Striated Muscle Esophagus Research Articles

Characterization and mechanism of the esophago-esophageal contractile reflex of the striated muscle esophagus

An esophago-esophageal contractile reflex (EECR) of the cervical esophagus has been identified in humans. The aim of this study was to characterize and determine the mechanisms of the EECR. Cats (n = 35) were decerebrated, electrodes were placed on pharynx and cervical esophagus, and esophageal motility was recorded using manometry. All areas of esophagus were distended to locate and quantify the EECR. The effects of esophageal perfusion of NaCl or HCl, vagus nerve or pharyngoesophageal nerve (PEN) transection, or hexamethonium administration (5 mg/kg iv) were determined. We found that distension of the esophagus at all locations activated EECR rostral to stimulus only. EECR response was greatest when the esophagus 2.5-11.5 cm from cricopharyngeus (CP) was distended. HCl perfusion activated repetitively an EECR-like response of the proximal esophagus only within 2 min, and after ~20 min EECR was inhibited. Transection of PEN blocked or inhibited EECR 1-7 cm from CP, and vagotomy blocked EECR at all locations. Hexamethonium blocked EECR at 13 and 16 cm from CP but sensitized its activation at 1-7 cm from CP. EECR of the entire esophagus exists, which is directed in the orad direction only. EECR of striated muscle esophagus is mediated by vagus nerve and PEN and inhibited by mechanoreceptors of smooth muscle esophagus. EECR of smooth muscle esophagus is mediated by enteric nervous system and vagus nerve. Activation of EECR of the striated muscle esophagus is initially sensitized by HCl exposure, which may have a role in prevention of supraesophageal reflux.NEW & NOTEWORTHY An esophago-esophageal contractile reflex (EECR) exists, which is directed in the orad direction only. EECR of the proximal esophagus can appear similar to and be mistaken for secondary peristalsis. The EECR of the striated muscle is mediated by the vagus nerve and pharyngoesophageal nerve and inhibited by mechanoreceptor input from the smooth muscle esophagus. HCl perfusion initially sensitizes activation of the EECR of the striated muscle esophagus, which may participate in prevention of supraesophageal reflux.

Tu1251 – Effect of Acute Esophageal Acid Exposure on Striated Muscle Esophagus and Ues Relaxation

Tu1251 – Effect of Acute Esophageal Acid Exposure on Striated Muscle Esophagus and Ues Relaxation

High Resolution Manofluorographic Study in Patients With Multiple System Atrophy: Possible Early Detection of Upper Esophageal Sphincter and Proximal Esophageal Abnormality.

Introduction: Multiple system atrophy (MSA) has detrimental effects on swallowing function. The swallowing function of patients with MSA has not been systematically characterized and the underlying pathophysiological mechanisms of dysphagia remain poorly understood.Objectives: To investigate the characteristics of swallow function in MSA using high-resolution manofluorography (HRMF).Methods: We conducted a retrospective review of twenty-five MSA patients who underwent HRMF from 2016 to 2017. HRMF was utilized on patients with only oral diet (Functional Oral Intake Scale (FOIS) >3). Pharyngoesophageal and proximal esophageal pressure profiles were evaluated and compared to established normative data. The frequency and characteristics of upper esophageal sphincter (UES) and proximal esophageal abnormalities during rest and swallow were calculated.Results: The ages of patient cohort in our study ranged from 48–81 years (median 65 years) with male predominance (68%). We observed a distinct abnormal deglutitive proximal esophageal contraction (ADPEC) in 14 (56% of patients), which appears to reflect a discoordinated response of the striated muscle esophagus. Deficient UES relaxation duration, impaired UES relaxation, hypertensive resting UES pressure and hypotensive resting UES pressure were detected in 8 patients (32%), 3 patients (12%), 1 patient (4%), and 11 patients (44%) respectively.Conclusions: In patients with MSA, abnormal UES resting pressure is common. A discoordinated proximal esophageal pressure response was identified and may be a pathognomonic manometry finding for MSA. These findings may serve as indications of early stage swallowing dysfunction in patients with MSA.

The enteric nervous system and gastrointestinal innervation: integrated local and central control.

The digestive system is innervated through its connections with the central nervous system (CNS) and by the enteric nervous system (ENS) within the wall of the gastrointestinal tract. The ENS works in concert with CNS reflex and command centers and with neural pathways that pass through sympathetic ganglia to control digestive function. There is bidirectional information flow between the ENS and CNS and between the ENS and sympathetic prevertebral ganglia.The ENS in human contains 200-600 million neurons, distributed in many thousands of small ganglia, the great majority of which are found in two plexuses, the myenteric and submucosal plexuses. The myenteric plexus forms a continuous network that extends from the upper esophagus to the internal anal sphincter. Submucosal ganglia and connecting fiber bundles form plexuses in the small and large intestines, but not in the stomach and esophagus. The connections between the ENS and CNS are carried by the vagus and pelvic nerves and sympathetic pathways. Neurons also project from the ENS to prevertebral ganglia, the gallbladder, pancreas and trachea.The relative roles of the ENS and CNS differ considerably along the digestive tract. Movements of the striated muscle esophagus are determined by neural pattern generators in the CNS. Likewise the CNS has a major role in monitoring the state of the stomach and, in turn, controlling its contractile activity and acid secretion, through vago-vagal reflexes. In contrast, the ENS in the small intestine and colon contains full reflex circuits, including sensory neurons, interneurons and several classes of motor neuron, through which muscle activity, transmucosal fluid fluxes, local blood flow and other functions are controlled. The CNS has control of defecation, via the defecation centers in the lumbosacral spinal cord. The importance of the ENS is emphasized by the life-threatening effects of some ENS neuropathies. By contrast, removal of vagal or sympathetic connections with the gastrointestinal tract has minor effects on GI function. Voluntary control of defecation is exerted through pelvic connections, but cutting these connections is not life-threatening and other functions are little affected.

Digestive and respiratory tract motor responses associated with eructation

We studied the digestive and respiratory tract motor responses in 10 chronically instrumented dogs during eructation activated after feeding. Muscles were recorded from the cervical area, thorax, and abdomen. The striated muscles were recorded using EMG and the smooth muscles using strain gauges. We found eructation in three distinct functional phases that were composed of different sets of motor responses: gas escape, barrier elimination, and gas transport. The gas escape phase, activated by gastric distension, consists of relaxation of the lower esophageal sphincter and diaphragmatic hiatus and contraction of the longitudinal muscle of the thoracic esophagus and rectus abdominis. All these motor events promote gas escape from the stomach. The barrier elimination phase, probably activated by rapid gas distension of the thoracic esophagus, consists of relaxation of the pharyngeal constrictors and excitation of dorsal and ventral upper esophageal sphincter distracting muscles, as well as rapid contraction of the diaphragmatic dome fibers. These motor events allow esophagopharyngeal air movement by promoting retrograde airflow and opening of the upper esophageal sphincter. The transport phase, possibly activated secondary to diaphragmatic contraction, consists of a retrograde contraction of the striated muscle esophagus that transports the air from the thoracic esophagus to the pharynx. We hypothesize that the esophageal reverse peristalsis is mediated by elementary reflexes, rather than a coordinated peristaltic response like secondary peristalsis. The phases of eructation can be activated independently of one another or in a different manner to participate in physiological events other than eructation that cause gastroesophageal or esophagogastric reflux.

A High-resolution View of Achalasia

High-resolution manometry (HRM) makes it possible to better evaluate spatial and temporal characteristics of esophageal motor function. This technology is revealing new observations regarding disordered motor function in esophageal diseases. The aim of this study was to define the essential features of achalasia using HRM. We performed HRM on 27 patients with achalasia, 10 patients with gastroesophageal reflux disease, and 10 controls. Ten 5 mL water swallows were recorded with a solid-state manometric assembly incorporating 36 circumferential sensors spaced at 1-cm intervals. The resting lower esophageal sphincter pressure was greater in achalasia than in controls or gastroesophageal reflux disease. There was an absence of peristalsis in the smooth muscle esophagus and failure of lower esophageal sphincter relaxation. The resting upper esophageal sphincter pressure was not different among the 3 groups. In addition to the typical manometric findings of achalasia, new observations are included. Esophageal shortening, pressurization of the esophagus, and rhythmic contractions of the upper esophageal sphincter and striated muscle esophagus were frequently observed. HRM demonstrates alterations of esophageal motor function in achalasia that are not easily observed with other manometric techniques.

Physiology of Normal Esophageal Motility

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.

Atropine effect on striated muscle esophagus in healthy subjects

Atropine effect on striated muscle esophagus in healthy subjects

Anatomy and Physiology of the Upper Esophageal Sphincter

The upper esophageal sphincter (UES) is composed of the cricopharyngeus (CP), thyropharyngeus (TP; inferior pharyngeal constrictor [IPC] in humans), and cranial cervical esophagus. All 3 muscles may at times function to maintain tone in the UES, but only the CP contracts and relaxes in all physiologic states consistent with the UES. The CP is a striated muscle composed of variable-sized small (25–35 μm) muscle fibers that are primarily type I (slow twitch), highly oxidative, and contain abundant (40%) endomysial elastic connective tissue. The fibers may attach to the connective tissue framework, forming a muscular net. In humans and rats, but not other animals, the CP has no median raphe. The optimum length of the CP for development of active tension is about 1.7 times resting length; therefore, in some respects the CP acts more like cardiac than striated muscle. A passive tone in the CP is present and increases through all degrees of stretch. The high compliance of the CP allows it to be opened by distraction of other muscles (e.g., geniohyoideus) or increased intraluminal pressure. The CP is innervated by branches of the vagus nerves: pharyngoesophageal (PE), superior laryngeal (SLN), and recurrent laryngeal (RLN); glossopharyngeal (GPN); and cervical sympathetics. Only the PE and SLN provide motor fibers to the CP. The GLN may be sensory; the sympathetics may innervate the mucosa, blood vessels, and glands; but no functional innervation by the RLN has been identified. Parasympathetic ganglia and various peptides (galanin, cGRP, VIP, neuropeptide Y, substance P, tyrosine hydroxylase) have been found in the CP, but their role in control of the CP is unknown. The motoneurons of the CP are found in the nucleus ambiguus, and the innervation is ipsilateral for animal species in which the CP has a median raphe. These motoneurons are topographically organized with other pharyngeal and laryngeal muscles and the striated muscle esophagus. Pharyngeal motoneurons often have a respiratory rhythm, but not a spontaneous background discharge. Therefore, the CP motoneurons may not generate CP tone. Various reflexes control the tone of the CP. Distension of the esophagus causes contraction of the CP and UES, which is mediated by a vago-vagal reflex. Pressure on the pharyngeal mucosa contracts the CP and UES and is mediated by a glossopharyngo-vagal reflex. Inflation of the lungs causes contraction of the CP and UES, which is mediated by a vago-vagal reflex. The pharyngo-UES and pulmonary-UES reflexes may generate the respiratory rhythm often observed on UES pressure or electromyographic activity. The UES or CP also contracts with arousal or with changes in posture. All of these reflexes and responses and the passive elastic properties of the CP may contribute to the generation of tone in the CP and UES.

Measurement of human esophageal tone in vivo

Background : Conventional perfused manometry has led to extensive study of phasic contractile activity in the human esophagus, but little is known about esophageal tonic activity. The aims of this study were to assess esophageal smooth and striated muscle tone and the effect of a smooth muscle relaxant (amyl nitrite, 0.3 mL inhalation) on this tone. Methods : Using a computerized isobaric recording system (barostat), esophageal tonic activity in 13 healthy subjects was recorded. Two parameters were analyzed: compliance and resistance to initial stretch (resting tone). Results : The smooth muscle esophagus was significantly more compliant but presented a greater resistance to initial stretch than the striated muscle section. Amyl nitrite affected only the smooth muscle section, significantly increasing compliance and decreasing the resistance to initial stretch. Significant chest pain and/or discomfort occurred only during striated muscle esophagus distension (10 of the 13 subjects at 25 mm Hg distending pressure). Conclusions : Active tone is present in the smooth muscle esophagus and can be modulated by a smooth muscle relaxant. Compliance and resting tone differ between the smooth and striated muscle segments of the esophagus. Assessment of tone in patients with esophageal motor disorders and noncardiac chest pain should provide further insights into these disorders.

Lower esophageal sphincter function in the cat: role of central innervation assessed by transient vagal blockade.

Studies were performed on four cats to assess the role of extrinsic vagal innervation in the control of lower esophageal sphincter (LES) function. Both cervical vagal nerves were blocked transiently by cooling. LES pressure was measured using a multilumen manometry tube. LES relaxation was assessed during intraesophageal balloon distension in both the striated and smooth muscle portions of the esophagus. Bilateral vagal nerve blockade lowered the mean LES pressure from 58 +/- 17 to 29 +/- 9 mmHg (P less than 0.01). During vagal blockade, balloon distension in the striated muscle esophagus further reduced sphincter pressure to 16 +/- 4 mmHg (P less than 0.01) and that in the smooth muscle esophagus to 15 +/- 3 mmHg (P less than 0.01). Swallow-induced LES relaxation was abolished during bilateral vagal nerve blockade. During vagal blockade, atropine reduced LES pressure to 10 +/- 1 mmHg, phentolamine to 13 +/- 6 mmHg, and hexamethonium to 10 +/- 4 mmHg (all P less than 0.01). We conclude that 1) normal LES tone in the cat is mediated primarily by two separate neural mechanisms: a vagal cholinergic mechanism and a nonvagal mechanism that utilizes both alpha-adrenergic and cholinergic receptors; 2) local, intramural mechanisms of high threshold are present in the striated and smooth muscle cat esophagus to allow distension-induced reflex inhibition of the LES; and 3) swallow-induced LES relaxation is dependent on vagally mediated central nervous system connections.

Effect of bilateral cervical vagotomy on balloon-induced lower esophageal sphincter relaxation in the dog

A study was performed in dogs to determine whether balloon distension within the striated muscle esophagus induces lower esophageal sphincter relaxation via a local intramural pathway or a central neural pathway. Bilateral vagosympathetic nerve blockade was produced by cooling the nerve trunks isolated in skin loops on either side of the neck. Sphincter pressure was measured before and during intraesophageal balloon distension, with and without nerve blockade. With the vagosympathetic nerves intact, balloon distension produced sphincter relaxation, sphincter shortening, and orad movement of the sphincter. The threshold for these responses increased progressively as distension was applied at more proximal levels. Bilateral vagosympathetic nerve blockade abolished all the lower esophageal sphincter responses to distension at any level within the esophagus, whether or not sphincter pressure was raised by pentagastrin infusion. Therefore, lower esophageal sphincter relaxation induced by distension of the dog striated muscle esophagus requires a central nervous system connection via the vagosympathetic nerve trunks. There is no direct intramural pathway for this response in the dog.