Oesophageal peristalsis in the cat: the role of central innervation assessed by transient vagal blockade

1985 ◽  
Vol 63 (2) ◽  
pp. 122-130 ◽  
Author(s):  
R. P. E. Reynolds ◽  
T. Y. El-Sharkawy ◽  
N. E. Diamant
Keyword(s):  
Smooth Muscle ◽  
Striated Muscle ◽  
Vagal Nerve ◽  
The Body ◽  
Nerve Blockade ◽  
Primary Peristalsis ◽  
Vagal Blockade ◽  
Central Innervation ◽  
Secondary Peristalsis

Studies were performed on five cats to assess the role of extrinsic vagal innervation in the control of peristalsis in the smooth muscle oesophagus. Transient vagal nerve blockade was accomplished by cooling the cervical vagosympathetic nerve trunks previously isolated in skin loops on each side of the neck. Peristalsis throughout the body of the oesophagus was monitored using a continuously perfused multilumen manometry tube. Striated and smooth muscle portions of the esophagus were delineated by abolishing smooth muscle activity with atropine. Secondary peristalsis was assessed by intra-oesophageal balloon distension studies. The threshold volume for balloon-induced secondary peristalsis was lower in the smooth muscle oesophagus. Unilateral vagal blockade reduced the incidence of primary and secondary peristalsis in the striated muscle oesophagus but not in the smooth muscle oesophagus. Bilateral vagal nerve blockade abolished primary swallow-induced peristalsis and secondary peristalsis in both the smooth and striated muscle cat oesophagus. Administration of cholinergic agents or adrenergic blocking agents failed to restore secondary peristalsis in the smooth muscle oesophagus during vagal cooling. We conclude that connections to the central nervous system via the vagal nerve trunks are required for normal secondary as well as primary peristalsis in both the smooth and striated muscle portions of the cat oesophagus.

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

1984 ◽  
Vol 246 (6) ◽  
pp. G666-G674 ◽  
Author(s):  
R. P. Reynolds ◽  
T. Y. El-Sharkawy ◽  
N. E. Diamant
Keyword(s):  
Smooth Muscle ◽  
Lower Esophageal Sphincter ◽  
Vagal Nerve ◽  
Sphincter Pressure ◽  
Cholinergic Mechanism ◽  
Nerve Blockade ◽  
Vagal Blockade ◽  
Balloon Distension ◽  
Esophageal Sphincter

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.

scholarly journals Nitric Oxide - Its Importance in Swallowing, Inflammatory Bowel Disease and Cirrhotic Cardiomyopathy

2001 ◽  
Vol 15 (8) ◽  
pp. 551-552
Author(s):  
ABR Thomson
Keyword(s):  
Nitric Oxide ◽  
Central Nervous System ◽  
Smooth Muscle ◽  
Esophageal Motility ◽  
Striated Muscle ◽  
Central Control ◽  
Solitary Tract ◽  
Esophageal Peristalsis ◽  
Primary Peristalsis

Nitric oxide is a neurotransmitter found in the central and peripheral nervous systems. Nitric oxide synthase (NOS) is localized in the central nervous system, including the nucleus of the solitary tract, nucleus ambiguus and dorsal motor nucleus of the vagus. These are regions that are implicated in the central control of swallowing and esophageal motility. In rats and rabbits, NOS has been shown to be present in the nucleus subcentralis of the nucleus of the solitary tract, and is thought to be responsible for the central programming of the striated muscle component of esophageal peristalsis. Beyak and co-workers from the University of Toronto, Toronto, Ontario provided evidence that the L-arginine-nitric oxide pathway is implicated in the central control of swallowing and esophageal motility. They studied oropharyngeal swallowing as well as esophageal peristalsis, and determined the functional role of brain stem nitric oxide by examining the effects of blockade of central nervous system NOS on swallowing, and on primary and secondary peristalsis. Administering NOS inhibitors intravenously or intracerebroventricularly into the fourth ventricle produced a number of oropharyngeal swallows and induced primary peristalsis in the smooth muscle portion of the esophageal body. NOS reduced the number of oropharyngeal swallows and the incidence of primary peristalsis in both smooth and striated muscle, and reduced the amplitude of peristalsis and smooth muscle contraction. This suggests that nitric oxide is a functional neurotransmitter in the central pattern generator responsible for swallowing and the central control of esophageal peristalsis. Peripherally administered NOS inhibitor can access structures within the blood-brain barrier to affect neuronal activity and physiological function. The central pattern generated for swallowing and esophageal peristalsis is suggested to be a serial network of linked neurons within the nucleus of the solitary tract and neighbouring reticular formation, and there is likely one subnetwork for the oropharyngeal phase and the other for the esophageal phase of swallowing. The neurosubstances mediating striated and smooth muscle peristalsis may be both anatomically and neurochemically distinct. The role of nitric oxide in the pathogenesis of esophageal motility disorders remains to be established.

Absence of a deglutitive inhibition equivalent with secondary peristalsis

2005 ◽  
Vol 288 (4) ◽  
pp. G671-G676 ◽  
Author(s):  
John E. Pandolfino ◽  
Guoxiang Shi ◽  
Qing Zhang ◽  
Peter J. Kahrilas
Keyword(s):  
Smooth Muscle ◽  
Lower Esophageal Sphincter ◽  
Intrinsic Property ◽  
Air Injection ◽  
Success Rates ◽  
Primary Peristalsis ◽  
No Inhibition ◽  
Lower Esophageal Sphincter Relaxation ◽  
Esophageal Sphincter ◽  
Secondary Peristalsis

This study aimed to determine the interactions between closely paired swallow-induced primary peristalsis (PP) and air injection-induced secondary peristalsis (SP). Ten subjects (7 men, 18–42 yr) were studied using a catheter, including two sleeves (upper and lower esophageal sphincters), a midesophageal infusion port, and seven esophageal and two pharyngeal recording sites. Ten iterations of PP and SP were induced by 5-ml water swallows and 20-ml intraesophageal air injections, respectively. Thereafter, the interactions between PP and SP, separated by 1- to 12-s intervals, were studied in all four possible sequences: paired swallows, swallow preceded by air injection, air injection preceded by swallow, and paired air injections. Tracings were analyzed for lower esophageal sphincter relaxation, presence and integrity of peristalsis, and event interaction. Eight subjects with success rates of both ≥90% PP and ≥80% SP were analyzed (PP 97 ± 2%, SP 90 ± 3%). During paired PP interactions and SP followed by PP, the first sequence was inhibited by the second with intervals < 4–6 s. However, no inhibition of the first peristaltic sequence was found in either PP followed by SP trials or SP followed by air injection. In contrast to swallowing or proximal esophageal distention, air injection into the lumen of the midesophagus does not inhibit an ongoing peristaltic event. Being that the elicitation of SP in the smooth muscle esophagus is intramurally mediated, this suggests that deglutitive inhibition is a centrally mediated phenomenon rather than an intrinsic property of peristalsis.

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

2019 ◽  
Vol 317 (3) ◽  
pp. G304-G313 ◽  
Author(s):  
Ivan M. Lang ◽  
Bidyut K. Medda ◽  
Reza Shaker
Keyword(s):  
Nervous System ◽  
Smooth Muscle ◽  
Vagus Nerve ◽  
Enteric Nervous System ◽  
Esophageal Motility ◽  
Striated Muscle ◽  
Cervical Esophagus ◽  
Proximal Esophagus ◽  
Secondary Peristalsis

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.

Role of vagus nerve in postprandial antropyloric coordination in conscious dogs

2005 ◽  
Vol 288 (3) ◽  
pp. G487-G495 ◽  
Author(s):  
Tomio Ueno ◽  
Kenichiro Uemura ◽  
Mary B. Harris ◽  
Theodore N. Pappas ◽  
Toku Takahashi
Keyword(s):  
Gastric Emptying ◽  
Vagus Nerve ◽  
Late Phase ◽  
Motor Pattern ◽  
The Body ◽  
Conscious Dogs ◽  
Solid Meal ◽  
Liquid Meal ◽  
Vagal Blockade

It is generally believed that gastric emptying of solids is regulated by a coordinated motor pattern between the antrum and pylorus. We studied the role of the vagus nerve in mediating postprandial coordination between the antrum and pylorus. Force transducers were implanted on the serosal surface of the body, antrum, pylorus, and duodenum in seven dogs. Dogs were given either a solid or a liquid meal, and gastroduodenal motility was recorded over 10 h. Gastric emptying was evaluated with radiopaque markers mixed with a solid meal. Dogs were treated with hexamethonium, NG-nitro-l-arginine methyl ester (l-NAME), or transient vagal nerve blockade by cooling. A postprandial motility pattern showed three distinct phases: early, intermediate, and late. In the late phase, profound pyloric relaxations predominantly synchronized with giant antral contractions that were defined as postprandial antropyloric coordination. A gastric emptying study revealed that the time at which gastric contents entered into the duodenum occurred concomitantly with antropyloric coordination. Treatment by vagal blockade or hexamethonium significantly reduced postprandial antral contractions and pyloric relaxations of the late phase. l-NAME changed pyloric motor patterns from relaxation dominant to contraction dominant. Solid gastric emptying was significantly attenuated by treatment with hexamethonium, l-NAME, and vagal blockade. Postprandial antropyloric coordination was not seen after feeding a liquid meal. It is concluded that postprandial antropyloric coordination plays an important role to regulate gastric emptying of a solid food. Postprandial antropyloric coordination is regulated by the vagus nerve and nitrergic neurons in conscious dogs.

scholarly journals Inactivation of carboxyl terminus of Hsc70-interacting protein prevents hypoxia-induced pulmonary arterial smooth muscle cells proliferation by reducing intracellular Ca2+ concentration

2019 ◽  
Vol 9 (3) ◽  
pp. 204589401987534 ◽  
Author(s):  
Fang Dong ◽  
Jun Zhang
Keyword(s):  
Smooth Muscle ◽  
Striated Muscle ◽  
Pulmonary Arteries ◽  
Underlying Mechanism ◽  
Carboxyl Terminus ◽  
Cell Phenotype ◽  
Interacting Protein ◽  
Aortic Smooth Muscle ◽  
Pulmonary Arterial

Carboxyl terminus of Hsc70-interacting protein (CHIP) is a 35-kDa cytoplasmic protein expressed in human striated muscle, brain, aortic smooth muscle, endothelial cells, and other tissues. Studies have confirmed that CHIP regulates cell growth, apoptosis, cell phenotype, metabolism, neurodegeneration, etc. However, whether CHIP is involved in pulmonary artery smooth muscle cell (PASMC) proliferation, a vital contributor to chronic hypoxia-induced pulmonary hypertension (CHPH), remains unknown. In this study, we first evaluated CHIP expression in the pulmonary arteries (PAs) of CHPH model rats. Subsequently, by silencing CHIP, we investigated the effect of CHIP on hypoxia-induced PASMC proliferation and the underlying mechanism. Our results showed that CHIP expression was upregulated in the PAs of CHPH model rats. Silencing CHIP significantly suppressed the hypoxia-triggered promotion of proliferation, [Ca2+]i, store-operated Ca2+ entry (SOCE), and some regulators of SOCE such as TRPC1 and TRPC6 in cultured PASMCs. These results indicate that CHIP likely contributes to hypoxia-induced PASMC proliferation by targeting the SOCE-[Ca2+]i pathway through the regulation of TRPC1 and TRPC6 in the PASMCs. In conclusion, the findings of the current study clarify the role of CHIP in hypoxia-induced PASMC proliferation.

scholarly journals The Contractile Mechanism in Obliquely Striated Body Wall Muscle of the Earthworm, Lumbricus Terrestris

1971 ◽  
Vol 8 (2) ◽  
pp. 413-425 ◽  
Author(s):  
M. F. KNAPP ◽  
P. J. MILL
Keyword(s):  
Body Wall ◽  
Striated Muscle ◽  
Lumbricus Terrestris ◽  
The Body ◽  
Band Width ◽  
Physiological Data ◽  
Muscle Fibres ◽  
Contraction Mechanism ◽  
Cross Links

Obliquely striated muscle fibres from the longitudinal and circular layers of the body wall of the earthworm were prepared in extended and contracted states for study in the electron microscope. Contracted fibres differ from extended ones in the following respects: (i) the I-bands are narrower, (ii) the A-bands are wider, and (iii) there are more rows of thick myofilaments in each A-band. The arrangement of the thick and thin myofilaments in interdigitating arrays and the occurrence of cross-links between the 2 types of myofilament indicate a classical sliding-filament mechanism of contraction as in cross-striated muscle, resulting in a reduction in the I-band width. The increase in the A-band width could be due to a moving apart of the myofilaments during contraction to preserve constant volume of the lattice. The third change, the increase in the number of rows of thick myofilaments in the A-band, can be explained only by a shearing of these filaments past one another in such a way as to increase the amount of their overlap. The role of the sliding-filament and shearing contraction mechanisms in bringing about the changes observed in earthworm muscle fibres is considered and the possible correlation of these mechanisms with certain physiological data is discussed. The function of the sarcoplasmic reticulum in the transmission of impulses to the interior of the fibre and/or in the control of the contraction mechanism is also discussed.

Effect of atropine on esophageal motor function in humans

1981 ◽  
Vol 240 (4) ◽  
pp. G290-G296 ◽  
Author(s):  
W. J. Dodds ◽  
J. Dent ◽  
W. J. Hogan ◽  
R. C. Arndorfer
Keyword(s):  
Smooth Muscle ◽  
Pulse Rate ◽  
Striated Muscle ◽  
Normal Subjects ◽  
Significant Inhibition ◽  
Species Variation ◽  
Primary Peristalsis ◽  
Neural Input ◽  
Manometric Studies ◽  
Esophageal Sphincter

In this study, we used a high-fidelity manometric recording system to quantitate the effects of atropine on lower esophageal sphincter (LES) pressure and primary peristalsis (1 degree P). A sleeve sensor recorded LES pressure, and seven recording orifices spaced at 3-cm intervals registered motor activity in the esophageal body. Five randomized manometric studies were done in each of five normal subjects. LES pressure and 1 degree P with wet swallows were recorded for 30 min before and 70 min after intravenous injection of saline or atropine, 3, 6, 12, and 24 micrograms/kg. We also studied the effect of atropine on LES pressure in five additional subjects, four dogs, four opossums, and six monkeys. In humans, saline and 3 micrograms/kg atropine caused no significant change in pulse rate, LES pressure, or the incidence of complete peristaltic sequences. The 6, 12, and 24 micrograms/kg atropine doses caused significant inhibition of LES pressure and the incidence of intact 1 degree P. Only the 12 and 24 micrograms/kg doses increased pulse rate. When 1 degree P occurred in the smooth muscle portion of the esophagus its appearance in the proximal portion of the smooth muscle segment was delayed for several seconds. The amplitude of 1 degree P was decreased 30-60% in the smooth muscle segment, but 1 degree P was not affected in the proximal striated muscle esophageal segment. Atropine reduced canine LES pressure substantially but caused no change in opossums or monkeys. We conclude that 1) basal LES tone in humans and dogs, unlike that of the opossum and monkey, is partially generated by cholinergic neural input, 2) cholinergic nerves elicit 1 degree P in human esophageal smooth muscle, and 3) species variation exists in esophageal responses to atropine.

Inositol trisphosphate, calcium and muscle contraction

1988 ◽  
Vol 320 (1199) ◽  
pp. 399-414 ◽  
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Phosphatase Activity ◽  
G Protein ◽  
Striated Muscle ◽  
Smooth Muscles ◽  
Physiological Role ◽  
Protein S ◽  
Storage Site

The identity of organelles storing intracellular calcium and the role of Ins(1,4,5) P 3 , in muscle have been explored with, respectively, electron probe X-ray microanalysis (EPMA) and laser photolysis of ‘caged’ compounds. The participation of G-protein(s) in the release of intracellular Ca 2+ was determined in saponin-permeabilized smooth muscle. The sarcoplasmic reticulum (SR) is identified as the major source of activator Ca 2+ in both smooth and striated muscle; similar (EPMA) studies suggest that the endoplasmic reticulum is the major Ca 2+ storage site in non-muscle cells. In none of the cell types did mitochondria play a significant, physiological role in the regulation of cytoplasmic Ca 2+ . The latency of guinea pig portal vein smooth muscle contraction following photolytic release of phenylephrine, an α 1 -agonist, is 1.5 ± 0.26 s at 20 °C and 0.6 ± 0.18 s at 30 °C; the latency of contraction after photolytic release of Ins(1,4,5) P 3 from caged Ins(1,4,5) P 3 is 0.5 ± 0.12 s at 20 °C. The long latency of α 1 -adrenergic Ca 2+ release and its temperature dependence are consistent with a process mediated by G-protein-coupled activation of phosphatidylinositol 4,5 bisphosphate (PtdIns(4,5) P 2 ) hydrolysis. GTPγS, a non-hydrolysable analogue of GTP, causes Ca 2+ release and contraction in permeabilized smooth muscle. Ins(1,4,5) P 3 has an additive effect during the late, but not the early, phase of GTPγS action, and GTPγS can cause Ca 2+ release and contraction of permeabilized smooth muscles refractory to Ins(l,4,5) P 3 . These results suggest that activation of G protein (s) can release Ca 2+ by, at least, two G-proteinregulated mechanisms: one mediated by Ins(1,4,5) P 3 and the other Ins(1,4,5) P 3 - independent. The Ins(1,4,5) P 3 , 5-phosphatase activity and the slow time-course (seconds) of the contractile response toIns(1,4,5) P 3 released with laser flash photolysis from caged Ins(1,4,5) P 3 in frog skeletal muscle suggest that Ins(1,4,5) P 3 is unlikely to be the physiological messenger of excitation-contraction coupling of striated muscle. In contrast, in smooth muscle the high Ins Ins(1,4,5) P 3 -5-phosphatase activity and the rate of force development after photolytic release of Ins(1,4,5) P 3 are compatible with a physiological role of Ins(1,4,5) P 3 as a messenger of pharmacomechanical coupling.

Gastric and duodenal motility in the cat: the role of central innervation assessed by transient vagal blockade

1986 ◽  
Vol 64 (6) ◽  
pp. 712-716 ◽  
Author(s):  
M. P. Bendeck ◽  
R. P. E. Reynolds
Keyword(s):  
Small Bowel ◽  
Contractile Activity ◽  
General Pattern ◽  
The Body ◽  
Complex Activity ◽  
Duodenal Motility ◽  
Vagal Blockade ◽  
Proximal Small Bowel ◽  
Vagal Innervation

Experiments were performed on four cats to characterize fasting gastric and small bowel motility and to assess the role of extrinsic vagal innervation in the control of that motor activity. A multilumen manometry tube was positioned to record pressure changes from the proximal small bowel and stomach. Transient vagal nerve blockade was accomplished by cooling the cervical vagosympathetic nerve trunks, previously isolated in skin loops on each side of the neck. Two characteristic patterns of basal activity were documented in the stomach: (i) regular phasic contractions of variable amplitude in the body of the stomach; and (ii) infrequent, irregular contractions of high amplitude in the distal antrum. In the duodenum, two predominant activity patterns were noted: (i) periods of continuous irregular activity; and (ii) irregular clusters of contractions separated by quiescent intervals. No typical migrating motor complex activity was seen in the basal gastric or small bowel recordings. Bilateral vagal blockade did not consistently change the general pattern of gastric or small bowel activity, but did appear to reduce gastric contractile activity, as measured by motility indices. We conclude that extrinsic vagal innervation does not play a major role in the control of fasting feline gastric and duodenal motility.

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