in healthy human volunteers. The EGJ pressure was monitored using a Dent sleeve device. Along with the pressure we concurrently monitored diaphragm electromyogram (EMG) using intra-esophageal bipolar electrodes that were placed on the nonpressure sensing surface of the sleeve device. Graded esophageal distensions were performed by graded inflations of a 2-cm-diameter balloon that was positioned 7 cm above the EGJ. The graded esophageal distensions caused a graded increase in the amplitude of lower esophageal sphincter (LES) relaxation (end-expiratory EGJ pressure). In a majority of the subjects, esophageal distension had no effect on spontaneous inspiratory EGJ pressure increase and diaphragm EMG. During sustained LES relaxation of greater than 70% induced by sustained esophageal distention, graded voluntary contractions of the diaphragm induced proportional increases in the EGJ pressure and diaphragm EMG. The EGJ pressure and diaphragm EMG were similar during diaphragmatic contraction both before and during esophageal distension. During a maximal and sustained diaphragm contraction, esophageal distension had no effect on the EGJ pressure. We conclude that there are two distinct sphincteric mechanisms at the EGJ, the LES and crural diaphragm, and they respond differently to distension of the distal esophagus.
7
Ladabaum, Uri, Morton B. Brown, Wenqin Pan, Chung Owyang, and William L. Hasler. "Effects of nutrients and serotonin 5-HT3 antagonism on symptoms evoked by distal gastric distension in humans." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 2 (February 1, 2001): G201—G208. http://dx.doi.org/10.1152/ajpgi.2001.280.2.g201.
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Distal gastric distension may contribute to meal-related dyspeptic symptoms. This study's aims were to determine the effects of distinct nutrient classes on symptoms induced by distal gastric distension and their dependence on 5-hydroxytryptamine3 (5-HT3) receptors. Nine healthy subjects rated pain, nausea, and bloating induced by isobaric distal gastric distensions (6–24 mmHg) during duodenal lipid, carbohydrate, protein, or saline perfusion after treatment with placebo or the 5-HT3 receptor antagonist granisetron (10 μg/kg iv). Distensions produced greater pain, nausea, and bloating with lipid at 1.5 kcal/min compared with saline ( P≤ 0.02), primarily because of greater distal gastric volumes at each distending pressure. In contrast, carbohydrate and protein had no significant effect. At 3 kcal/min, lipid increased symptoms through a volume-independent as well as a volume-dependent effect. Granisetron did not affect symptom perception or gastric pressure-volume relationships. In conclusion, isobaric distal gastric distension produces more intense symptoms during duodenal lipid compared with saline perfusion. Symptom perception during distal gastric distension is unaffected by 5-HT3 receptor antagonism.
8
Hibberd, Timothy J., Garreth R. Kestell, Melinda A. Kyloh, Simon J. H. Brookes, David A. Wattchow, and Nick J. Spencer. "Identification of different functional types of spinal afferent neurons innervating the mouse large intestine using a novel CGRPα transgenic reporter mouse." American Journal of Physiology-Gastrointestinal and Liver Physiology 310, no. 8 (April 15, 2016): G561—G573. http://dx.doi.org/10.1152/ajpgi.00462.2015.
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Spinal afferent neurons detect noxious and physiological stimuli in visceral organs. Five functional classes of afferent terminals have been extensively characterized in the colorectum, primarily from axonal recordings. Little is known about the corresponding somata of these classes of afferents, including their morphology, neurochemistry, and electrophysiology. To address this, we made intracellular recordings from somata in L6/S1 dorsal root ganglia and applied intraluminal colonic distensions. A transgenic calcitonin gene-related peptide-α (CGRPα)-mCherry reporter mouse, which enabled rapid identification of soma neurochemistry and morphology following electrophysiological recordings, was developed. Three distinct classes of low-threshold distension-sensitive colorectal afferent neurons were characterized; an additional group was distension-insensitive. Two of three low-threshold classes expressed CGRPα. One class expressing CGRPα discharged phasically, with inflections on the rising phase of their action potentials, at low frequencies, to both physiological (<30 mmHg) and noxious (>30 mmHg) distensions. The second class expressed CGRPα and discharged tonically, with smooth, briefer action potentials and significantly greater distension sensitivity than phasically firing neurons. A third class that lacked CGRPα generated the highest-frequency firing to distension and had smaller somata. Thus, CGRPα expression in colorectal afferents was associated with lower distension sensitivity and firing rates and larger somata, while colorectal afferents that generated the highest firing frequencies to distension had the smallest somata and lacked CGRPα. These data fill significant gaps in our understanding of the different classes of colorectal afferent somata that give rise to distinct functional classes of colorectal afferents. In healthy mice, the majority of sensory neurons that respond to colorectal distension are low-threshold, wide-dynamic-range afferents, encoding both physiological and noxious ranges.
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Manthey, M. W., B. T. Massey, R. C. Arndorfer, and W. J. Hogan. "Determinants of lower esophageal sphincter relaxation induced by esophageal balloon distension in humans." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 6 (June 1, 1996): G1022—G1027. http://dx.doi.org/10.1152/ajpgi.1996.270.6.g1022.
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The determinants of the lower esophageal sphincter relaxation response to esophageal distension have not previously been systematically examined in humans. In this study, 14 healthy subjects were tested using a manometry catheter with a sleeve device and three balloons spaced 5 cm apart. Subjects had up to five distensions with each balloon at four different diameters and two different durations of inflation. The results indicated that 1,170 separate distensions were available for analysis. Sphincter relaxation occurred more frequently (P < 0.005) with larger balloon diameters, yet occurred in only 84% of inflations at the largest diameter. Sphincter relaxation was more often observed with the proximal balloon (P < 0.005) during longer distensions (P < 0.05) and when esophageal contractions occurred above the balloon (P < 0.005). Once sphincter relaxation occurred, its magnitude was essentially independent of balloon site and diameter, distension duration, and the presence of proximal contractions. In conclusion, even large balloon distensions do not uniformly produce or maintain lower esophageal sphincter relaxation. Sphincter relaxation is more likely with proximal esophageal distension. The association of sphincter relaxation with vagally mediated proximal contractions suggests vagal modulation of this response.
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Willing, A. E., and H. R. Berthoud. "Gastric distension-induced c-fos expression in catecholaminergic neurons of rat dorsal vagal complex." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 1 (January 1, 1997): R59—R67. http://dx.doi.org/10.1152/ajpregu.1997.272.1.r59.
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Functionally specific vagal afferents were stimulated by gastric balloon distension in unanesthetized rats, followed by double c-fos/dopamine beta-hydroxylase (DBH) immunocytochemistry, to identify second-order neurons in the dorsal vagal complex. Continuous and repeated phasic distension with similar volumes produced similar numbers and patterns of c-fos expression, with most of the activated neurons in the medial and commissural nucleus of the solitary tract (NTS) and dorsal motor nucleus (DMNX). Larger distension activated significantly more neurons in all responsive areas but there was no differential effect. In most NTS subnuclei and the DMNX, a small (3-5%) proportion of gastric distension-activated neurons was DBH-immunoreactive (DBH-IR), and this proportion did not significantly change with type of distension. With continuous and repeated small distensions, 10-12% and, with the large distension, 22-30% of all DBH-IR neurons expressed c-fos. The results suggest a large degree of convergence between rapidly adapting mucosal receptors and slowly adapting tension receptors, but not between low- and high-threshold tension receptors, and a relatively minor role of catecholaminergic second-order neurons in the dissemination of distension signals in the brain.
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Delgado-Aros, Silvia, Heather J. Chial, Michael Camilleri, Lawrence A. Szarka, Frank T. Weber, Jutta Jacob, Irene Ferber, Sanna McKinzie, Duane D. Burton, and Alan R. Zinsmeister. "Effects of a κ-opioid agonist, asimadoline, on satiation and GI motor and sensory functions in humans." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 4 (April 1, 2003): G558—G566. http://dx.doi.org/10.1152/ajpgi.00360.2002.
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To compare the effects of the κ-opioid agonist asimadoline and placebo on visceral sensation and gastrointestinal (GI) motor functions in humans, 91 healthy participants were randomized in a double-blind fashion to 0.15, 0.5, or 1.5 mg of asimadoline or placebo orally twice a day for 9 days. We assessed satiation (nutrient drink test), colonic compliance, tone, perception of colonic distension (barostat), and whole gut transit (scintigraphy). Treatment effect was assessed by analysis of covariance. Asimadoline increased nutrient drink intake ( P = 0.03). Asimadoline decreased colonic tone during fasting ( P = 0.03) without affecting postprandial colonic contraction, compliance, or transit. Gas scores in response to colonic distension were decreased with 0.5 mg of asimadoline at low levels (8 mmHg above operating pressure) of distension ( P = 0.04) but not at higher levels of distension. Asimadoline at 1.5 mg increased gas scores at 16 mmHg of distension ( P = 0.03) and pain scores at distensions of 8 and 16 mmHg ( P = 0.003 and 0.03, respectively) but not at higher levels of distension. Further studies of this compound in diseases with altered satiation or visceral sensation are warranted.
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Khan, M. I., N. W. Read, and D. Grundy. "Effect of varying the rate and pattern of gastric distension on its sensory perception and motor activity." American Journal of Physiology-Gastrointestinal and Liver Physiology 264, no. 5 (May 1, 1993): G824—G827. http://dx.doi.org/10.1152/ajpgi.1993.264.5.g824.
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The aim of the present study was to see if varying the rate and pattern of gastric distension affected its motor and sensory responses to distension. A balloon was used to carry out distensions in male volunteers at constant rates of 20, 50, 100, and 200 ml/min. In addition rapid (75 ml/s) intermittent distensions (RID) were carried out with the use of a large hand-held syringe. Subjects were asked to indicate the first perception of the balloon, fullness, and discomfort. Increasing the rate of ramp distension caused all sensations to occur at higher volumes and higher pressures and reduced the frequency and amplitude of phasic oscillations in gastric pressure. During RID, the same sensations were experienced at much reduced volumes but were poorly sustained. These data suggest that ramp and RID are likely to induce gastric sensations by activating different populations of receptors. The responses to ramp distension are compatible with the activation of stretch receptors situated in parallel with the muscle elements, whereas RID appear to be activating a different population of rapidly adapting mechanoreceptors possibly situated in the mucosa.
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Lingenfelser, T., W. M. Sun, G. S. Hebbard, J. Dent, and M. Horowitz. "Effects of duodenal distension on antropyloroduodenal pressures and perception are modified by hyperglycemia." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 3 (March 1, 1999): G711—G718. http://dx.doi.org/10.1152/ajpgi.1999.276.3.g711.
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Marked hyperglycemia (blood glucose ∼15 mmol/l) affects gastrointestinal motor function and modulates the perception of gastrointestinal sensations. The aims of this study were to evaluate the effects of mild hyperglycemia on the perception of, and motor responses to, duodenal distension. Paired studies were done in nine healthy volunteers, during euglycemia (∼4 mmol/l) and mild hyperglycemia (∼10 mmol/l), in randomized order, using a crossover design. Antropyloroduodenal pressures were recorded with a manometric, sleeve-side hole assembly, and proximal duodenal distensions were performed with a flaccid bag. Intrabag volumes were increased at 4-ml increments from 12 to 48 ml, each distension lasting for 2.5 min and separated by 10 min. Perception of the distensions and sensations of fullness, nausea, and hunger were evaluated. Perceptions of distension ( P < 0.001) and fullness ( P < 0.05) were greater and hunger less ( P < 0.001) during hyperglycemia compared with euglycemia. Proximal duodenal distension stimulated pyloric tone ( P < 0.01), isolated pyloric pressure waves ( P < 0.01), and duodenal pressure waves ( P< 0.01). Compared with euglycemia, hyperglycemia was associated with increases in pyloric tone ( P < 0.001), the frequency ( P < 0.05) and amplitude ( P < 0.01) of isolated pyloric pressure waves, and the frequency of duodenal pressure waves ( P < 0.001) in response to duodenal distension. Duodenal compliance was less ( P < 0.05) during hyperglycemia compared with euglycemia, but this did not account for the effects of hyperglycemia on perception. We conclude that both the perception of, and stimulation of pyloric and duodenal pressures by, duodenal distension are increased by mild hyperglycemia. These observations are consistent with the concept that the blood glucose concentration plays a role in the regulation of gastrointestinal motility and sensation.
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Bouras, Ernest P., Terence J. O’Brien, Michael Camilleri, Michael K. O’Connor, and Brian P. Mullan. "Cerebral topography of rectal stimulation using single photon emission computed tomography." American Journal of Physiology-Gastrointestinal and Liver Physiology 277, no. 3 (September 1, 1999): G687—G694. http://dx.doi.org/10.1152/ajpgi.1999.277.3.g687.
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Central processing of visceral information in humans is incompletely understood. We aimed to demonstrate the feasibility of single photon emission computed tomography (SPECT) and to quantitate the changes in regional cerebral blood flow during rectal distension. Ten healthy volunteers underwent randomized sham and active rectal distensions on separate days, during which cerebral blood flow was assessed by intravenous technetium-99m ethyl cysteinate dimer (99mTc-ECD) SPECT. Three-dimensional coregistration of brain images was used to quantitate activation in four preselected cerebral foci and two control regions. Paired analysis compared blood flow during sham and active distensions. There was increased right anterior cingulate gyrus activity (6.5 ± 2.9%, P = 0.03) with active rectal distension. A 5.4 ± 2.4% reduction in blood flow in the superior parieto-occipital control region ( P = 0.04) suggested blood “redistribution” during stimulation. Marked variability in activation of the frontal cortex, thalamus/basal ganglia complex, and mesiotemporal lobe was noted. Thus rectal distension increases activity in the right anterior cingulate gyrus on average; other foci of cerebral activation are quite variable, suggesting a lack of specific cerebral projections during rectal stimulation.
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Sengupta, J. N., D. Kauvar, and R. K. Goyal. "Characteristics of vagal esophageal tension-sensitive afferent fibers in the opossum." Journal of Neurophysiology 61, no. 5 (May 1, 1989): 1001–10. http://dx.doi.org/10.1152/jn.1989.61.5.1001.
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1. Single-unit vagal afferent activity was recorded from 35 fibers that demonstrated evoked response to distension in the smooth muscle portion of the esophagus in anesthetized opossums. 2. The conduction velocities, measured in 22 fibers, varied from 1.0 to 21.33 m/s. Eight fibers (36%) had conduction velocities in the range of C-fibers (less than 2.5 m/s), whereas 14 (64%) had velocities in the range of A delta-fibers (3.16-21.33 m/s). All fibers were spontaneously active with an average discharge rate of 7.3 +/- 1.0 imp/s (mean +/- SE; range, 1.2-23 imp/s). 3. Esophageal distension produced a reproducible increase in discharge rate that adapted slowly to sustained distension. The average threshold pressure of the endings was 10 mmHg. The saturation pressure was 70 mmHg with cumulative, stepwise distension and 56 mmHg with graded, discrete distensions, respectively. 4. The discharge rate at the saturation pressure was 46 +/- 7 imp/s with cumulative, stepwise distensions and was 59 +/- 4 imp/s with graded, discrete distensions. The difference in maximum discharge between these two modes of distension was not statistically significant (P greater than 0.05). 5. Esophageal peristaltic contraction was associated with bursts of spike discharge with an average rate of 53.6 +/- 4.7 imp/s. 6. Two types of fibers were identified based on their duration of spike discharge associated with peristaltic contraction. The short-activity fibers showed a short duration of response consisting of approximately 3 s of spike bursts in response to swallows. These short-activity fibers were not activated by either stretch or contraction of the longitudinal esophageal muscle. The long-activity fibers showed a long duration of response consisting of approximately 10 s of activity in response to swallows. These long-activity fibers could be activated by longitudinal muscle stretch or contraction. 7. It is concluded that esophageal tension-sensitive mechano-receptors associated with vagal afferents are activated by physiological peristalsis and are present "in series" with either circular or longitudinal muscle layers.
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Hammer, H. F., S. F. Phillips, M. Camilleri, and R. B. Hanson. "Rectal tone, distensibility, and perception: reproducibility and response to different distensions." American Journal of Physiology-Gastrointestinal and Liver Physiology 274, no. 3 (March 1, 1998): G584—G590. http://dx.doi.org/10.1152/ajpgi.1998.274.3.g584.
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Increasing interest is focusing on the role of intestinal tone, distensibility, and mechanosensation in the genesis of abdominal symptoms. Experimental approaches usually feature balloon distension of the bowel with measurements of perception, tone, and compliance and/or elastance; however, the methodologies are standardized incompletely. We examined the reproducibility of repeated assessments of sensory perception, basal tone, and compliance and/or elastance of the rectum during distension. We also evaluated the response to inflations that varied in regard to control of pressure or volume, pattern of distension, and rate of inflation. Five healthy volunteers were studied under two separate protocols. The first featured a series of experiments on each of 5 days; the other consisted of 2 separate days of study. Repeated distensions evoked reproducible responses of sensation and compliance and/or elastance on a single day, providing a conditioning distension preceded them. Day-to-day variability was also sufficiently small to allow valid comparisons to be made on different days in healthy persons. The configuration of the distension profile (phasic, staircase, or ramp) and the rate of inflation (from 1 to 40 ml/s) had little effect on distensibility or perception. Perceptions were sometimes transient and sometimes constant, but no relationship was found between these temporal features and the magnitude of the stimulus. These observations help provide a basis as to how the responses to rectal distension can be best studied.
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Ness, T. J., and G. F. Gebhart. "Interactions between visceral and cutaneous nociception in the rat. II. Noxious visceral stimuli inhibit cutaneous nociceptive neurons and reflexes." Journal of Neurophysiology 66, no. 1 (July 1, 1991): 29–39. http://dx.doi.org/10.1152/jn.1991.66.1.29.
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1. Nocigenic inhibition is the inhibition of neural, behavioral, or reflex responses to a nociceptive test stimulus produced by another, conditioning, nociceptive stimulus. The present study examines whether a natural noxious visceral stimulus, colorectal distension, used as a conditioning stimulus would inhibit neuronal or reflex responses to noxious cutaneous stimuli. Segmental effects of colorectal distension have been previously characterized; hence conditioning effects of colorectal distension on stimuli applied at sites distant (heterosegmental effects) and adjacent (perisegmental effects) to those areas of the spinal cord that receive the greatest afferent input from the colon were examined. The conditioning effects of colorectal distension were compared with those of noxious pinch. 2. Heterosegmental effects of colorectal distension were studied in 129 neurons located in the area of the trigeminal nucleus caudalis and cervical spinal dorsal horn. Steady-state activity (spontaneous activity or activity evoked by sustained pressure) of 106 of 129 trigeminal-cervical dorsal horn neurons was inhibited by both noxious colorectal distension (100 mmHg, 20 s) and noxious pinch of the tail; all neurons inhibited by colorectal distension were also inhibited by noxious pinch. Inhibition was graded with the intensity of the distending stimulus. The class 2-class 3 classification system (neurons excited by nonnoxious and noxious or only by noxious cutaneous stimuli, respectively) was roughly predictive of susceptibility to nocigenic inhibition, because 74 of 75 class 2 neurons tested were inhibited by noxious colorectal distension or noxious pinch and only 32 of 54 class 3 neurons were similarly inhibited. Five neurons were excited by colorectal distension, all of which were class 3 neurons. 3. Perisegmental effects of colorectal distension were observed in 100 L3-L5 spinal dorsal horn neurons. The spontaneous activities and responses during noxious test heating of the glabrous skin of the hindpaw of these neurons were affected in the same way by noxious (conditioning) colorectal distension. All neurons inhibited by colorectal distension (51 class 2 and 8 class 3 neurons) were also inhibited by noxious pinch of the nose or forepaw. The magnitude of the nocigenic inhibition of responses during heating of the hindpaw was graded with the intensity and duration of the noxious conditioning colorectal distension, was a function of the number of preceding distensions given to the rat, and outlasted the distending stimulus. Conditioning colorectal distension also produced a parallel shift to the right in stimulus-response functions relating responses of neurons to the intensity of the noxious test stimulus (42-50 degrees C).(ABSTRACT TRUNCATED AT 400 WORDS)
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Verhagen, M. A. M. T., C. K. Rayner, J. M. Andrews, G. S. Hebbard, S. M. Doran, M. Samsom, and M. Horowitz. "Physiological changes in blood glucose do not affect gastric compliance and perception in normal subjects." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 3 (March 1, 1999): G761—G766. http://dx.doi.org/10.1152/ajpgi.1999.276.3.g761.
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Marked hyperglycemia (blood glucose ∼14 mmol/l) slows gastric emptying and affects the perception of sensations arising from the gut. Elevation of blood glucose within the physiological range also slows gastric emptying. This study aimed to determine whether physiological changes in blood glucose affect proximal gastric compliance and/or the perception of gastric distension in the fasting state. Paired studies were conducted in 10 fasting healthy volunteers. On a single day, isovolumetric and isobaric distensions of the proximal stomach were performed using an electronic barostat while the blood glucose concentration was maintained at 4 and 9 mmol/l in random order. Sensations were quantified using visual analog scales. The blood glucose concentration had no effect on the pressure-volume relationship during either isovolumetric or isobaric distensions or the perception of gastric distension. At both blood glucose concentrations, the perceptions of fullness, nausea, bloating, and abdominal discomfort, but not hunger or desire to eat, were related to intrabag volume ( P ≤ 0.002) and pressure ( P ≤ 0.01). We conclude that, in the fasted state, elevations of blood glucose within the physiological range do not affect proximal gastric compliance or the perception of gastric distension.
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Feinle, C., and N. W. Read. "Ondansetron reduces nausea induced by gastroduodenal stimulation without changing gastric motility." American Journal of Physiology-Gastrointestinal and Liver Physiology 271, no. 4 (October 1, 1996): G591—G597. http://dx.doi.org/10.1152/ajpgi.1996.271.4.g591.
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The involvement of 5-hydroxytryptamine3 (5-HT3) receptors in gastric motor and sensory responses to distension and duodenal lipid was investigated. Subjects were studied on four occasions during which isotonic saline or 20% Intralipid (2 kcal/ml) was infused intraduodenally (1 ml/min) while the proximal stomach was distended with air (100 ml/min). Subjects received either 8 mg ondansetron (5-HT3 antagonist) or placebo orally in random order. Intragastric pressure was recorded continuously, and subjects reported gastric sensations. Gastric motor and sensory responses to distension during duodenal saline were similar with placebo and ondansetron. Intraduodenal lipid decreased gastric tonic and phasic pressure activity, and this was not influenced by ondansetron. Lipid also induced meal-like fullness followed by nausea during distensions. Ondansetron reduced nausea and did not affect meal-like fullness but increased volumes and pressures at which sensations were reported. Intestinal 5-HT3 receptors are involved in induction of nausea but not of meal-like fullness by intraduodenal lipid and gastric distension. 5-HT3 receptor antagonism reduces gastric sensitivity to distension during intraduodenal lipid infusion.
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Thumshirn, Miriam, Michael Camilleri, Russell B. Hanson, Donald E. Williams, Alfred J. Schei, and Patricia P. Kammer. "Gastric mechanosensory and lower esophageal sphincter function in rumination syndrome." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 2 (August 1, 1998): G314—G321. http://dx.doi.org/10.1152/ajpgi.1998.275.2.g314.
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Our hypothesis was that rumination syndrome is associated with gastric sensory and motor dysfunction. We studied gastric and somatic sensitivity, reflex relaxation of the lower esophageal sphincter (LES), and gastric compliance and accommodation postprandially and postglucagon. A barostatically controlled gastric bag and esophageal manometry were used to compare gastric sensorimotor functions and LES relaxation to gastric distension in 12 patients with rumination syndrome and 12 controls. During bag distensions, patients had greater nausea, bloating, and aggregate score, but not pain, compared with controls ( P < 0.05). At 4 and 8 mmHg gastric distension, LES tone reduction was greater in patients than in controls ( P < 0.05). Gastric compliance, accommodation to a standard meal, and response to glucagon were not different in patients and controls; however, 6 of 12 patients had no gastric accommodation; the latter patients had significantly greater pain perception during distension ( P < 0.05) but normal somatic sensitivity compared with healthy controls. Rumination syndrome is characterized by higher gastric sensitivity and LES relaxation during gastric distension. A subgroup of patients also had absent postprandial accommodation.
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Tipnis, Neelesh A., Poong-Lyul Rhee, and Ravinder K. Mittal. "Distension during gastroesophageal reflux: effects of acid inhibition and correlation with symptoms." American Journal of Physiology-Gastrointestinal and Liver Physiology 293, no. 2 (August 2007): G469—G474. http://dx.doi.org/10.1152/ajpgi.00019.2007.
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We studied spontaneous gastroesophageal reflux (GER)-induced esophageal distension using ultrasound imaging and its role in the genesis of esophageal symptoms before and during esomeprazole therapy. Ten controls and 10 GER disease (GERD) patients were studied by combined impedance, esophageal pH, manometry, and ultrasonography before and during esomeprazole therapy. Physiological data and symptoms were recorded for 2 h following a standardized meal. From ultrasound images, the esophageal cross-sectional area (CSA) at the peak of GER-induced distension was determined and compared between controls vs. patients, symptomatic vs. asymptomatic GER episodes, and before vs. during esomeprazole in GERD patients. The mean lumen CSA is greater in the patients than controls (271 ± 71 mm2 vs. 163 ± 56 mm2, P = 0.001) but not different among asymptomatic reflux episodes, and those associated with regurgitation (290 ± 110 mm2) or heartburn (271 ± 67 mm2). Eight chest pain episodes associated with reflux revealed a tendency toward larger mean esophageal distension (459 ± 40 mm2) compared with asymptomatic reflux (268 ± 70 mm2, P = 0.058). Following esomeprazole treatment, most GER episodes were nonacidic and asymptomatic except in two patients in whom cyclical reflux was associated with large esophageal distensions. Esomeprazole did not alter the lumen CSA during GER. Esophageal distension is greater in the GERD subjects compared with controls; however, it is unlikely that the GER-induced distension of the esophagus plays a significant role in the genesis of heartburn sensation. Esomeprazole therapy does not alter the GER-induced distension of the esophagus.
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Harraf, F., M. Schmulson, L. Saba, N. Niazi, R. Fass, J. Munakata, D. Diehl, H. Mertz, B. Naliboff, and E. A. Mayer. "Subtypes of constipation predominant irritable bowel syndrome based on rectal perception." Gut 43, no. 3 (September 1, 1998): 388–94. http://dx.doi.org/10.1136/gut.43.3.388.
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Background—Patients who complain of constipation can be divided into those who have lost the natural call to stool, but develop abdominal discomfort after several days without a bowel movement (no urge); and those who experience a constant sensation of incomplete evacuation (urge).Aims—To determine whether the two groups differ in symptoms, colonic transit, and perceptual responses to controlled rectal distension.Methods—Forty four patients with constipation were evaluated with a bowel symptom questionnaire, colonic transit (radiopaque markers), and rectal balloon distension. Stool (S) and discomfort (D) thresholds to slow ramp (40 ml/min) and rapid phasic distension (870 ml/min) were determined with an electronic distension device. Fifteen healthy controls were also studied.Results—All patients had Rome positive irritable bowel syndrome (IBS); 17 were no urge and 27 urge. Mean D threshold to phasic rectal distensions was 28 (3) mm Hg in no urge, 27 (3) mm Hg in urge (NS), but higher in the control group (46 (2) mm Hg; p<0.01). Sixty seven per cent of no urge and 69% of urge were hypersensitive for D. Slow ramp distension thresholds were higher in no urge (S: 26 (3); D: 45 (4) mm Hg) compared with urge (S: 16 (2); D: 31 (3) mm Hg; p<0.01), or with controls (S: 15 (1); D: 30 (3); p<0.01).Conclusions—Hyposensitivity to slow rectal distension is found in patients with IBS who complain of constipation and have lost the call to stool even though their sensitivity to phasic distension is increased.
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Kern, Mark K., Safwan Jaradeh, Ronald C. Arndorfer, Andrzej Jesmanowicz, James Hyde, and Reza Shaker. "Gender differences in cortical representation of rectal distension in healthy humans." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 6 (December 1, 2001): G1512—G1523. http://dx.doi.org/10.1152/ajpgi.2001.281.6.g1512.
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Cerebral cortical processing of information relayed via visceral afferents is poorly understood. We determined and compared cortical activity caused by various levels of rectal distension in healthy male and female subjects. Twenty-eight healthy, young (20–44 yr) volunteer subjects (13 male, 15 female) were studied with a paradigm-driven functional magnetic resonance imaging (fMRI) technique during barostat-controlled rectal distension at perception threshold and 10 mmHg below and above perception threshold. Male subjects showed localized clusters of fMRI activity primarily in the sensory and parietooccipital regions, whereas female subjects also showed activity in the anterior cingulate and insular regions. A progressive increase in maximum percent fMRI signal change and total volume of cortical activity was associated with the intensity of rectal distension pressure in both genders. Regions of cortical activity for below-threshold stimuli showed less substantial signal intensity and volume than responses for threshold and above-threshold stimuli. Volume of cortical activity during rectal distension in women was significantly higher than that for men for all distensions. We conclude that 1) there are substantial differences in female cortical activation topography during rectal distension compared with males; 2) intensity and volume of registered cortical activity due to rectal stimulation are directly related to stimulus strength; and 3) rectal stimulation below perception level is registered in the cerebral cortex.
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Choi, Kym Ja. "Abdominal Distension." Journal of the Korean Medical Association 44, no. 1 (2001): 80. http://dx.doi.org/10.5124/jkma.2001.44.1.80.
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Yang, Dae Hyun. "Abdominal Distension." Journal of the Korean Medical Association 44, no. 4 (2001): 427. http://dx.doi.org/10.5124/jkma.2001.44.4.427.
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Mukhtar, A. "Abdominal distension." Postgraduate Medical Journal 78, no. 921 (July 1, 2002): 432. http://dx.doi.org/10.1136/pmj.78.921.432.
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Bangalore, Harish, Javeed Ahmed, John Bible, Esse Natasha Menson, Andrew Durward, and Cheuk Yan William Tong. "ABDOMINAL DISTENSION." Pediatric Infectious Disease Journal 30, no. 3 (March 2011): 260–62. http://dx.doi.org/10.1097/inf.0b013e318207691c.
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Berkley, Karen J., and Charles F. Badland. "Uterine Distension." Clinical Journal of Pain 7, no. 1 (March 1991): 66. http://dx.doi.org/10.1097/00002508-199103000-00113.
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Ray, P. "Distension thoracique." Annales françaises de médecine d'urgence 2, no. 2 (January 21, 2012): 112. http://dx.doi.org/10.1007/s13341-012-0161-5.
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Bharucha, Adil E., Rolf D. Hubmayr, Irene J. Ferber, and Alan R. Zinsmeister. "Viscoelastic properties of the human colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 2 (August 1, 2001): G459—G466. http://dx.doi.org/10.1152/ajpgi.2001.281.2.g459.
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Our objectives were to characterize colonic viscoelastic properties of the human descending colon by assessing pressure-volume (P-V) relationships during barostatic balloon distension. In 16 healthy subjects, a balloon was inflated to 44 mmHg and then deflated to 0 mmHg in 4-mmHg steps at 10, 30, and 60 ml/min, allowing volume fluctuations to stabilize at each pressure increment. Thereafter, these “quasi-static” P-V curves were compared with “dynamic” distensions to 300 ml, at 1 and 10 ml/s, before and after intravenous atropine in another five subjects. During quasi-static curves, balloon volume stabilized at each pressure increment. Quasi-static P-V curves were reproducible within individuals and approximated to a power exponential function and revealed hysteresis, indicative of viscoelasticity. Body mass index influenced quasi-static P-V curves during inflation but not during deflation. The colon was less compliant during dynamic distensions at 10 ml/s than during quasi-static distensions. Atropine increased quasi-static compliance and attenuated differences between quasi-static and rapid distensions. We conclude that colonic viscoelastic properties can be assessed by quasi-static P-V curves. Rapid colonic distension activated neural reflexes, thereby reducing colonic compliance compared with quasi-static distensions.
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Ng, Clinton, Mark Danta, Gillian Prott, Caro-Anne Badcock, John Kellow, and Allison Malcolm. "Modulatory influences on antegrade and retrograde tonic reflexes in the colon and rectum." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 5 (November 2004): G962—G966. http://dx.doi.org/10.1152/ajpgi.00460.2003.
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Tonic reflexes in the colon and rectum are likely to be important in health and in disorders of gastrointestinal function. The aim of this study was to evaluate the fasting and postprandial “colorectal” and “rectocolic” reflexes in response to 2-min isobaric distensions of the colon and rectum, accounting for enteric sensation, compliance, and distending balloon volume. In 14 healthy fasting subjects, a dual barostat assembly was positioned (descending colon and rectum). A 2-min phasic distension was performed in the colon and rectum in random order while the opposing balloon volume was recorded. Sensation (phasic distension) and compliance (ramp distension) were also determined. The experiment was repeated postprandially. Colonic distension resulted in significant rectal tonic contraction in the fasting (rectal volume change: −35.4 ± 8.4 ml, P < 0.01) and postprandial (−22.2 ± 8.4 ml, P < 0.01) states. After adjustment for colonic sensitivity, for compliance, and for distending balloon volume, the rectal volume change remained significant; the extent of the tonic response, however, correlated significantly with increasing pain score ( P < 0.01). In contrast, rectal distension did not produce a significant tonic response in the colon (fasting: −6.5 ± 7.3 ml; postprandial: 2.7 ± 7.3 ml), either unadjusted or adjusted for rectal sensitivity, compliance, and distending balloon volume. In conclusion, the colorectal reflex, but not the rectocolic reflex, can be readily demonstrated both before and after a meal in response to a 2-min isobaric distension in the colon and rectum, respectively. Although the presence of the colorectal reflex does not depend on colonic sensitivity or the volume of the distending colonic balloon, these factors modulate the reflex, especially in the fasting state.
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Brennan, T. J., U. T. Oh, S. F. Hobbs, D. W. Garrison, and R. D. Foreman. "Urinary bladder and hindlimb afferent input inhibits activity of primate T2-T5 spinothalamic tract neurons." Journal of Neurophysiology 61, no. 3 (March 1, 1989): 573–88. http://dx.doi.org/10.1152/jn.1989.61.3.573.
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1. Extracellular recordings were made from 41 spinothalamic tract (STT) neurons on the left side of the T2-T5 spinal segments of 20 monkeys (Macaca fascicularis) anesthetized with alpha-chloralose. Manipulation of the left triceps-chest region and electrical stimulation of cardiopulmonary sympathetic afferent fibers excited these cells. 2. Isotonic urinary bladder distensions (UBD) to pressures between 20 and 80 cmH2O reduced the spontaneous activity in 33 of 41 cells. Cell activity was significantly reduced by UBD at 20 cmH2O. Distensions to 40, 60, and 80 cmH2O produced progressively greater reductions in spontaneous discharge. Activity was decreased throughout distension in 29 cells (tonic inhibition) and at the onset of distension in 3 neurons (phasic inhibition). In one cell, inhibition followed a brief excitation at the onset of distension (phasic excitation-tonic inhibition). Spontaneous bladder contractions also inhibited STT cell activity. 3. Inhibition by UBD was observed in STT cells characterized as wide dynamic range, high threshold, and high threshold inhibitory. No correlation existed between cell type or laminar location and inhibition by urinary bladder distension. Cells excited by cardiopulmonary sympathetic afferent A delta- and C-fibers had a significantly greater tendency to be inhibited by UBD (17 of 18) than cells activated by A delta- but not C-fibers (13 of 20). 4. Urinary bladder distension and pinch of the hindlimbs also reduced activity of STT cells excited by input from cardiopulmonary sympathetic afferents and from the proximal forelimb. 5. Urinary bladder distension to 40, 60, or 80 cmH2O produced a greater absolute but smaller relative reduction in the firing frequency of STT cells as spontaneous activity increased. Thus the magnitude of this inhibitory effect may depend on whether the inhibitory effect is measured as an absolute or relative change in cell activity. 6. Convergent inhibitory input from somatic regions also was observed. Noxious pinch of the hamstring region of the right hindlimb decreased activity in 32 of 39 cells. Left hindlimb pinch inhibited 21 of 38 cells, and 15 of 29 cells were inhibited by right triceps pinch. 7. Convergent inhibitory input from the hamstring region of the hindlimbs and from the urinary bladder to upper thoracic STT cells may be important for coding the intensity and location of noxious visceral and somatic stimuli and for organizing the appropriate sequence of motor responses when multiple noxious stimuli are present.
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Feinle, Christine, David Grundy, and Michael Fried. "Modulation of gastric distension-induced sensations by small intestinal receptors." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 1 (January 1, 2001): G51—G57. http://dx.doi.org/10.1152/ajpgi.2001.280.1.g51.
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Duodenal lipid exacerbates gastrointestinal sensations during gastric distension. Using luminal application of the local anesthetic benzocaine, we investigated the role of intestinal receptors in the induction of these sensations. Nine healthy subjects were studied on five occasions, during which isotonic saline or 20% lipid (2 kcal/min), combined with (duodenal or jejunal) 0.75% benzocaine or vehicle at 2.5 ml/min, was infused intraduodenally before and during gastric distension. Intragastric pressures and volumes, gastrointestinal sensations, and plasma CCK levels were determined. Duodenal lipid combined with vehicle increased gastric volume (in ml: saline, −10 ± 18; lipid/vehicle, 237 ± 30) and plasma CCK [mean levels (pmol/l): saline, 2.0 ± 0.2; lipid/vehicle, 8.0 ± 1.6] and, during distensions, induced nausea (scores: saline, 3 ± 2: lipid/vehicle, 58 ± 19) and decreased pressures at which fullness and discomfort occurred. Duodenal but not jejunal benzocaine attenuated the effect of lipid on gastric volume, plasma CCK, and nausea during distension (135 ± 38 and 216 ± 40 ml, 4.6 ± 0.6 pmol/l and not assessed, and 37 ± 12 and 64 ± 21 for lipid + duodenal benzocaine and lipid + jejunal benzocaine, respectively) and on pressures for sensations. In conclusion, intestinal receptors modulate gastrointestinal sensations associated with duodenal lipid and gastric distension. There is also the potential for local neural mechanisms to regulate CCK release and thereby reduce afferent activation indirectly.
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Knapp, M. F., M. N. Hicks, R. J. Linden, and D. A. S. G. Mary. "EVIDENCE AGAINST ANP AS A NATRIURETIC HORMONE DURING ATRIAL DISTENSION." Journal of Endocrinology 109, no. 2 (May 1986): R5—R8. http://dx.doi.org/10.1677/joe.0.109r005.
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ABSTRACT To determine whether natriuresis attributable to atrial natriuretic peptides (ANP) is obtained in response to atrial stretch after blockade of the afferent input and reflex diuresis from atrial receptors, urine flow and sodium excretion were measured in response to distension of a balloon in the left atrium with the vagi at 37 and 9°C. It is known that during such a distension ANP plasma concentration is increased by the same amount whether or not the afferent vagal fibres are intact. In 11 chloralose anaesthetized dogs 22 distensions with the vagi at 37°C increased urine flow 117.5% and increased sodium excretion 28.7%. In 11 distensions with the vagi at 9°C, urine flow did not change but sodium excretion decreased significantly (−20.9%). Thus natriuresis could not be demonstrated in response to atrial stretch in anaesthetised dogs after blockade of the atrial receptor reflex. These results imply that under these conditions, in which ANP is reportedly released into plasma, ANP is not acting as a hormone. The results must call into question the suggestion that ANP is released into plasma in a concentration capable of causing a natriuresis as its normal physiological function.
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Gao, Chunwen, Lars Arendt-Nielsen, Weiming Liu, Poul Petersen, Asbjørn Mohr Drewes, and Hans Gregersen. "Sensory and biomechanical responses to ramp-controlled distension of the human duodenum." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 3 (March 1, 2003): G461—G471. http://dx.doi.org/10.1152/ajpgi.00456.2001.
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The aim of this study was to develop a new method for investigation of the relationship among the mechanical stimulus, the biomechanical properties, and the visceral perception evoked by volume/ramp-controlled distension in the human duodenum in vivo. An impedance planimetric probe for balloon distension was placed in the third part of the duodenum in seven healthy volunteers. Distension of the duodenum was done at infusion rates of 10, 25, and 50 ml/min. The pump was reversed when level 7 was reached on a visual analog scale ranging from 0 to 10. Distensions were done with and without the administration of the antimuscarinic drug butylscopolamine. The total circumferential tension (Ttotal) and the passive circumferential tension (Tpassive) were determined from the distension tests without and with the administration of butylscopolamine, respectively. Ttotal and Tpassive showed an exponential behavior as a function of strain (a measure of deformation). The active circumferential tension (Tactive) was computed as Ttotal−Tpassive and showed a bell-shaped behavior as a function of strain. At low distension intensities, the intensity of sensation at 10 ml/min was significantly higher than that obtained at 25 and 50 ml/min. The coefficient of variation at the pain threshold for circumferential strain (average 4.34) was closer to zero compared with those for volume (8.72), pressure (31.22), and circumferential tension (31.55). This suggests that the mechanoreceptors in the gastrointestinal wall depend primarily on circumferential strain. The stimulus-response functions provided evidence for the existence of low- and high-threshold mechanoreceptors in the human duodenum. Furthermore, the data suggest that high-threshold receptors are nonadapting.
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Ng, Clinton, Mark Danta, John Kellow, Caro-Anne Badcock, Ross Hansen, and Allison Malcolm. "Attenuation of the colorectal tonic reflex in female patients with irritable bowel syndrome." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 3 (September 2005): G489—G494. http://dx.doi.org/10.1152/ajpgi.00527.2004.
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Alterations in normal intestinointestinal reflexes may be important contributors to the pathophysiology of irritable bowel syndrome (IBS). Our aims were to compare the rectal tonic responses to colonic distension in female IBS patients with predominant constipation (IBS-C) and with predominant diarrhea (IBS-D) to those in healthy females, both fasting and postprandially. Using a dual barostat assembly, 2-min colonic phasic distensions were performed during fasting and postprandially. Rectal tone was recorded before, during, and after the phasic distension. Colonic compliance and colonic sensitivity in response to the distension were also evaluated fasting and postprandially. Eight IBS-C patients, 8 IBS-D patients, and 8 age- and sex-matched healthy subjects ( group N) participated. The fasting increments in rectal tone in response to colonic distension in both IBS-C (rectal balloon volume change −4.6 ± 6.1 ml) and IBS-D (−7.9 ± 4.9 ml) were significantly reduced compared with group N (−34 ± 9.7 ml, P = 0.01). Similar findings were observed postprandially ( P = 0.02). When adjusted for the colonic compliance of individual subjects, the degree of attenuation in the rectal tonic response in IBS compared with group N was maintained (fasting P = 0.007; postprandial P = 0.03). When adjusted for colonic sensitivity there was a trend for the attenuation in the rectal tonic response in IBS patients compared with group N to be maintained (fasting P = 0.07, postprandial P = 0.08). IBS patients display a definite attenuation of the normal increase in rectal tone in response to colonic distension (colorectal reflex), fasting and postprandially. Alterations in colonic compliance and sensitivity in IBS are not likely to contribute to such attenuation.
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Rouillon, J. M., F. Azpiroz, and J. R. Malagelada. "Reflex changes in intestinal tone: relationship to perception." American Journal of Physiology-Gastrointestinal and Liver Physiology 261, no. 2 (August 1, 1991): G280—G286. http://dx.doi.org/10.1152/ajpgi.1991.261.2.g280.
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Using an original technique, we demonstrated a modulation of intestinal tonic muscular activity (intestinal tone) by intestino-intestinal reflexes. In 11 healthy volunteers we quantitated intestinal tone variations as changes in the air volume within a flaccid bag (12 cm long) located in the proximal jejunum and maintained at a constant pressure by an electronic barostat. Validation studies with glucagon showed significant intestinal relaxation (117 +/- 10% delta vol; P less than 0.05). In six healthy volunteers, graded balloon distensions (1 min duration at 10-min intervals in 8-ml stepwise increments) were randomly performed 8 cm orad, 8 cm caudad, and 20 cm caudad to the bag of the barostat. Perception was scored (0-6) by a questionnaire. Distensions at the three sites induced similar perception; at the threshold for discomfort (score greater than or equal to 5) distension also induced intestinal relaxatory responses (43 +/- 10%, 34 +/- 5%, and 32 +/- 4% delta vol from orad to caudad, respectively; P less than 0.05 for all). However, while unperceived orad distensions (13 +/- 2 ml) induced reflex relaxation (21 +/- 6% delta vol; P less than 0.05), 20-cm-caudad distensions at higher levels (16 +/- 2 ml, 2.7 +/- 0.5 perception score; P less than 0.05) did not (1 +/- 7% delta vol). This dissociation between perception and intestinal tone reflexes suggests that both responses to intestinal distension are mediated by specific mechanisms.
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Takeda, Torahiko, Ghassan Kassab, Jianmin Liu, James L. Puckett, Rishi R. Mittal, and Ravinder K. Mittal. "A novel ultrasound technique to study the biomechanics of the human esophagus in vivo." American Journal of Physiology-Gastrointestinal and Liver Physiology 282, no. 5 (May 1, 2002): G785—G793. http://dx.doi.org/10.1152/ajpgi.00394.2001.
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The objectives of this study were to validate a novel ultrasound technique and to use it to study the circumferential stress-strain properties of the human esophagus in vivo. A manometric catheter equipped with a high-compliance bag and a high-frequency intraluminal ultrasonography probe was used to record esophageal pressure and images. Validation studies were performed in vitro followed by in vivo studies in healthy human subjects. Esophageal distensions were performed with either an isovolumic (5–20 ml of water) or with an isobaric (10–60 mmHg) technique. Sustained distension was also performed for 3 min in each subject. The circumferential wall stress and strain were calculated. In vitro studies indicate that the ultrasound technique can make measurements of the esophageal wall with an accuracy of 0.01 mm. The in vivo studies provide the necessary data to compute the Kirchhoff's stress, Green's strain, and Young's elastic modulus during esophageal distensions. The stress-strain relationship revealed a linear shape, the slope of which corresponds to the Young's modulus. During sustained distensions, we found dynamic changes of stress and strain during the period of distension. We describe and validate a novel ultrasound technique that allows measurement of biomechanical properties of the esophagus in vivo in humans.
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Feinle, Christine, David Grundy, Bärbel Otto, and Michael Fried. "Relationship between increasing duodenal lipid doses, gastric perception, and plasma hormone levels in humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 5 (May 1, 2000): R1217—R1223. http://dx.doi.org/10.1152/ajpregu.2000.278.5.r1217.
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Duodenal lipid causes gastric relaxation, CCK secretion, and nausea. Vasopressin has been implicated in motion sickness-related nausea. We hypothesized that increasing doses of lipid enhance gastric relaxation and CCK-vasopressin secretion, resulting in a dose-related exacerbation of nausea. Nine healthy subjects received isotonic saline or lipid (1, 2, or 3 kcal/min, L1, L2, L3) duodenally. Changes in gastric volume, sensations, and plasma hormone levels were assessed during infusions and isobaric gastric distensions. Lipid infusions increased gastric volume, plasma CCK (but not vasopressin) levels, and gastric compliance during distensions, compared with saline. Plasma CCK levels were related to the dose of lipid administered [CCK levels at 30 min (pmol/l), saline: 1.1 ± 0.2, L1: 1.8 ± 0.2, L2: 3.0 ± 0.2, L3: 4.3 ± 0.6]. During distensions, nausea increased in intensity with increasing doses of lipid [score (where 0 is no sensation and 100 is strongest sensation), saline: 7 ± 4, L1: 19 ± 7, L2: 44 ± 7, L3: 66 ± 8]; however, no further rise in plasma CCK occurred. Because neither lipid nor distension alone induced significant nausea, we conclude that the interaction between these stimuli together with a modulation by CCK is responsible for the effects observed. Vasopressin is not involved in lipid- and distension-induced nausea.
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Bonchek, Lawrence I. "Balloon Distension Systems." Annals of Thoracic Surgery 43, no. 4 (April 1987): 458. http://dx.doi.org/10.1016/s0003-4975(10)62836-6.
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Dimitri, Wade. "Balloon Distension Systems." Annals of Thoracic Surgery 43, no. 4 (April 1987): 458. http://dx.doi.org/10.1016/s0003-4975(10)62837-8.
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Salamon, Samuel M. "Capsular Bag Distension." Journal of Cataract & Refractive Surgery 18, no. 5 (September 1992): 537. http://dx.doi.org/10.1016/s0886-3350(13)80117-4.
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KONICK-McMAHAN, JOANNE. "JUGULAR VEIN DISTENSION." Nursing 19, no. 2 (February 1989): 100–103. http://dx.doi.org/10.1097/00152193-198902000-00036.
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Hohenauer, Peter, and Martin W. Dünser. "Massive gastric distension." Wiener klinische Wochenschrift 123, no. 19-20 (August 10, 2011): 592. http://dx.doi.org/10.1007/s00508-011-1599-y.
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Larsson, Marie H., Maria Sapnara, Evan A. Thomas, Joel C. Bornstein, Erik Lindström, David J. Svensson, and Henrik Sjövall. "Pharmacological analysis of components of the change in transmural potential difference evoked by distension of rat proximal small intestine in vivo." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 1 (January 2008): G165—G173. http://dx.doi.org/10.1152/ajpgi.00264.2007.
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The reflex response to distension of the small intestine in vivo is complex and not well understood. The aim of this study was to characterize the neural mechanisms contributing to the complex time course of the intestinal secretory response to distension. Transmucosal potential difference (PD) was used as a marker for mucosal chloride secretion, which reflects the activity of the secretomotor neurons. Graded distensions (5, 10, and 20 mmHg) of distal rat duodenum with saline for 5 min induced a biphasic PD response with an initial peak (rapid response) followed by a plateau (sustained response). The rapid response was significantly reduced by the neural blockers tetrodotoxin and lidocaine (given serosally) and by intravenous (iv) administration of the ganglionic blocker hexamethonium and the NK1 receptor antagonist SR-140333. Serosal TTX and iv SR-140333 significantly reduced the sustained response, which was also reduced by the NK3 receptor antagonist talnetant and by the vasoactive intestinal polypeptide (VPAC) receptor antagonist [4Cl-d-Phe6, Leu17]-VIP. Serosal lidocaine and iv hexamethonium had no significant effect on this component. Inhibition of nitric oxide synthase had no effect on any of the components of the PD response to distension. The PD response to distension thus seems to consist of two components, a rapidly activating and adapting component operating via nicotinic transmission and NK1 receptors, and a slow component operating via VIP-ergic transmission and involving both NK1 and NK3 receptors.
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Siproudhis, L., E. Bellissant, F. Juguet, H. Allain, J.-F. Bretagne, and M. Gosselin. "Perception of and adaptation to rectal isobaric distension in patients with faecal incontinence." Gut 44, no. 5 (May 1, 1999): 687–92. http://dx.doi.org/10.1136/gut.44.5.687.
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BACKGROUNDPerception of, and adaptation of the rectum to, distension probably play an important role in the maintenance of continence, but perception studies in faecal incontinence provide controversial conclusions possibly related to methodological biases. In order to better understand perception disorders, the aim of this study was to analyse anorectal adaptation to rectal isobaric distension in subjects with incontinence.PATIENTS/METHODSBetween June 95 and December 97, 97 consecutive patients (nine men and 88 women, mean (SEM) age 55 (1) years) suffering from incontinence were evaluated and compared with 15 healthy volunteers (four men and 11 women, mean age 48 (3) years). The patients were classified into three groups according to their perception status to rectal isobaric distensions (impaired, 22; normal, 61; enhanced, 14). Anal and rectal adaptations to increasing rectal pressure were analysed using a model of rectal isobaric distension.RESULTSThe four groups did not differ with respect to age, parity, or sex ratio. Magnitude of incontinence, prevalence of pelvic disorders, and sphincter defects were similar in the incontinent groups. When compared with healthy controls, anal pressure and rectal adaptation to distension were decreased in incontinent patients. When compared with incontinent patients with normal perception, patients with enhanced perception experienced similar rectal adaptation but had reduced anal pressure. In contrast, patients with impaired perception showed considerably decreased rectal adaptation but had similar anal pressure.CONCLUSIONAbnormal sensations during rectal distension are observed in one third of subjects suffering from incontinence. These abnormalities may reflect hyperreactivity or neuropathological damage of the rectal wall.
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Lent, C. M., and M. H. Dickinson. "On the termination of ingestive behaviour by the medicinal leech." Journal of Experimental Biology 131, no. 1 (September 1, 1987): 1–15. http://dx.doi.org/10.1242/jeb.131.1.1.
Full textAbstract:
Hungry leeches, Hirudo medicinalis, ingest blood meals averaging 890% of their mass in 29 min. Ingestion is terminated as a result of distension of the body: experimentally distending leeches as they feed causes an immediate cessation of ingestion and inhibits any subsequent biting behaviour; if distension is circumvented by various experimental procedures, leech ingestive periods are prolonged significantly. Ingestion is not terminated as a result of fatigue, chemical cues or mass change. Distension also underlies satiation, for removing blood from the crops of recently fed leeches qualitatively alters their satiated behaviour to biting. Biting is not a defensive reaction to injury. In rostral ganglia, impulses of the serotonergic Retzius (RZ) and LL neurones evoke the physiological components of ingestion. Localized warming of the prostomial lip induces impulses in these large effector neurones. Distending the body wall tonically hyperpolarizes the RZ and LL cells. This inhibitory response to distension is conducted from the mid-body to the anterior neurones via the ventral nerve cord. Distensive inhibition antagonizes the synaptic excitation evoked in RZ and LL neurones by thermal stimulation. Thus, a stimulus which evokes feeding synaptically excites 5-HT neurones and a stimulus which terminates ingestion inhibits them. The integration of these inputs controls the expression of leech feeding behaviour and these connections match precisely a model proposed to regulate the ingestive behaviour of blowflies.
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Yu, Shaoyong, and Ann Ouyang. "Effect of synthetic cationic protein on mechanoexcitability of vagal afferent nerve subtypes in guinea pig esophagus." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 6 (December 2011): G1052—G1058. http://dx.doi.org/10.1152/ajpgi.00015.2011.
Full textAbstract:
Eosinophilic esophagitis is characterized by increased infiltration and degranulation of eosinophils in the esophagus. Whether eosinophil-derived cationic proteins regulate esophageal sensory nerve function is still unknown. Using synthetic cationic protein to investigate such effect, we performed extracellular recordings from vagal nodose or jugular neurons in ex vivo esophageal-vagal preparations with intact nerve endings in the esophagus. Nerve excitabilities were determined by comparing action potentials evoked by esophageal distensions before and after perfusion of synthetic cationic protein poly-l-lysine (PLL) with or without pretreatment with poly-l-glutamic acid (PLGA), which neutralized cationic charges of PLL. Perfusion with PLL did not evoke action potentials in esophageal nodose C fibers but increased their responses to esophageal distension. This potentiation effect lasted for 30 min after washing out of PLL. Pretreatment with PLGA significantly inhibited PLL-induced mechanohyperexcitability of esophageal nodose C fibers. In esophageal nodose Aδ fibers, perfusion with PLL did not evoke action potentials. In contrast to nodose C fibers, both the spontaneous discharges and the responses to esophageal distension in nodose Aδ fibers were decreased by perfusion with PLL, which can be restored after washing out PLL for 30–60 min. Pretreatment with PLGA attenuated PLL-induced decrease in spontaneous discharge and mechanoexcitability of esophageal nodose Aδ fibers. In esophageal jugular C fibers, PLL neither evoked action potentials nor changed their responses to esophageal distension. Collectively, these data demonstrated that synthetic cationic protein did not evoke action potential discharges of esophageal vagal afferents but had distinctive sensitization effects on their responses to esophageal distension.
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Belay, Tsegay, Kim Chun IL, and Peter Schiavone. "Mechanics of a lipid bilayer subjected to thickness distension and membrane budding." Mathematics and Mechanics of Solids 23, no. 1 (September 13, 2016): 67–84. http://dx.doi.org/10.1177/1081286516666136.
Full textAbstract:
We study the distension-induced gradient capillarity in membrane bud formation. The budding process is assumed to be primarily driven by diffusion of transmembrane proteins and acting line tensions on the protein-concentrated interface. The proposed model, based on the Helfrich-type potential, is designed to accommodate inhomogeneous elastic responses of the membrane, non-uniform protein distributions over the membrane surface and, more importantly, the thickness distensions induced by bud formations in the membrane. The latter are employed via the augmented energy potential of bulk incompressibility in a weakened manner. By computing the variations of the proposed membrane energy potential, we obtained the corresponding equilibrium equation (membrane shape equation) describing the morphological transitions of the lipid membrane undergoing bud formation and the associated thickness distensions. The effects of lipid distension on the shape equation and the necessary adjustments to the accompanying boundary conditions are also derived in detail. The resulting shape equation is solved numerically for the parametric representation of the surface which has one-to-one-correspondence with the membrane surface under consideration. The proposed model successfully predicts the bud formation phenomenon on a flat lipid membrane and the associated thickness distensions of the membrane and demonstrates a smooth transition from one phase to the other (including necking domains). It is also found that the final deformed configuration is energetically favorable and therefore is stable. Finally, we show that the inhomogeneous thickness deformation on the membrane in response to transmembrane protein diffusion makes a significant contribution to the budding and necking processes of the membrane.
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Penagini, R., A. Picone, and P. A. Bianchi. "Effect of morphine and naloxone on motor response of the human esophagus to swallowing and distension." American Journal of Physiology-Gastrointestinal and Liver Physiology 271, no. 4 (October 1, 1996): G675—G680. http://dx.doi.org/10.1152/ajpgi.1996.271.4.g675.
Full textAbstract:
The effect of morphine on esophageal motility has been little explored. In eight healthy volunteers, we studied the effect of intravenous morphine (100 micrograms/kg) followed 60 min later by intravenous naloxone (80 micrograms/kg) and of intravenous naloxone alone (80 micrograms/kg) on the esophageal motor response to swallowing and 30-s intraluminal distensions(4, 6, 8, and 10 ml) during two separate experiments. Morphine increased (P < 0.01) the velocity but did not alter the amplitude or duration of primary peristalsis, and it decreased the duration and magnitude of swallow-induced lower esophageal sphincter (LES) relaxation (P < 0.01). It also markedly increased contractile activity below the balloon at high distending volumes (P < 0.05) and decreased the magnitude of distension-induced LES relaxation (P < 0.05) but did not affect contractile activity above the balloon. All effects were reversed by naloxone. The latter alone did not influence the esophageal response to swallowing or distension. The conclusions are that 1) morphine exerts effects on the response of the human esophagus to swallowing and intraluminal distension that are consistent with an action at the level of the inhibitory neural pathways, 2) these effects occur through opioid receptors, and 3) endogenous opioids do not seem to control esophageal motility, at least through mu-receptors.