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Rattan S, Cao W, Katz PO, Goyal RK. In the memory of our following colleagues, and friends. Neurogastroenterol Motil 2022; 34:e14393. [PMID: 35583082 DOI: 10.1111/nmo.14393] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/20/2022] [Accepted: 04/21/2022] [Indexed: 02/08/2023]
Affiliation(s)
- Satish Rattan
- Department of Medicine, Division of Gastroenterology & Hepatology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania, USA
| | - Weibiao Cao
- Department of Pathology & Medicine, Rhode Island Hospital and The Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA
| | - Philip O Katz
- Weill Cornell Medicine, New York Presbyterian Hospital, New York, New York, USA
| | - Raj K Goyal
- Department of Medicine, Divisions of Gastroenterology and Hepatology. VA Boston Healthcare System, Beth Israel Deaconess Hospital and Harvard medical School, Boston, Massachusetts, USA
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Pharmacologic Treatment of Esophageal Dysmotility. Dysphagia 2017. [DOI: 10.1007/174_2017_127] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/18/2022]
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Boeckxstaens G, Camilleri M, Sifrim D, Houghton LA, Elsenbruch S, Lindberg G, Azpiroz F, Parkman HP. Fundamentals of Neurogastroenterology: Physiology/Motility - Sensation. Gastroenterology 2016; 150:S0016-5085(16)00221-3. [PMID: 27144619 DOI: 10.1053/j.gastro.2016.02.030] [Citation(s) in RCA: 78] [Impact Index Per Article: 8.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/03/2016] [Accepted: 02/09/2016] [Indexed: 12/14/2022]
Abstract
The fundamental gastrointestinal functions include motility, sensation, absorption, secretion, digestion and intestinal barrier function. Digestion of food and absorption of nutrients normally occurs without conscious perception. Symptoms of functional gastrointestinal disorders are often triggered by meal intake suggesting abnormalities in the physiological processes are involved in the generation of symptoms. In this manuscript, normal physiology and pathophysiology of gastrointestinal function, and the processes underlying symptom generation are critically reviewed. The functions of each anatomical region of the digestive tract are summarized. The pathophysiology of perception, motility, mucosal barrier, and secretion in functional gastrointestinal disorders as well as effects of food, meal intake and microbiota on gastrointestinal motility and sensation are discussed. Genetic mechanisms associated with visceral pain and motor functions in health and functional gastrointestinal disorders are reviewed. Understanding the basis for digestive tract functions is essential to understand dysfunctions in the functional gastrointestinal disorders.
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Affiliation(s)
- Guy Boeckxstaens
- Department of Gastroenterology, Translational Research Center for Gastrointestinal Disorders (TARGID), University Hospital Leuven, KU Leuven, Leuven, Belgium
| | | | - Daniel Sifrim
- Wingate Institute of Neurogastroenterology, Bart's and the London School of Medicine, Queen Mary, University of London, London, UK
| | - Lesley A Houghton
- Division of Gastroenterology and Hepatology, Mayo Clinic, Jacksonville, FL, USA
| | - Sigrid Elsenbruch
- Institute of Medical Psychology and Behavioral Immunobiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany
| | - Greger Lindberg
- Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden
| | - Fernando Azpiroz
- Digestive Diseases Department, University Hospital Vall D'Hebron, Autonomous University of Barcelona, Barcelona, Spain
| | - Henry P Parkman
- Department of Medicine, Temple University School of Medicine, Philadelphia, PA, USA.
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Li KL, Chen JH, Zhang Q, Huizinga JD, Vadakepeedika S, Zhao YR, Yu WZ, Luo HS. Habitual rapid food intake and ineffective esophageal motility. World J Gastroenterol 2013; 19:2270-2277. [PMID: 23599655 PMCID: PMC3627893 DOI: 10.3748/wjg.v19.i14.2270] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/24/2012] [Revised: 11/19/2012] [Accepted: 01/21/2013] [Indexed: 02/06/2023] Open
Abstract
AIM: To study non-cardiac chest pain (NCCP) in relation to ineffective esophageal motility (IEM) and rapid food intake.
METHODS: NCCP patients with a self-reported habit of fast eating underwent esophageal manometry for the diagnosis of IEM. Telephone interviews identified eating habits of additional IEM patients. Comparison of manometric features was done among IEM patients with and without the habit of rapid food intake and healthy controls. A case study investigated the effect of 6-mo gum chewing on restoration of esophageal motility in an IEM patient. The Valsalva maneuver was performed in IEM patients and healthy controls to assess the compliance of the esophagus in response to abdominal pressure increase.
RESULTS: Although most patients diagnosed with NCCP do not exhibit IEM, remarkably, all 12 NCCP patients who were self-reporting fast eaters with a main complaint of chest pain (75.0%) had contraction amplitudes in the mid and distal esophagus that were significantly lower compared with healthy controls [(23.45 mmHg (95%CI: 14.06-32.85) vs 58.80 mmHg (95%CI: 42.56-75.04), P < 0.01 and 28.29 mmHg (95%CI: 21.77-34.81) vs 50.75 mmHg (95%CI: 38.44-63.05), P < 0.01, respectively)]. In 7 normal-eating IEM patients with a main complaint of sensation of obstruction (42.9%), the mid amplitude was smaller than in the controls [30.09 mmHg (95%CI: 19.48-40.70) vs 58.80 mmHg (95%CI: 42.56-75.04), P < 0.05]. There was no statistically significant difference in manometric features between the fast-eating and normal-eating groups. One NCCP patient who self-reported fast eating and was subsequently diagnosed with IEM did not improve with proton-pump inhibition but restored swallow-induced contractions upon 6-mo gum-chewing. The Valsalva maneuver caused a markedly reduced pressure rise in the mid and proximal esophagus in the IEM patients.
CONCLUSION: Habitual rapid food intake may lead to IEM. A prospective study is needed to validate this hypothesis. Gum-chewing might strengthen weakened esophageal muscles.
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Abstract
The primary role of the esophagus is to propel swallowed food or fluid into the stomach and to prevent or clear gastroesophageal reflux. This function is achieved by an organized pattern that involves a sensory pathway, neural reflexes, and a motor response that includes esophageal tone, peristalsis, and shortening. The motor function of the esophagus is controlled by highly complex voluntary and involuntary mechanisms. There are three different functional areas in the esophagus: the upper esophageal sphincter, the esophageal body, and the LES. This article focused on anatomy and physiology of the esophageal body.
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Affiliation(s)
- E Yazaki
- Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
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Sifrim D, Jafari J. Deglutitive inhibition, latency between swallow and esophageal contractions and primary esophageal motor disorders. J Neurogastroenterol Motil 2012; 18:6-12. [PMID: 22323983 PMCID: PMC3271255 DOI: 10.5056/jnm.2012.18.1.6] [Citation(s) in RCA: 34] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/09/2011] [Revised: 12/12/2011] [Accepted: 12/20/2011] [Indexed: 01/03/2023] Open
Abstract
Swallowing induces an inhibitory wave that is followed by a contractile wave along the esophageal body. Deglutitive inhibition in the skeletal muscle of the esophagus is controlled in the brain stem whilst in the smooth muscle, an intrinsic peripheral control mechanism is critical. The latency between swallow and contractions is determined by the pattern of activation of the inhibitory and excitatory vagal pathways, the regional gradients of inhibitory and excitatory myenteric nerves, and the intrinsic properties of the smooth muscle. A wave of inhibition precedes a swallow-induced peristaltic contraction in the smooth muscle part of the human oesophagus involving both circular and longitudinal muscles in a peristaltic fashion. Deglutitive inhibition is necessary for drinking liquids which requires multiple rapid swallows (MRS). During MRS the esophageal body remains inhibited until the last of the series of swallows and then a peristaltic contraction wave follows. A normal response to MRS requires indemnity of both inhibitory and excitatory mechanisms and esophageal muscle. MRS has recently been used to assess deglutitive inhibition in patients with esophageal motor disorders. Examples with impairment of deglutitive inhibition are achalasia of the LES and diffuse esophageal spasm.
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Affiliation(s)
- Daniel Sifrim
- Barts and The London School of Medicine and Dentistry, Queen Mary, University of London, London, UK
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Abstract
The esophagus consists of 2 different parts. In humans, the cervical esophagus is composed of striated muscles and the thoracic esophagus is composed of phasic smooth muscles. The striated muscle esophagus is innervated by the lower motor neurons and peristalsis in this segment is due to sequential activation of the motor neurons in the nucleus ambiguus. Both primary and secondary peristaltic contractions are centrally mediated. The smooth muscle of esophagus is phasic in nature and is innervated by intramural inhibitory (nitric oxide releasing) and excitatory (acetylcholine releasing) neurons that receive inputs from separate sets of preganglionic neurons located in the dorsal motor nucleus of vagus. The primary peristalsis in this segment involves both central and peripheral mechanisms. The primary peristalsis consists of inhibition (called deglutitive inhibition) followed by excitation. The secondary peristalsis is entirely due to peripheral mechanisms and also involves inhibition followed by excitation. The lower esophageal sphincter (LES) is characterized by tonic muscle that is different from the muscle of the esophageal body. The LES, like the esophageal body smooth muscle, is also innervated by the inhibitory and excitatory neurons. The LES maintains tonic closure because of its myogenic property. The LES tone is modulated by the inhibitory and the excitatory nerves. Inhibitory nerves mediate LES relaxation and the excitatory nerves mediate reflex contraction or rebound contraction of the LES. Clinical disorders of esophageal motility can be classified on the basis of disorders of the inhibitory and excitatory innervations and the smooth muscles.
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Bredenoord AJ, Weusten BLAM, Timmer R, Smout AJPM. Gastro-oesophageal reflux of liquids and gas during transient lower oesophageal sphincter relaxations. Neurogastroenterol Motil 2006; 18:888-93. [PMID: 16961691 DOI: 10.1111/j.1365-2982.2006.00817.x] [Citation(s) in RCA: 23] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/26/2022]
Abstract
Some transient lower oesophageal sphincter relaxations (TLOSRs) are accompanied by gastro-oesophageal reflux and others are not. We aimed to investigate what factors determine the occurrence and type of reflux during TLOSRs. In 12 healthy subjects prolonged high-resolution manometry was performed. Reflux was detected using pH-impedance monitoring. A total of 219 TLOSRs were detected; no differences were observed between the duration of TLOSRs with liquid-containing reflux (20.2 +/- 1.0 s), gas reflux (17.0 +/- 1.0 s) and no reflux (19.0 +/- 1.0 s). Trans-sphincteric pressure gradient was similar in TLOSRs with liquid reflux (1.6 +/- 0.1 kPa), gas reflux (1.5 +/- 0.1 kPa) and no reflux (1.7 +/- 0.3 kPa). Prevalence, duration and amplitude of oesophageal pre-contractions and sphincteric after-contractions were not different for TLOSRs with and without reflux. The total number of TLOSRs decreased significantly from 8.2 +/- 0.8 in the first to 5.7 +/- 0.5 in the second and 4.4 +/- 0.6 in the third 70-min recording period. The number of TLOSRs accompanied by liquid-containing reflux decreased from 4.7 +/- 0.9 to 3.0 +/- 0.4 to 1.6 +/- 0.4, while the numbers of TLOSRs with gas reflux remained unchanged (2.1 +/- 0.6-2.1 +/- 0.7-2.2 +/- 0.6). Besides, time after the meal, no differences were observed in the characteristics of TLOSRs with and without gastro-oesophageal reflux. We conclude that factors, other than TLOSR characteristics, are important of whether or not a TLOSR is reflux-related.
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Affiliation(s)
- A J Bredenoord
- Department of Gastroenterology, Sint Antonius Hospital, Nieuwegein, The Netherlands.
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Tutuian R, Jalil S, Katz PO, Castell DO. Effect of interval between swallows on oesophageal pressures and bolus movement in normal subjects - Studies with combined multichannel intraluminal impedance and oesophageal manometry. Neurogastroenterol Motil 2004; 16:23-9. [PMID: 14764202 DOI: 10.1046/j.1365-2982.2003.00460.x] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/08/2023]
Abstract
The effect of closely spaced swallows to decrease peristalsis ('deglutitive inhibition') is believed to be due to both central inhibitory impulses and smooth muscle refractoriness. Ten volunteers (three females, age 26-65) were given both four pairs and two series of four swallows at 5-, 10-, 15-s intervals and control swallows at 30-s intervals. Oesophageal function was assessed using combined multichannel intraluminal impedance and oesophageal manometry (MII-OM). Swallows were considered manometrical effective if distal oesophageal pressures >/=30 mmHg. Complete bolus transit was defined as bolus exiting from all three distal impedance segments. During swallowing at 5-s intervals the majority of initial swallows were ineffective with incomplete bolus transit while the last swallow in both series and pairs was manometrically effective with complete bolus transit. During swallowing at 10-15-s intervals the number of manometric ineffective swallows and swallows with incomplete bolus transit progressively increased with the number of swallows. The functional information obtained by MII-OM indicates pooling of liquid in the distal oesophagus that is cleared by the last swallow determined by, previously reported, neural inhibition occurring during swallowing spaced 5 s apart whereas incomplete bolus transit is related to manometrically ineffective swallows resulting from muscle refractoriness occurring during swallowing at 10-15-s intervals.
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Affiliation(s)
- R Tutuian
- Medical University of South Carolina, Charleston, SC 29425, USA.
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Abstract
BACKGROUND/AIMS Primary esophageal motility disorders (achalasia, diffuse esophageal spasm, and intermediate forms) are suggested to be caused by different degrees of inhibitory dysfunction; however, direct evidence for this hypothesis has never been presented in humans. The aim of this study was to measure the degree of inhibition that precedes deglutitive contractions in patients with primary motility disorders. METHODS Deglutitive inhibition was examined in patients with primary motility disorders: 9 with achalasia, 6 with symptomatic diffuse esophageal spasm, and 5 with intermediate forms. An artificial high-pressure zone was created in the esophageal body by inflating a balloon to a critical level, and pressure changes were measured at the interface between the balloon and esophageal wall. Inhibition was visualized as a relaxation of the artificial high-pressure zone. RESULTS An inverse relationship was found between the degree of inhibition and the propagation velocity of the deglutitive contraction (r = 0.75; P < 0.001). Normally propagated contractions were preceded by an inhibition of 84.2% +/- 3.6%; fast-propagating contractions were preceded by partial inhibition of 40.6% +/- 6.2%; and, in case of simultaneous contractions, inhibition was absent, i.e., 2.6% +/- 1.6%. CONCLUSIONS The spectrum of primary motility disorders is an expression of a progressively failing deglutitive inhibition.
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Affiliation(s)
- D Sifrim
- Department of Medical Research, University of Leuven, Belgium
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Abstract
BACKGROUND Simultaneous and spontaneous contractions are frequently recorded in patients with esophageal motility disorders. The aim was to investigate the pathogenesis of swallow-induced simultaneous and spontaneous contractions. METHODS The pathogenesis was studied in patients with normal peristaltic contractions (control group) and in patients with functional dysphagia with either simultaneous contractions (group A), with peristaltic but prolonged contractions (group B), and with frequent spontaneous contractions (group C). RESULTS Simultaneous contractions had latencies of 2.9 +/- 0.2 seconds compared with 6.4 +/- 0.2 seconds for normal peristaltic contractions and 5.8 +/- 0.4 seconds for prolonged peristaltic contractions. Paired swallows at intervals of 5 seconds generated one peristaltic sequence after the second swallow in subjects with normal peristalsis and two sets of contractions in patients with simultaneous contractions. Ten consecutive swallows taken at 5-second intervals inhibited the spontaneous contractions evoked by bethanechol in control subjects but had no significant effect on the spontaneous contractions of subjects with simultaneous contractions. Atropine reduced the frequency, force, and duration of the spontaneously generated contractions in group C. CONCLUSIONS The shorter latency of simultaneous contractions may be caused by a defective deglutitive inhibitory reflex, and spontaneous contractions appear to be generated by swallow independent discharges of acetylcholine.
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Affiliation(s)
- J Behar
- Department of Medicine, Rhode Island Hospital, Providence
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Abstract
To explore the involvement of NO in normal peristalsis, the effects of inhibitors of NO synthase, including N omega-nitro-L-arginine (L-NNA) and N omega-nitro-L-arginine methyl ester (L-NAME), on esophageal peristaltic contractions induced by diverse stimuli that may involve different neuronal circuits were studied. Studies were performed in opossums. Experimental conditions in vivo included primary peristalsis (P) induced by pharyngeal stroking, short-train (1 second) electrical stimulation of the vagus nerve which caused peristaltic (S) contractions, and long-train (10 second) electrical stimulation of the vagus nerves which caused contractions at the onset of (A contractions) and after (B contractions) the stimulation period. In vitro experiments were performed on strips of esophageal circular muscle using electrical field stimulation which caused contractions at the onset of (on contractions) and after (off contractions) the stimulation period. The administration of L-NAME significantly decreased the latency period and reduced the latency gradient for P contractions, thereby increasing the velocity of peristalsis. Concomitant administration of atropine prolonged the latency period but did not restore the latency gradient. L-NAME abolished B contractions in a dose-dependent fashion. In vitro, L-NAME caused dose-dependent inhibition of off contractions and augmentation of on contractions. These studies support the hypothesis that NO may be involved in (a) both the latency period and the latency gradient, as well as in the contraction amplitude of esophageal peristalsis; and (b) esophageal B and off contractions.
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Affiliation(s)
- S Yamato
- Center for Swallowing and Motility Disorders, Charles A. Dana Research Institute, Boston, Massachusetts
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Mulè F. The avian oesophageal motor function and its nervous control: some physiological, pharmacological and comparative aspects. COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY. A, COMPARATIVE PHYSIOLOGY 1991; 99:491-8. [PMID: 1679687 DOI: 10.1016/0300-9629(91)90121-r] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/28/2022]
Abstract
1. This paper deals with the avian oesophageal motor function and it attempts to draw some comparative aspects between neural regulation of the avian and mammalian oesophagus. 2. Different from the mammalian oesophagus, the avian oesophagus, presents at rest electrical activity associated to spontaneous contractions. 3. Swallowing elicits peristaltic contraction, characterized by an inhibitory and an excitatory component. 4. Non-adrenergic, non-cholinergic neurons are responsible for the inhibitory component. 5. Contrarily to what observed in mammals, where the peripheral mechanism are important for the peristaltic sequence, the primary peristaltism of birds seems to be entirely mediated by extrinsic nervous system.
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Affiliation(s)
- F Mulè
- Dipartimento di Biologia cellulare e dello Sviluppo, Università di Palermo, Italy
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Abstract
We review recent studies on the central neural control of esophageal motility, emphasizing the anatomy and chemical coding of esophageal pathways in the spinal cord and medulla. Sympathetic innervation of the proximal esophagus is derived primarily from cervical and upper thoracic paravertebral ganglia, whereas that of the lower esophageal sphincter and proximal stomach is derived from the celiac ganglion. In addition to noradrenaline, many sympathetic fibers in the esophagus contain neuropeptide Y (NPY), and both noradrenaline and NPY appear to decrease blood flow and motility. Preganglionic neurons innervating the cervical and upper thoracic ganglia are located at lower cervical and upper thoracic spinal levels. The preganglionic innervation of the celiac ganglion arises from lower thoracic spinal levels. Both acetylcholine (ACh) and enkephalin (ENK) have been localized in sympathetic preganglionic neurons, and it has been suggested that ENK acts to pre-synaptically inhibit ganglionic transmission. Spinal afferents from the esophagus are few, but have been described in lower cervical and thoracic dorsal root ganglia. A significant percentage contain calcitonin gene-related peptide (CGRP) and substance P (SP). The central distribution of spinal afferents, as well as their subsequent processing within the spinal cord, have not been addressed. Medullary afferents arise from the nodose ganglion and terminate peripherally both in myenteric ganglia, where they have been postulated to act as tension receptors, and, to a lesser extent, in more superficial layers. Centrally, these afferents appear to end in a discrete part of the nucleus of the solitary tract (NTS) termed the central subnucleus. The transmitter specificity of the majority of these afferents remains unknown. The central subnucleus, in turn, sends a dense and topographically discrete projection to esophageal motor neurons in the rostral portion of the nucleus ambiguous (NA). Both somatostatin-(SS) and ENK-related peptides have been localized in this pathway. Finally, motor neurons from the rostral NA innervate striated portions of the esophagus. In addition to ACh, these esophageal motor neurons contain CGRP, galanin (GAL), N-acetylaspartylglutamate (NAAG), and brain natriuretic peptide (BNP). The physiological effect of these peptides on esophageal motility remains unclear. Medullary control of smooth muscle portions of the esophagus have not been thoroughly investigated.
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Affiliation(s)
- E T Cunningham
- Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205
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Abstract
The present study was performed to characterize the interaction between two closely timed swallows, with particular attention being paid to short swallow intervals (less than 6-8 s) when the first wave is still traversing the esophagus and the effect of afferent stimulation in the form of bolus size. The contractile response of the esophagus to paired swallows (2-8 ml) over a range of swallow intervals (1.5-20 s) was studied in 13 normal humans using a 7-lumen perfused manometry catheter. At the shortest swallow intervals (less than 4 s), the first swallow wave is arrested in the striated muscle, while the second progresses normally. As swallow intervals lengthen (3-8 s), the first wave is arrested in the striated muscle, or is arrested or attenuated in the smooth muscle esophagus, but can continue for up to 3 s after initiation of the second swallow. The second wave is then arrested in the striated muscle, while beyond, a rapid or nonperistaltic low-amplitude wave occurs 3-5 s after the second swallow. At longer swallow intervals (greater than 6-8 s), the nonperistaltic second wave is replaced abruptly by a low-amplitude peristaltic wave of low velocity that traverses the entire esophagus. A larger first bolus increases the swallow interval required for this abrupt change, whereas a larger second bolus shortens the interval. The larger second bolus also increases the amplitude and decreases the velocity of the peristaltic second wave in both striated and smooth muscle portions. At swallow intervals greater than 10-15 s, two normal peristaltic waves occur. These studies demonstrate that each swallow of a closely timed pair directly affects the other. Not only does the second wave inhibit the first, but the first swallow and its wave markedly affect the second swallow wave. These interactions involve both the striated and the smooth muscle esophagus, and the latter interaction in particular is highly sensitive to afferent stimulation. This suggests that the interactions are predominantly neurogenic and have a significant central neural component.
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Abstract
The influence of two successive vagal stimuli on esophageal contractions was studied by recording intraluminal pressures in the smooth muscle portion of the opossum esophagus. The esophageal contraction in response to the first or second stimulus in a pair of vagal stimuli was inhibited depending on the interstimulus interval, the frequency of the stimulus, and the esophageal site. The esophageal contraction in response to the first vagal stimulus was inhibited by a second vagal stimulus if the latter stimulus was applied before the peak of the first contraction. This phenomenon is termed initial inhibition. Initial inhibition is a graded phenomenon. It was greater at higher frequencies than at lower frequencies (p less than 0.001), and was significantly greater in the distal esophagus than in the proximal esophagus (p less than 0.01). The term "refractoriness" has been used to denote inhibition of the second esophageal contraction by the first. Refractoriness was observed during and beyond the duration of the first esophageal response. Refractoriness was also observed at all esophageal levels; however, the interstimulus intervals that demonstrated refractoriness were significantly greater in the distal than in the proximal esophagus (p less than 0.01). Refractoriness was complete (effective refractory period) during the ascending phase of the first contraction. Refractoriness was incomplete after the peak of the contraction (relative refractory period). These studies show gradients of durations and degrees of initial inhibition and refractoriness along the esophagus. The gradient is responsible for the peristaltic nature of esophageal contraction. The gradients of initial inhibition and refractoriness determine esophageal response to multiple successive swallows.
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Crist J, Gidda JS, Goyal RK. Intramural mechanism of esophageal peristalsis: roles of cholinergic and noncholinergic nerves. Proc Natl Acad Sci U S A 1984; 81:3595-9. [PMID: 6587375 PMCID: PMC345556 DOI: 10.1073/pnas.81.11.3595] [Citation(s) in RCA: 77] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/20/2023] Open
Abstract
We examined the role of peripheral cholinergic and noncholinergic mechanisms in esophageal peristalsis. Intramural nerve elements in rings of circular muscle from six different levels of the opossum esophagus were stimulated transmurally so as to cause neurally mediated muscle contractions. Stimulus frequency was varied from 2 to 40 Hz. An increase in stimulus frequency caused an increase in latencies of contractions in rings from distal esophageal sites and a decrease in latencies in rings from proximal sites. This resulted in a marked slowing of the calculated peristaltic speed. Increasing stimulus frequency also caused an increase in duration and amplitude of contractions. These effects were reversed by atropine (0.1 microM), suggesting that higher stimulus frequencies recruited more cholinergic nerves. In the presence of atropine, increasing the stimulus frequency caused an increase in latencies of contraction at all sites, suggesting that increasing stimulation frequency applied to noncholinergic nerves causes an increase in latencies of contraction at all sites. The results of this study indicate that both noncholinergic and cholinergic nerves play a role in the peripheral mechanism of esophageal peristalsis. Cholinergic nerve stimulation reduces the latency and enhances the amplitude and duration of contractions seen with noncholinergic nerve stimulation alone. The influence of cholinergic innervation is most prominent proximally and decreases distally along the smooth muscle portion of the esophagus. This peripherally located gradient of cholinergic innervation plays an important role in determining the speed and amplitude of esophageal peristalsis.
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