Relevant bibliographies by topics / Smooth nerve

Academic literature on the topic 'Smooth nerve'

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Published: 21 July 2023

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Journal articles on the topic "Smooth nerve"

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Valic, Zoran, Edward H. Vidruk, Stephen B. Ruble, John B. Buckwalter, and Philip S. Clifford. "Parasympathetic innervation of canine tracheal smooth muscle." Journal of Applied Physiology 90, no. 1 (January 1, 2001): 23–28. http://dx.doi.org/10.1152/jappl.2001.90.1.23.

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To investigate whether efferent parasympathetic fibers to the tracheal smooth muscle course through the pararecurrent nerve rather than the recurrent or the superior laryngeal nerve, we stimulated all three nerves in anesthetized dogs. We also recorded the pararecurrent nerve activity response to bronchoconstrictor stimuli and compared it with pressure changes inside a saline-filled cuff of an endotracheal tube. Electrical stimulation (30 s, 100 Hz, 0.1 ms, 10 mA) increased tracheal cuff pressure by 21.0 ± 3.2 and 1.3 ± 0.7 cmH2O for the pararecurrent and the recurrent laryngeal nerve, respectively. Stimulation of the superior laryngeal nerve increased tracheal cuff pressure before, but not after, sectioning of the ramus anastomoticus, which connects it to the pararecurrent nerve. Intravenous administration of sodium cyanide increased pararecurrent nerve activity by 208 ± 51% and tracheal cuff pressure by 14.4 ± 3.5 cmH2O. Elevation of end-tidal Pco 2 to 50 Torr increased pararecurrent nerve activity by 49 ± 19% and tracheal cuff pressure by 8.4 ± 3.6 cmH2O. Further elevation to 60 Torr increased pararecurrent nerve activity by 101 ± 33% and tracheal cuff pressure by 11.3 ± 2.9 cmH2O. These results lead us to the conclusion that parasympathetic efferent fibers reach the smooth muscle of the canine trachea via the pararecurrent nerve.
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Canning, B. J., and A. Fischer. "Localization of cholinergic nerves in lower airways of guinea pigs using antisera to choline acetyltransferase." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 4 (April 1, 1997): L731—L738. http://dx.doi.org/10.1152/ajplung.1997.272.4.l731.

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Primary antiserum to choline acetyltransferase (ChAT), a specific marker for cholinergic nerves, was used to characterize the distribution of cholinergic nerve fibers and nerve cell bodies in guinea pig airways. ChAT immunoreactive nerve fibers were localized to the smooth muscle throughout the conducting airways and in the lamina propria of the trachea and large bronchi. Likewise, all nerve cell bodies in the ganglia intrinsic to the trachea and bronchi displayed a cholinergic phenotype. By contrast, ChAT immunoreactive nerve fibers were infrequently seen in the lamina propria of the peripheral airways and were absent in the airway epithelium. No evidence for colocalization of ChAT and the enzyme synthesizing the putative relaxant neurotransmitter nitric oxide was observed. These results provide further evidence for the key role played by cholinergic nerves in regulating airway smooth muscle tone and bronchial blood flow and provide further evidence that acetylcholine is not coreleased with the neurotransmitter(s) mediating relaxations of airway smooth muscle.
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Undem, B. J., A. C. Myers, H. Barthlow, and D. Weinreich. "Vagal innervation of guinea pig bronchial smooth muscle." Journal of Applied Physiology 69, no. 4 (October 1, 1990): 1336–46. http://dx.doi.org/10.1152/jappl.1990.69.4.1336.

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We isolated the guinea pig right bronchus with the vagus nerves intact and evaluated the changes in isometric tension of the smooth muscle in response to nerve stimulation. Brief (10-s) trains of electrical field stimulation or vagus nerve stimulation caused a biphasic contraction: the "first phase" sensitive to atropine and the "second phase" sensitive to capsaicin. The two phases could be dissociated by adjusting the stimulus intensity; greater stimulus intensities (pulse durations or voltage) were required to evoke the capsaicin-sensitive phase. When stimulated at 30-min intervals, the magnitude of both phases of the contractions declined over a 2-h period of repeated stimulation; however, this was prevented by indomethacin. Stimulation of the left vagus nerve resulted in a monophasic contraction of the right bronchus, with little evidence of a capsaicin-sensitive phase. Blocking neurotransmission through the bronchial ganglion, as monitored by intracellular recording techniques, abolished the first-phase contraction but had no effect on the capsaicin-sensitive phase. Selective blockade of muscarinic M1 receptors had no effect on vagus nerve-mediated contractions. The results demonstrate that the left and right vagus nerves carry preganglionic fibers to the right bronchial ganglion. The right but not the left vagus nerve also carries capsaicin-sensitive afferent fibers that, when stimulated, result in a persistent contraction of the right bronchus. Finally, we provide functional and electrophysiological evidence supporting the hypothesis that capsaicin-sensitive afferent neurons communicate with postganglionic motoneurons within the bronchus.
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Mitchell, R. A., D. A. Herbert, and D. G. Baker. "Inspiratory rhythm in airway smooth muscle tone." Journal of Applied Physiology 58, no. 3 (March 1, 1985): 911–20. http://dx.doi.org/10.1152/jappl.1985.58.3.911.

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In anesthetized paralyzed open-chested cats ventilated with low tidal volumes at high frequency, we recorded phrenic nerve activity, transpulmonary pressure (TPP), and either the tension in an upper tracheal segment or the impulse activity in a pulmonary branch of the vagus nerve. The TPP and upper tracheal segment tension fluctuated with respiration, with peak pressure and tension paralleling phrenic nerve activity. Increased end-tidal CO2 or stimulation of the carotid chemoreceptors with sodium cyanide increased both TPP and tracheal segment tension during the increased activity of the phrenic nerve. Lowering end-tidal CO2 or hyperinflating the lungs to achieve neural apnea (lack of phrenic activity) caused a decrease in TPP and tracheal segment tension and abolished the inspiratory fluctuations. During neural apnea produced by lowering end-tidal CO2, lung inflation caused no further decrease in tracheal segment tension and TPP. Likewise, stimulation of the cervical sympathetics, which caused a reduction in TPP and tracheal segment tension during normal breathing, caused no further reduction in these parameters when the stimulation occurred during neural apnea. During neural apnea the tracheal segment tension and TPP were the same as those following the transection of the vagi or the administration of atropine (0.5 mg/kg). Numerous fibers in the pulmonary branch of the vagus nerve fired in synchrony with the phrenic nerve. Only these fibers had activity which paralleled changes in TPP and tracheal tension. We propose that the major excitatory input to airway smooth muscle arises from cholinergic nerves that fire during inspiration, which have preganglionic cell bodies in the ventral respiratory group in the region of the nucleus ambiguus and are driven by the same pattern generators that drive the phrenic and inspiratory intercostal motoneurons.
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Huizinga, Jan D., David E. Reed, Irene Berezin, Xuan-Yu Wang, Diana T. Valdez, Louis W. C. Liu, and Nicholas E. Diamant. "Survival dependency of intramuscular ICC on vagal afferent nerves in the cat esophagus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 2 (February 2008): R302—R310. http://dx.doi.org/10.1152/ajpregu.00398.2007.

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Interstitial cells of Cajal (ICC) have been proposed as stretch receptors for vagal afferent nerves in the stomach based on immunohistochemical studies. The aim of the present study was to use electron microscopy and the anterograde degeneration technique to investigate ultrastructural features and survival dependency of ICC associated with vagal afferent innervation of the cat esophagus. This is the first report on the ultrastructural characteristics of ICC in the cat esophagus. Intramuscular ICC (ICC-IM) were identified throughout the musculature, whereas ICC in the myenteric plexus were rare. ICC-IM were particularly numerous in septa aligned with smooth muscle bundles. They were in synapse-like contact with nerve varicosities and in gap junction contact with smooth muscle cells. Smooth muscle cells also made contact with ICC through peg and socket junctions. Precision damage through small-volume injection of saline in the center of the nodose ganglion from the lateral side, known to selectively affect sensory nerves, was followed within 24 h by degeneration of a subset of nerve varicosities associated with ICC-IM, as well as degeneration of the associated ICC-IM. Smooth muscle cells were not affected. Nerves of Auerbachs plexus and associated ICC were not affected. In summary, ICC-IM aligning the esophageal muscle bundles form specialized synapse-like contacts with vagal afferent nerves as well as gap junction and peg-and-socket contacts with smooth muscle cells. This is consistent with a role of ICC-IM as stretch receptors associated with vagal afferent nerves; the ICC-vagal nerve interaction appears essential for the survival of the ICC.
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Conklin, J. L., and C. Du. "Guanylate cyclase inhibitors: effect on inhibitory junction potentials in esophageal smooth muscle." American Journal of Physiology-Gastrointestinal and Liver Physiology 263, no. 1 (July 1, 1992): G87—G90. http://dx.doi.org/10.1152/ajpgi.1992.263.1.g87.

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Electrical field stimulation (EFS) of nerves intrinsic to the opossum lower esophageal sphincter (LES) produces LES relaxation, an increase in its guanosine 3',5'-cyclic monophosphate (cGMP) content, and hyperpolarization of its circular muscle membrane potential difference. Activation of esophageal nerves produces an analogous hyperpolarization of the circular esophageal smooth muscle. These studies test the hypothesis that cGMP is an intracellular mediator of this hyperpolarization. The transmembrane potential difference of circular smooth muscle cells was recorded with glass microelectrodes. Nerve-mediated smooth muscle hyperpolarization was evoked by EFS (1 ms, 50 V pulses). Forskolin, an activator of adenylate cyclase, and sodium nitroprusside, an activator of guanylate cyclase, produced hyperpolarization. Cystamine and methylene blue, inhibitors of guanylate cyclase, blocked the hyperpolarization elicited by sodium nitroprusside, but not that by forskolin. Both also reversibly abolished the hyperpolarization evoked by EFS. Membrane-permeable derivatives of cGMP produced a concentration-dependent hyperpolarization. These data support the hypothesis that cGMP is an intracellular mediator of nerve-induced esophageal smooth muscle hyperpolarization.
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Stauss, Harald M., Erling A. Anderson, William G. Haynes, and Kevin C. Kregel. "Frequency response characteristics of sympathetically mediated vasomotor waves in humans." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 4 (April 1, 1998): H1277—H1283. http://dx.doi.org/10.1152/ajpheart.1998.274.4.h1277.

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In a recent study, we demonstrated that transmission from peripheral sympathetic nerves to vascular smooth muscles is strongest in the frequency band from 0.2 to 0.5 Hz in conscious rats. In contrast, sympathetic modulation of vasomotor tone in humans is suggested to be reflected in the power spectrum of arterial blood pressure in a frequency range centered around ∼0.1 Hz. Therefore, we addressed whether frequency response characteristics of sympathetic transmission from peripheral sympathetic nerves to vascular smooth muscles in humans differ from those in rats. In 12 male subjects, skin-sympathetic fibers of the left median nerve were electrically stimulated via microneurography needles with stimulation frequencies ranging from 0.01 to 0.5 Hz. Simultaneously, blood flow in the innervated skin area at the palm of the ipsilateral hand was recorded by a laser-Doppler device. The skin blood flow in the same area of the contralateral hand was recorded as a control. Median nerve stimulation produced transient decreases in skin blood flow in the ipsilateral hand. At frequencies ranging from 0.025 to 0.10 Hz, median nerve stimulation evoked high-power peaks at the same frequencies in the skin blood flow power spectra of the ipsilateral but not of the contralateral hand. The greatest responses were found in the frequency range from 0.075 to 0.10 Hz. Therefore, these data indicate that the transmission from peripheral sympathetic nerves to cutaneous vascular smooth muscles in humans is slower than in rats. In addition, the frequency range believed to be most important in sympathetic modulation of vasomotor activity in humans corresponds to the frequency band of the greatest response of cutaneous vascular smooth muscle contraction to sympathetic nerve stimulation.
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Du, C., J. Murray, J. N. Bates, and J. L. Conklin. "Nitric oxide: mediator of NANC hyperpolarization of opossum esophageal smooth muscle." American Journal of Physiology-Gastrointestinal and Liver Physiology 261, no. 6 (December 1, 1991): G1012—G1016. http://dx.doi.org/10.1152/ajpgi.1991.261.6.g1012.

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Activation of intrinsic nonadrenergic noncholinergic (NANC) esophageal nerves during peristalsis or by electrical field stimulation (EFS) in vitro produces a hyperpolarization followed by a depolarization of the circular smooth muscle of the opossum esophagus. N omega-nitro-L-arginine (L-NNA), an inhibitor of nitric oxide synthase, and nitric oxide (NO) were used to test the hypothesis that NO or a NO-containing compound is a mediator of this NANC nerve-induced hyperpolarization of circular esophageal smooth muscle. The transmembrane potential difference of esophageal circular smooth muscle cells was recorded with glass microelectrodes. Nerve-mediated membrane responses were evoked by single electrical pulses of 0.5 ms duration and 50 V amplitude. L-NNA abolished the initial hyperpolarization and reduced the amplitude of and the time to maximal depolarization. L-Arginine (1 mM), the substrate for NO synthase, antagonized the effect of L-NNA. Exogenous NO produced hyperpolarization of the smooth muscle membrane potential and attenuated the amplitudes of EFS-induced hyperpolarization and depolarization. The effect of NO was blocked neither by L-NNA nor by tetrodotoxin (1 microM). The data support the hypothesis that NO or a NO-containing compound mediates NANC nerve-induced responses of the esophageal smooth muscle membrane.
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Wu, Zhong-Xin, Brian E. Satterfield, and Richard D. Dey. "Substance P released from intrinsic airway neurons contributes to ozone-enhanced airway hyperresponsiveness in ferret trachea." Journal of Applied Physiology 95, no. 2 (August 2003): 742–50. http://dx.doi.org/10.1152/japplphysiol.00109.2003.

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Exposure to ozone (O3) induces airway hyperresponsiveness mediated partly through the release of substance P (SP) from nerve terminals in the airway wall. Although substantial evidence suggests that SP is released by sensory nerves, SP is also present in neurons of airway ganglia. The purpose of this study was to investigate the role of intrinsic airway neurons in O3-enhanced airway responsiveness in ferret trachea. To remove the effects of sensory innervation, segments of ferret trachea were maintained in culture conditions for 24 h before in vitro exposure to 2 parts/million of O3 or air for 1 h. Sensory nerve depletion was confirmed by showing that capsaicin did not affect tracheal smooth muscle responsiveness to cholinergic agonist or contractility responses to electrical field stimulation (EFS). Contractions of isolated tracheal smooth muscle to EFS were significantly increased after in vitro O3 exposure, but the constrictor response to cholinergic agonist was not altered. Pretreatment with CP-99994, an antagonist of the neurokinin 1 receptor, attenuated the increased contraction to EFS after O3 exposure but had no effect in the air exposure group. The number of SP-positive neurons in longitudinal trunk ganglia, the extent of SP innervation to superficial muscular plexus nerve cell bodies, and SP nerve fiber density in tracheal smooth muscle all increased significantly after O3 exposure. The results show that release of SP from intrinsic airway neurons contributes to O3-enhanced tracheal smooth muscle responsiveness by facilitating acetylcholine release from cholinergic nerve terminals.
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Gonda, T., E. E. Daniel, T. J. McDonald, J. E. Fox, B. D. Brooks, and M. Oki. "Distribution and function of enteric GAL-IR nerves in dogs: comparison with VIP." American Journal of Physiology-Gastrointestinal and Liver Physiology 256, no. 5 (May 1, 1989): G884—G896. http://dx.doi.org/10.1152/ajpgi.1989.256.5.g884.

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The distribution of nerves containing galanin-immunoreactive (GAL-IR) material was compared to the distribution of neurons containing vasoactive intestinal polypeptide (VIP) immunoreactivity in the canine gastrointestinal tract. The actions of intra-arterially administered galanin and VIP on motility in the gastric antrum and corpus and the intestines were also studied. All sphincter muscles contained galanin- and VIP-immunoreactive nerve profiles. VIP-immunoreactive nerve profiles were present in all layers of the stomach, small intestine, and colon. GAL-IR nerve somata were common in the submucous plexus of ileum and colon and in the myenteric plexus of the terminal antrum, as were nerve processes in various layers. In the small intestine, galanin inhibited contractile responses to field stimulation of intrinsic nerves and also reduced the contractions after nerve blockade with tetrodotoxin (TTX). VIP often enhanced field-stimulated contractions at low doses but inhibited these and the contractions after TTX at higher doses. In the stomach and colon, both peptides inhibited responses to field stimulation; whether these effects were due to actions on smooth muscle was not tested. The distribution and actions of galanin in gut are consistent with the hypothesis that it acts at smooth muscle sites and possibly at prejunctional sites.
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Dissertations / Theses on the topic "Smooth nerve"

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Savage, Madelyn Clare. "Neurotransmitter interactions in molluscan visceral smooth muscle." Thesis, Lancaster University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246102.

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Hallén, Katarina. "Nerve-induced release of nitric oxide in gastrointestinal and erectile tissue /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-081-8/.

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Lim, S. P. "Electrical basis for inhibition and excitation in non-propulsive autonomically innervated smooth muscle." Thesis, University of Glasgow, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377171.

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Makwana, R. "Pharmacological analysis of cannabinoid receptor activity in isolated nerve-smooth muscle and epithelial preparations." Thesis, University of Hertfordshire, 2007. http://hdl.handle.net/2299/1182.

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This study was directed at characterising the cannabinoid receptor activity modulating the electrical field stimulation (EFS) evoked contractions of the rat isolated ileum myenteric plexus longitudinal muscle (MPLM) preparation, and the capsaicin, nicotine and veratridine evoked secretory responses of the rat isolated colonic submucosal plexus-mucosal (SPM) preparation. EFS of the MPLM preparation with single pulses at a repetition frequency of 0.05 Hz elicited a transient twitch contraction immediately in response to each electrical pulse. In contrast, stimulation of the MPLM preparation with 2 second trains of pulses every minute at a frequency of 30 Hz elicited a rapid transient rebound contraction on termination of each train of EFS. The non-selective cannabinoid receptor agonists AEA, CP 55,940, D9-THC and WIN 55,212-2 inhibited both EFS-evoked twitch and rebound contractions of the rat ileum MPLM elicited by 0.05 Hz and 30 Hz EFS respectively. The inhibition of the twitch contractions was competitively antagonised by the cannabinoid CB1 receptor antagonist / inverse agonist SR 141716 with pKB values of 8.60. In contrast, SR 141716 only antagonised the ability of AEA, D9-THC and WIN 55,212-2 but not CP 55,940 to inhibit the rebound contractions with pA2 values of 6.60. These observations extended to the inhibitory effect of WIN 55,212-2 on the twitch and rebound contractions of the guinea-pig ileum MPLM. The CB2 antagonist / inverse agonist SR 144528 did not alter the effects of the agonists. Additionally, the inhibitory effect of AEA was refractory to the vanilloid TRPV1 receptor antagonist capsazepine. WIN 55,212-3 a stereoisomer of WIN 55,212-2 was without effect on the rat MPLM. SR 141716 alone concentration-dependently increased the twitch contractions but inhibited the rebound contractions. Both types of the EFS-evoked contractions were abolished by the Na+ channel blocker tetrodotoxin or the muscarinic acetylcholine (ACh) receptor antagonist atropine but not the nicotinic ACh receptor antagonist hexamethonium. None of the cannabinoids altered the contractions to exogenously applied ACh. These data suggested that the cannabinoid agonists inhibited the twitch contractions through a stereospecific presynaptic CB1 receptor-mediated reduction in the release of ACh. Additionally, the inhibition of the rebound contractions occurred because of an inhibition of ACh release by a novel stereospecific presynaptic non-CB1 -non CB2 -non -TRPV1 site. The ability of SR 141716 to inhibit the rebound contractions and antagonise AEA, D9-THC and WIN 55,212-2 may be though partial agonism at the non-CB1-non CB2-non-TRPV1 site. The ability of SR 141716 to potentiate the twitch contractions by increasing the release of ACh suggested that the CB1 receptor was constitutively active or was subjected to a tonic activation by endocannabinoid agonists. A comparison between the maximal enhancement of the twitch contractions of the rat and the guinea-pig ileum MPLM caused by three CB1 receptor antagonists/inverse agonists AM 251, SR 141716 and O-2050 showed that each cannabinoid had a different maximum. This suggested inverse agonism. These data were supported with studies showing the lack of effect of three fatty acid amide hydrolase (FAAH) inhibitors AA-5HT, PMSF, URB–597 and VDM-11, an inhibitor of the AEA uptake transporter on EFS-evoked contractions. These studies showed that all three FAAH inhibitors increased the potency of exogenously applied AEA but not WIN 55,212-2, and that VDM-11 had no effect on the potency of exogenously applied AEA. This data suggested that a functional endocannabinoid tone and the uptake transporter were not present in the MPLM, but FAAH was present. These data provide supporting evidence that SR 141716 behaved as an inverse agonist in the MPLM to augment twitch contractions. The interaction between CP 55,940 or WIN 55,212-2 with SR 141716 was investigated using the rat colonic SPM sheet. Both CP 55,940 and WIN 55,212-2 attenuated the secretory responses to capsaicin and nicotine in a SR 141716 sensitive manner. SR 140333, a neurokinin 1 receptor antagonist, abolished the capsaicin and nicotine. This suggested that CP 55,940 and WIN 55,212-2 inhibited the capsaicin and nicotine response through a CB1 receptor-mediated inhibition of the release of substance P or neurokinin A. The sensitivity of the veratridine response to TTX and a-chymotrypsin and the failure of the cannabinoids to attenuate the response suggested the absence of the CB1 receptor on the neurones releasing the undetermined neuropeptide. Together, these data suggest that both the CB1 receptor and non-CB1-non-CB2 -non-TRPV1 receptor can mediate the inhibitory effects of cannabinoid agonists in the rat ileum MPLM depending on the frequency of EFS. These data also show that SR 141716 is an inverse agonist in the MPLM. In the SPM preparation, the CB1 receptor appears to be involved in the modulation of some forms of peptidergic transmission.
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Mustafa, Seham M. D. "An analysis of the effects of cooling and nerve stimulation on ovine airway smooth muscle." Thesis, University of Bath, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321848.

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Hasan, Tahseen. "Transcutaneous electrical nerve stimulation (TENS) and temporary S3 nerve root stimulation in idiopathic detrusor instability and characterization of the human detrusor smooth muscle contraction." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310132.

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Kemi, Cecilia. "Studies on neuroimmune interactions in allergic inflammation with focus on neurotrophins /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-885-1/.

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Tollet, Cecilia Jenny. "The origin and early development of the intrinsic innervation in the foetal mouse lung." University of Western Australia. School of Biomedical and Chemical Sciences, 2003. http://theses.library.uwa.edu.au/adt-WU2004.0060.

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In this study, the origin and development of the intrinsic innervation in the foetal mouse lung is described and experimental evidence is provided to support the involvement of glial cell line-derived neurotrophic factor (GDNF) in the guidance of nerves and neuronal precursors in the developing lung. Antibodies were used to stain for neuronal precursors, neurones, nerve fibres, primordial epithelium and smooth muscle. These structures were revealed in whole mounts of foetal mouse lungs by immunofluorescence and confocal microscopy, and their spatial and temporal distribution was mapped from the onset of lung development and through the pseudoglandular period. The results showed that neuronal precursors, positive for neural crest cell markers, were present in the vagal tract of the foregut at embryonic day 10 (E10), the time of the evagination of the lung buds. These neural crest-derived cells (NCC) migrated into the lung at E11, along nerve processes directed from the vagus to the smooth musclecovered trachea and emerging lobar bronchi. During E11-E14, a network of nerves and ganglia became established along the dorsal trachea, and large ganglia formed a plexus at the ventral hilum. Nerve trunks issued from these ganglia, travelled along the smooth muscle-covered bronchi, providing a pathway for migrating NCC. To investigate the role of GDNF in the innervation of the lung, an in vitro model of left lung lobes was established. Lung growth and tubule branching was comparable to that in vivo, and neural tissue and smooth muscle continued to grow and thrive. A significant increase in nerve growth occurred when explants were cultured with GDNF compared to controls. Nerves extended, and NCC migrated towards GDNF-impregnated beads suggesting that GDNF may be the molecule guiding nerve fibres and NCC in the lung. The migrating NCC were negative for GDNF-family receptor α1 (GFRα1) during their migration into the lung while the nerves were positive. Since GDNF needs to be associated with its binding receptor, GFRα1, for cellular signalling, GDNF may induce the migration of the NCC if they migrate along the GFRα1-positive nerve fibres. It is concluded that neural tissue and smooth muscle become integral components of the lung shortly after the onset of lung development. The results show that the migration of neural crest-derived cells into the lung and the establishment of the innervation requires coordinated cross-talk between NCC, nerves and smooth muscle throughout development.
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Stefani, Davide. "Representations up to homotopy and perfect complexes over differentiable stacks." Electronic Thesis or Diss., Sorbonne université, 2019. http://www.theses.fr/2019SORUS687.

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Cette thèse concerne l’étude de la géométrie des champs dans le contexte de la géométrie différentiable, utilisant les outils de la théorie de l’homotopie et des catégories supérieures. Ces techniques deviennent nécessaires pour traiter des généralisation aux champs d’objets géométriques fondamentales, tels que les fibrés tangent et cotangent, les formes sur un champs, leurs automorphismes et plus en général les complexes parfaits, qui sont un des objets principaux dans ce travail. Dans la première partie de cette thèse nous faisons une récapitulation des champs différentiables supérieurs, leur homotopie et cohomologie. Dans la deuxième partie nous étudions les représentations à homotopie près des groupoïdes de Lie et nous les relions avec une théorie des complexes parfaits sur les champs différentiables. Parmi nos résultat, nous montrons que une représentation à homotopie près d’un groupoïde de Lie est exactement un module cohésive sur la dg-algèbre des fonctions lisses et que les dg-catégories correspondants sont Morita invariantes. Ça nous permets de donner une définition de dg-catégorie des complexes parfaits sur un champ différentiable. De plus nous construisons un 2-groupoide de Lie des automorphismes des complexes des fibrés vectoriels de longueur 2, qui est un analogue supérieur du champs classifiant BGL_n. Nous concluons avec une définition du 2-champs différentiable des complexes parfaits de amplitude [0,1] par le biais d’une présentation par un 2-groupoide de Lie
This thesis is concerned with the geometry of stacks in the differential geometry context using homotopical and higher categorical techniques. These techniques becomes necessary to deal with simple stack generalizations of crucial objects such as tangent and cotangent bundles, forms on a stack, their automorphisms and more generally perfect complexes, which are one of the main object of study of this work. In the first part of this thesis we give an overview of higher and differentiable stacks, their homotopy theory and cohomology theories. In the second part we study one representation up to homotopy of Lie groupoids and rely them with a theory of perfect complex over differentiable stacks. Among our results, we show that a representation up to homotopy on a Lie groupoid is the same as a cohesive module on its dg-algebra of smooth functions and that the correspondent dg-categories are Morita invariant. This allows us to give a definition of dg-category of perfect complexes on a differentiable stack. We moreover construct a Lie 2-groupoid of automorphisms of 2-terms complexes of vector bundles, which is a higher analogue of the classifying stack BGL_n. We conclude by giving a definition of the differentiable 2-stack of perfect complexes of amplitude [0,1] by means of a Lie 2-groupoid presenting it
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鳥橋, 茂子, and Shigeko Torihashi. "腸管平滑筋運動におけるカハールの介在細胞と壁内神経 (特集. Neurogastroenterologyの幕開け）." 日本メディカルセンター, 2003. http://hdl.handle.net/2237/7893.

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Books on the topic "Smooth nerve"

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M, Vanhoutte Paul, Shepherd John T. 1919-, International Union of Physiological Sciences. Congress, and International Symposium on Mechanisms of Vasodilatation (4th : 1986 : Rochester, Minn.), eds. Vasodilatation: Vascular smooth muscle, peptides, autonomic nerves, and endothelium. New York: Raven Press, 1988.

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2

Manlapaz, Mariel, and Perin Kothari. Neuromuscular Disorders and Anesthesia. Edited by David E. Traul and Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0029.

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The various neuromuscular diseases present with different airway, cardiovascular, pulmonary, and anesthetic considerations. It is useful to categorize these different diseases into nerve, neuromuscular junction, and primary muscle diseases. Understanding their pathophysiology is paramount in choosing the right anesthetic drugs (for example, depolarizing versus nondepolarizing and regional versus general anesthesia). Knowing their manifestations such as autonomic dysfunction, skeletal/cardiac/smooth/bulbar muscle involvement, or tendency for tonic contraction, allows for expectant perioperative management. Finally appreciating their association with certain disease states such as malignant hyperthermia or endocrine dysfunction can prevent complications. A brief review of myotonic dystrophy is presented here, followed by a brief summary of anesthetic considerations for various neuromuscular diseases.
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Vanhoutte, Paul M. Vasodilatation: Vascular Smooth Muscle, Peptides, Autonomic Nerves, and Endothelium. Raven Pr, 1988.

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Snape, Jr, and Stephen M. Collins. Effects of Immune Cells and Inflammation on Smooth Muscle and Enteric Nerves. Taylor & Francis Group, 2020.

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Effects of immune cells and inflammation on smooth muscle and enteric nerves. Boca Raton, Fla: CRC Press, 1991.

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Snape, Jr, and Stephen M. Collins. Effects of Immune Cells and Inflammation on Smooth Muscle and Enteric Nerves. Taylor & Francis Group, 2020.

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Snape, Jr, and Stephen M. Collins. Effects of Immune Cells and Inflammation on Smooth Muscle and Enteric Nerves. Taylor & Francis Group, 2020.

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Snape, Jr, and Stephen M. Collins. Effects of Immune Cells and Inflammation on Smooth Muscle and Enteric Nerves. Taylor & Francis Group, 2020.

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9

The use of TENS for non-painful conditions. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199673278.003.0010.

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Peripheral nerves consist of afferent and efferent neurones with different functions. TENS can be used to excite somatic efferents to influence the activity of skeletal muscle, and autonomic efferents to influence the activity of smooth muscle, cardiac muscle, and glands. There are physiological rationale to support the use of TENS to manage various non-painful conditions. Clinical experience suggests TENS is often beneficial. The purpose of this chapter is to describe the mechanism of action, clinical use and clinical efficacy for TENS when used to manage non-painful conditions. The chapter covers the effects of TENS on the autonomic nervous system, circulatory system, tissue regeneration, and psychomotor conditions. It also considers the use of TENS for incontinence, constipation, ileus and gastrointestinal discomfort, post-surgical symptoms, and antiemesis.
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Book chapters on the topic "Smooth nerve"

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Smoller, Bruce R., and Kim M. Hiatt. "Tumors of Fat, Nerve, and Smooth Muscle." In Dermal Tumors: The Basics, 103–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-19085-8_5.

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Rotterdam, Heidrun, and Horatio T. Enterline. "Gastric Smooth Muscle, Nerve Sheath, and Related Tumors." In Pathology of the Stomach and Duodenum, 257–85. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3550-7_11.

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Aickin, C. Claire. "Chloride Transport across the Sarcolemma of Vertebrate Smooth and Skeletal Muscle." In Chloride Channels and Carriers in Nerve, Muscle, and Glial Cells, 209–49. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4757-9685-8_7.

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Watson, Nikki. "Autoregulation of Cholinergic Neurotransmission in Airways Nerves." In Airways Smooth Muscle, 261–78. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-7558-5_10.

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Barnes, Peter J. "Modulation of Neurotransmitter Release from Airways Nerves." In Airways Smooth Muscle, 209–59. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-7558-5_9.

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Satchell, David. "Use of Purine Nucleotide and Nucleoside Metabolising Enzymes as Tools to Determine the Presence of Purinergic Nerve Transmission in Smooth Muscle." In Advances in Experimental Medicine and Biology, 435–40. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5676-9_64.

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Collins, S. M. "Gastritis and Altered Motility; the Ability of a Mucosal Inflammatory Reaction to Alter Enteric Nerve and Smooth Muscle in the Gut." In Helicobacter pylori, Gastritis and Peptic Ulcer, 370–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75315-2_54.

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Springall, David R., and Julia M. Polak. "Immunocytochemistry and Molecular Biology in the Identification of Peptide-Containing Nerves." In Airways Smooth Muscle, 189–208. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-7558-5_8.

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Krstić, Radivoj V. "Endings of Autonomic Nerves in the Smooth Musculature." In General Histology of the Mammal, 368–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70420-8_180.

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Ogawa, Rei. "Ideal Wound Closure Methods for Minimizing Scarring After Surgery." In Textbook on Scar Management, 185–91. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_21.

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AbstractWound-healing phenomena are the result of a cascade of complex biochemical events that can be categorized into four general overlapping phases: coagulation, inflammation, proliferation, and remodeling. Significantly, all four phases of wound healing are influenced by both intrinsic and extrinsic mechanical forces. These mechanical forces provoke chronic inflammation of the dermis, namely, the unceasing influx and activation of inflammatory cells, the persistent generation of blood vessels and nerve fibers, and the constant production of collagen by the activated fibroblasts. This chronic inflammation blocks the conversion of the granulation tissue into dermis-like tissue by the remodeling process and results in an immature hypertrophic scar that is red, elevated, hard, and painful. These observations suggest that, to prevent pathological scarring after surgery, it is necessary to ensure that the sutures cause the wound edges to adhere to each other without any tension, even when strong extrinsic forces are placed on the wound. This will allow the granulation tissue to convert smoothly into dermis-like tissue, thereby yielding minimal scarring. Another way to prevent pathological scar formation in high-tension areas is to use zigzag suturing techniques such as the Z-plasty.
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Conference papers on the topic "Smooth nerve"

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Bult, H., H. Fret, A. G. Herman, F. Jordaens, F. A. M. Peeters, and T. J. Verbeuren. "ENDOTHELIUM CURTAILS THE TRANSFER OF PLATELET SEROTONIN INTO THE BLOOD VESSEL WALL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643795.

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Blood platelets are the principal source of serotonin (5-hydroxytryptamine, 5HT) in the circulation. As it is assumed that 5HT release by activated platelets can influence vascular tone, we investigated whether platelet derived 5HT can penetrate from the lumen into the vessel wall. Venous blood was collected from pentobarbitone anaesthetized dogs on 5.8 mM EDTA, platelet rich plasma was prepared and incubated with 3H-5HT and 14c-adenine. After washing, a platelet suspension (PS, 108/ml) was made in Ca2+ free Krebs'. A segment of each saphenous vein was removed and de-endothelialized for about half (2-3 cm) of its length. The PS was perfused (37°C, 3 ml/min) for 15 min (4 dogs) or 30 min (4 dogs) through the lumen in the absence (one V. saphena) or presence (contralateral vein) of 0.1 unit thrombin/ml. Thereafter, 1 cm of the area with and the area without endothelium was excised, and these segments were washed 24 times with 5 ml Krebs. The 3H and 14c content of wash fluid and solubilized tissue was measured. The 12th wash contained 1.0 unit thrombin in order to verify that the 3H was not derived from adhering platelets. The 14c data indicated that - at low shear stress -similar platelet numbers adhere to the intima with or without endothelium, but in the absence of endothelium thrombin-induced aggregates remain loosely attached to the intima. The wash procedure removed the majority of these adhering platelets, as well as their 3H. In all tissues 3H accumulated, eg 708 dpm after 15 min and 1673 dpm after 30 min perfusion followed by washout. Both values were 7 to 10 fold enhanced when the platelet release reaction was induced with thrombin. In addition, endothelial denudation doubled the 3h accumulation under both circumstances. Previous experiments with soluble 5HT indicated that 70 % of the 3h is present in the adrenergic nerve terminals of the vessel. Application of the PS to the outside of the vessel led to a larger 3h accumulation, but then there was no indication of a difference between area's with or without endothelium.In conclusion, removal of the endothelial metabolic barrier enhanced vascular accumulation of 5HT, but the occurrence of a release reaction appeared to be more important in determining the access of platelet derived 5HT to vascular smooth muscle cells and adrenergic nerve endings.
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Marsh, B., A. Fryer, D. B. Jacoby, and M. G. Drake. "TRPA1 Agonists Have Opposing Effects on Airway Nerves Versus Airway Smooth Muscle." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2845.

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