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Journal articles on the topic 'Laryngeal chemoreflex'

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Published: 10 December 2022

Last updated: 28 January 2023

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1

Goding, George S., and Kerri Johnson Pernell. "Effect of a Second Laryngeal Stimulation during Recovery from the Laryngeal Chemoreflex." Otolaryngology–Head and Neck Surgery 114, no. 1 (January 1996): 84–90. http://dx.doi.org/10.1016/s0194-59989670288-7.

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The laryngeal chemoreflex is a potential mechanism for sudden infant death. In experimental protocols in which a full recovery is allowed between stimuli, no laryngeal chemoreflex responses result in a fatal outcome. In the clinical situation there are no controls to prevent repeated laryngeal stimulation before a full recovery. The effect of a laryngeal stimulus applied during or soon after a laryngeal chemoreflex-induced apnea was investigated. Eighteen piglets were divided into groups aged 10 to 12 days, 17 to 21 days, and 32 to 36 days. Laryngeal stimulation was performed under normoxic conditions with water applied to the mucosa. Baseline respiratory and cardiovascular response data were measured. After recovery an initial stimulation was applied, followed by a second stimulation during the apnea or 5, 30, 60, or 120 seconds after restoration of breathing. No profound apneas occurred with baseline laryngeal stimulation. In piglets aged 32 to 36 and 17 to 21 days, a second laryngeal stimulus resulted in a shortened apnea duration. The response varied in piglets aged 10 to 12 days with profound apneas observed In 2 of 6 subjects and 4 of 30 trials. Piglets aged 17 to 36 days are less susceptible to the laryngeal chemoreflex during the immediate recovery period. In piglets aged 10 to 12 days, the laryngeal chemoreflex response may be more severe after a second Stimulus.

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2

Chan, Kenneth, Linda K. Kullama, Linda Day, Anthony Ogundipe, and Michael G. Ross. "Ovine Fetal Laryngeal Chemoreflex Thresholds and Respiratory Effects." Otolaryngology–Head and Neck Surgery 116, no. 1 (January 1997): 91–96. http://dx.doi.org/10.1016/s0194-59989770356-5.

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In newborn infants, laryngeal contact with solutions of low chloride concentration or pH evokes swallowing, laryngeal adduction, and respiratory inhibition (laryngeal chemoreflex). To determine whether the laryngeal chemoreflex is present during fetal life and its effect on fetal respiratory activity, eight time-bred ewes (128 ± 2 days) were prepared with fetal electrocortical diaphragm and esophageal electrodes and a nasopharyngeal catheter. After a 60-minute control period, increasing volumes (0.1 to 1.0 ml/kg) of 0.15 mol/L NaCl or distilled water (0.05 to 1.0 ml/kg) and decreasing concentrations of NaCl (0.15 to 0.02 mol/L) at a fixed volume (0.3 ml/kg) were sequentially administered through the nasopharyngeal catheter (38° C). The minimum water volume that stimulated swallowing was significantly less than the minimum 0.15 mol/L NaCl volume (0.10 ± 0.02 vs. 0.70 ± 0.05 ml/kg). The maximum NaCl concentration that stimulated swallowing was 0.04 ± 0.01 mol/L. During the control period, respiratory activity averaged 14.6 ± 0.7 breaths/minute and did not change during absent swallow responses or isotonic saline-induced swallows. However, respiratory activity significantly decreased during water (4.7 ± 0.6 breaths/minute) and hypotonic saline-induced swallow responses (3.7 ± 0.7 breaths/minute). Fetal electrocortical activity did not change during absent or stimulated swallows. We conclude that laryngeal water or hypotonic saline solution may stimulate fetal swallowing and suppress fetal respiratory activity, similar to the newborn laryngeal chemoreflex. We speculate that an exaggeration of the laryngeal chemoreflex apnea response in the newborn may predispose to sudden infant death syndrome.

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3

Goding, George S. "Correlation of Laryngeal Chemoreflex Severity With Laryngeal Muscle Response." Laryngoscope 108, no. 6 (June 1998): 863–72. http://dx.doi.org/10.1097/00005537-199806000-00015.

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4

Park, Han-Q., Won-Pyo Hong, Kwang-Moon Kim, Myung-Sang Kim, Young-Ho Kim, and Dong-Young Kim. "Age Dependence of Laryngeal Chemoreflex in Puppies." Annals of Otology, Rhinology & Laryngology 110, no. 10 (October 2001): 956–63. http://dx.doi.org/10.1177/000348940111001012.

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Previously collected data have indicated that the laryngeal chemoreflex (lcr) response is exaggerated during a critical period of postnatal development in several experimental animals. These animals had fewer anatomic and physiological similarities to humans than do puppies. This investigation of the lcr in 14 anesthetized puppies was undertaken to determine age-related differences in the response to stimulation of the supraglottic laryngeal mucosa by saline solution, distilled water, cow's milk, and acid at pH 1.0. The dogs were divided into 3 age groups: group 1 consisted of 4 dogs that were 2 weeks old, and in groups 2 and 3 there were 5 puppies each, of 4 and 6 weeks of age, respectively. The lcr response (laryngospasm, apnea, respiratory depression, and bradycardia) was found in the puppies only after stimulation of the laryngeal mucosa with acid at pH 1.0, and it was more easily achieved in the 4- and 6-week age groups than in the 2-week group. These findings suggest that the lcr is an age-dependent response that appears in dogs only after 2 weeks of age. The important implication of this finding is that postnatal neural maturation may influence the laryngeal reflex in humans to some extent.

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5

Woodson, Gayle E., and George Brauel. "Arterial chemoreceptor influences on the laryngeal chemoreflex." Otolaryngology–Head and Neck Surgery 107, no. 6_part_1 (December 1992): 775–82. http://dx.doi.org/10.1177/019459988910700612.1.

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Prolonged apnea and cardiovascular changes have been elicited in infant animals by the application of water to the laryngeal mucosa. Previous reports have produced conflicting evidence in regard to the possible role of arterial chemoreceptors in modulating this reflex. The present study was designed to determine the effect of carotid body stimulation or suppression on the duration of apnea and severity of cardiovascular changes in response to water in the larynx of piglets. The role of swallowing in terminating the apnea was also Investigated. Hypoxia and isoproterenol, both carotid body stimuli, caused decreased apnea duration. Hyperoxia was associated with prolonged apnea duration; however, dopamine, which inhibits carotid body chemoreceptors, produced no significant change. Hypotension and bradycardia were only observed after prolonged apnea or chemoreceptor stimulation, supporting the concept that the cardiovascular component of the laryngeal chemoreflex is a result of changes in blood gas concentration rather than a direct response to laryngeal chemostimulatlon. The Interval between water application and Initiation of swallowing was not significantly affected by hypoxia or carotid body stimulation and swallowing did not always occur before resumption of breathing.

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6

Wang, Deqiang, Timothy M. McCulloch, Nancy M. Bauman, Debra M. Jaffe, Richard J. H. Smith, Michael P. Porter, and Anthony D. Sandler. "Role of Substance P in the Laryngeal Chemoreflex." Annals of Otology, Rhinology & Laryngology 107, no. 7 (July 1998): 575–80. http://dx.doi.org/10.1177/000348949810700706.

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The laryngeal chemoreflex (LCR) is a potentially life-threatening reflex that is elicited in immature animals by the topical application of water to the laryngeal mucosa. The reflex response is characterized by immediate apnea and laryngeal adduction and delayed cardiovascular instability. The cardiorespiratory changes of the LCR may be life-threatening, particularly in very immature animals such as piglets under 2 weeks of age. The afferent and efferent limbs of the LCR are mediated through the vagus nerve, but the neuromediators responsible for the reflex changes have not yet been clearly elucidated. Previous agonist and antagonist studies in immature dogs demonstrated that substance P, a sensory tachykinin, mediates the life-threatening esophagolaryngeal adductor reflex elicited by distal esophageal sensory nerve stimulation. This study was conducted to determine if substance P also plays a role in mediating the LCR. The LCR response was compared before and after treatment with intravenous substance P antagonist (Pfizer CP-96,345–1) in eight piglets (mean 27.7 days of age). The laryngeal and cardiovascular responses of the animals following intravenous administration of the tachykinins substance P, neurokinin a, and neurokinin B were also assessed. Pretreatment with substance P antagonist did not alter the LCR's duration of apnea (p > .10), laryngeal adductor response, or early change in mean arterial pressure (p > .10), although the early maximal heart rate response was significantly altered (p < .01). Intravenous substance P, neurokinin a, and neurokinin B did not reproduce the laryngeal respiratory response of the LCR. We conclude that substance P, neurokinin a, and neurokinin B are not key neurotransmitters of the LCR.

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7

Pathak, Shivani, Laurie Slovarp, Matthew S. Clary, and Marie E. Jetté. "Laryngeal Chemoreflex in Health and Disease: A Review." Chemical Senses 45, no. 9 (October 14, 2020): 823–31. http://dx.doi.org/10.1093/chemse/bjaa069.

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Abstract The larynx plays a key role in airway protection via the laryngeal chemoreflex (LCR). This involuntary reflex can be evoked when hazardous substances activate mucosal receptors, which send signals to be processed within the brainstem. Although the LCR is meant to be protective, the reflex can become hyperstimulated, even to benign stimuli, which can result in pathological disorders, such as chronic cough and inducible laryngeal obstruction. In this review, we will outline the mechanism of the LCR and its associated pathological disorders.

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8

Wei, Wan, Xiuping Gao, Lei Zhao, Jianguo Zhuang, Yang Jiao, and Fadi Xu. "Liquiritin apioside attenuates laryngeal chemoreflex but not mechanoreflex in rat pups." American Journal of Physiology-Lung Cellular and Molecular Physiology 318, no. 1 (January 1, 2020): L89—L97. http://dx.doi.org/10.1152/ajplung.00306.2019.

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Liquiritin apioside (LA), a main flavonoid component of licorice, reportedly suppresses cough responses to inhalation of aerosolized capsaicin [CAP; a stimulant to transient receptor potential vanilloid 1 (TRPV1)] in conscious guinea pigs via acting on peripheral nerves. However, the evidence of LA having a direct effect on airway sensory fibers is lacking. Considering the important role laryngeal chemoreceptors and mechanoreceptors play in triggering apnea and cough, we studied whether LA suppressed the apneic responses to stimulation of these receptors via directly acting on the superior laryngeal nerve (SLN). Intralaryngeal delivery of chemical [CAP, HCl, and distilled water (DW)] and mechanical [an air-pulse (AP)] stimulations was applied in anesthetized rat pups to evoke the apnea. These stimuli were repeated after intralaryngeal LA treatment or peri-SLN LA treatment to determine the direct effect of LA on the SLN. Our results showed that all stimuli triggered an immediate apnea. Intralaryngeal LA treatment significantly attenuated the apneic response to chemical but not mechanical stimulations. The same attenuation was observed after peri-SLN LA treatment. Owing that TRPV1 receptors of laryngeal C fibers are responsible for the CAP-triggered apneas, the LA impact on the activity of laryngeal C neurons retrogradely traced by DiI was subsequently studied using a patch-clamp approach. LA pretreatment significantly altered the electrophysiological kinetics of CAP-induced currents in laryngeal C neurons by reducing their amplitudes, increasing the rise times, and prolonging the decay times. In conclusion, our results, for the first time, reveal that LA suppresses the laryngeal chemoreceptor-mediated apnea by directly acting on the SLN (TRPV1 receptors of laryngeal C fibers).

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9

Downs, Daniel H., Kerri Johnson, and George S. Goding. "The effect of antitastamines on the laryngeal chemoreflex." Laryngoscope 105, no. 8 (August 1995): 857–61. http://dx.doi.org/10.1288/00005537-199508000-00017.

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10

Boyer, H. C., D. H. Downs, G. S. Goding, and K. J. Pernell. "Effect of Topical Diphenhydramine on the Laryngeal Chemoreflex." Archives of Otolaryngology - Head and Neck Surgery 122, no. 10 (October 1, 1996): 1112–16. http://dx.doi.org/10.1001/archotol.1996.01890220078013.

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11

GODINGJR, G., and K. PERNELL. "Effect of a second laryngeal stimulation during recovery from the laryngeal chemoreflex." Otolaryngology - Head and Neck Surgery 114, no. 1 (January 1996): 84–90. http://dx.doi.org/10.1016/s0194-5998(96)70288-7.

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12

Davies, A. M., J. S. Koenig, and B. T. Thach. "Upper airway chemoreflex responses to saline and water in preterm infants." Journal of Applied Physiology 64, no. 4 (April 1, 1988): 1412–20. http://dx.doi.org/10.1152/jappl.1988.64.4.1412.

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Laryngeal chemoreflex (LCR) responses elicited by fluid irrigation of the larynx have been described repeatedly in animals, whereas evidence for a similar reflex in human infants is extremely limited. Using nasopharyngeal catheters to instill small volumes of warm saline or water into the pharynx, we examined the incidence and characteristics of such a reflex in nine premature infants. Saline and water elicited the same pattern of responses, which frequently included swallows, central apnea, and airway obstruction and less commonly featured coughs, prolonged apnea, and arousal. With the exception of arousal, the incidence of these responses was significantly greater after delivery of water stimuli than after saline bolus administration. We therefore deduce chemoreceptor involvement in generation of these reflex responses and propose a laryngeal site for this sensory system, as in animals. Since greater potency of water compared with saline was demonstrable in all the infants studied, we further conclude that most preterm infants possess an upper airway chemoreflex.

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13

Vollestad, N. K., O. M. Sejersted, R. Bahr, J. J. Woods, and B. Bigland-Ritchie. "Motor drive and metabolic responses during repeated submaximal contractions in humans." Journal of Applied Physiology 64, no. 4 (April 1, 1988): 1421–27. http://dx.doi.org/10.1152/jappl.1988.64.4.1421.

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Laryngeal chemoreflex (LCR) responses elicited by fluid irrigation of the larynx have been described repeatedly in animals, whereas evidence for a similar reflex in human infants is extremely limited. Using nasopharyngeal catheters to instill small volumes of warm saline or water into the pharynx, we examined the incidence and characteristics of such a reflex in nine premature infants. Saline and water elicited the same pattern of responses, which frequently included swallows, central apnea, and airway obstruction and less commonly featured coughs, prolonged apnea, and arousal. With the exception of arousal, the incidence of these responses was significantly greater after delivery of water stimuli than after saline bolus administration. We therefore deduce chemoreceptor involvement in generation of these reflex responses and propose a laryngeal site for this sensory system, as in animals. Since greater potency of water compared with saline was demonstrable in all the infants studied, we further conclude that most preterm infants possess an upper airway chemoreflex.

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14

Milerad, Joseph, and Håkan W. Sundell. "Reduced inspiratory drive following laryngeal chemoreflex apnea during hypoxia." Respiration Physiology 116, no. 1 (June 1999): 35–45. http://dx.doi.org/10.1016/s0034-5687(99)00035-3.

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15

CHAN, K., L. KULLAMA, L. DAY, A. OGUNDIPE, and M. ROSS. "Ovine fetal laryngeal chemoreflex thresholds and respiratory effects☆☆☆★." Otolaryngology - Head and Neck Surgery 116, no. 1 (January 1997): 91–96. http://dx.doi.org/10.1016/s0194-5998(97)70356-5.

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16

Heman-Ackah, Yolanda D., and George S. Goding. "Laryngeal chemoreflex severity and end-apnea Pao2 and Paco2." Otolaryngology–Head and Neck Surgery 121, no. 2_suppl (August 1999): P144. http://dx.doi.org/10.1016/s0194-5998(99)80248-4.

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17

Heman-Ackah, Yolanda D., Kerri J. Pernell, and George S. Goding. "The laryngeal chemoreflex: An evaluation of the normoxic response." Laryngoscope 119, no. 2 (February 2009): 370–79. http://dx.doi.org/10.1002/lary.20007.

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18

Cohen, Scott, Paul Kileny, Ramon M. Esclamado, and Steven Telian. "Correlation between the Laryngeal Brain Stem Evoked Response and the Laryngeal Chemoreflex in the Porcine Model." Annals of Otology, Rhinology & Laryngology 102, no. 2 (February 1993): 92–99. http://dx.doi.org/10.1177/000348949310200203.

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The laryngeal brain stem evoked response (LBR) represents the neural activity involved in laryngeal reflex pathways. The laryngeal chemoreflex (LCR) is a centrally mediated response consisting of apnea and hemodynamic changes that result from laryngeal stimulation. The purpose of this study is to determine the characteristics of the LBR that are predictive of LCR severity in the porcine model. The duration of apnea resulting from stimulation of the supraglottic larynx defined LCR severity. The LBR tracings were recorded from electrodes flanking the brain stem following direct electrical stimulation of the superior laryngeal nerve. The LBR peak latencies from piglets demonstrating prolonged LCR apnea were compared to those without an exaggerated LCR response. Two LBR peak latencies demonstrated a statistically significant difference between the two piglet groups. These peak latencies appear to be indicators of susceptibility to exaggerated laryngeal reflex sensitivity. Thus, the LBR may prove useful in identifying and evaluating subjects predisposed to conditions associated with dysfunctional laryngeal reflex activity.

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19

McCulloch, Timothy M., Mark A. Richardson, Paul W. Flint, and Michael J. Bishop. "Lidocaine Effects on the Laryngeal Chemoreflex, Mechanoreflex, and Afferent Electrical Stimulation Reflex." Annals of Otology, Rhinology & Laryngology 101, no. 7 (July 1992): 583–89. http://dx.doi.org/10.1177/000348949210100707.

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The use of lidocaine hydrochloride as either a topical or intravenous agent has become a common practice for minimizing laryngospasm and the reflex cardiovascular effects resulting from upper airway manipulation. The efficacy and mechanism of action of lidocaine for this purpose remain unclear. We evaluated the effect of lidocaine on the laryngeal chemoreflex (LCR), mechanoreflex (LMR), and superior laryngeal nerve electrical stimulation adductor reflex (SLN-ESAR) in piglets. Cardiopulmonary responses were used to assess LCR and LMR. Latency following SLN stimulation was used to assess SLN-ESAR. Intravenous lidocaine hydrochloride at 3 mg/kg produced no suppression of the LCR, LMR, or latency (SLN-ESAR onset latency before lidocaine 11.7 ± 0.7 milliseconds, after lidocaine 12.2 ± 0.5 milliseconds; peak latency before lidocaine 13.2 ± 0.2 milliseconds, after lidocaine 13.4 ± 0.4 milliseconds). Topically applied lidocaine at the same dose eliminated both LCR and LMR responses in all animals, with return of reflex responses 15 minutes after application. No effect on the SLN-ESAR was seen with application of topical lidocaine. This study supports topical lidocaine as a suppressant of laryngeal mucosal neuroreceptors without central neural reflex effects. Intravenous lidocaine did not affect peripheral neuroreceptors, nor did it significantly affect the latency of the SLN-ESAR neural reflex arc. Intravenous and topical lidocaine differ in mechanism of action and efficacy with regard to modulation of reflex effects induced by laryngeal stimulation.

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20

Curran, A. K., L. Xia, J. C. Leiter, and D. Bartlett. "Elevated body temperature enhances the laryngeal chemoreflex in decerebrate piglets." Journal of Applied Physiology 98, no. 3 (March 2005): 780–86. http://dx.doi.org/10.1152/japplphysiol.00906.2004.

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Hyperthermia and reflex apnea may both contribute to sudden infant death syndrome (SIDS). Therefore, we investigated the effect of increased body temperature on the inhibition of breathing produced by water injected into the larynx, which elicits the laryngeal chemoreflex (LCR). We studied decerebrated, vagotomized, neonatal piglets aged 3–15 days. Blood pressure, end-tidal CO2, body temperature, and phrenic nerve activity were recorded. To elicit the LCR, we infused 0.1 ml of distilled water through a polyethylene tube passed through the nose and positioned just rostral to the larynx. Three to five LCR trials were performed with the piglet at normal body temperature. The animal's core body temperature was raised by ∼2.5°C, and three to five LCR trials were performed before the animal was cooled, and three to five LCR trials were repeated. The respiratory inhibition associated with the LCR was substantially prolonged when body temperature was elevated. Thus elevated body temperature may contribute to the pathogenesis of SIDS by increasing the inhibitory effects of the LCR.

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21

Dragomir, Andrei, Yasemin Akay, Aidan K. Curran, and Metin Akay. "Investigating the complexity of respiratory patterns during the laryngeal chemoreflex." Journal of NeuroEngineering and Rehabilitation 5, no. 1 (2008): 17. http://dx.doi.org/10.1186/1743-0003-5-17.

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22

Goding, George S., Mark A. Richardson, and Ronald E. Trachy. "Laryngeal Chemoreflex: Anatomic and Physiologic Study by use of the Superior Laryngeal Nerve in the Piglet." Otolaryngology–Head and Neck Surgery 97, no. 1 (July 1987): 28–38. http://dx.doi.org/10.1177/019459988709700106.

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The laryngeal chemoreflex (LCR) was investigated in 21 piglets (ages 6 to 80 days old) with the use of physiologic and histologic techniques. The central projection of the superior laryngeal nerve (SLN) was determined in 14 animals by use of horseradish peroxidase-wheat germ agglutinin. Ipsilateral labeling of the solitary tract nucleus was seen. The caudal extent of the labeling varied with age. Sensory labeling of the nucleus ambiguus was present bilaterally in three younger animals and unilaterally in older piglets. Bilateral labeling of the nucleus dorsomedialis was seen in all ages. Apneic and cardiovascular response to water stimulation of laryngeal mucosa and the laryngeal adductor reflex (LAR) were examined in 16 piglets. Blunting of the apneic and cardiovascular response was seen after sacrifice of a single SLN. Hypoxia did not significantly affect the LAR or apnea duration in animals with only one intact SLN. A contralateral LAR was found in younger animals. Relevance to the LCR is also discussed.

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23

Heman-Ackah, Yolanda D., and George S. Goding. "Effects of Intralaryngeal Carbon Dioxide and Acetazolamide on the Laryngeal Chemoreflex." Annals of Otology, Rhinology & Laryngology 109, no. 10 (October 2000): 921–28. http://dx.doi.org/10.1177/000348940010901005.

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24

Cleland-Zamudio, Suzanne S., Mark Mahowald, George S. Goding, and Kerri J. Pernell. "Effect of Sleep State on the Laryngeal Chemoreflex in Neonatal Piglets." Annals of Otology, Rhinology & Laryngology 108, no. 3 (March 1999): 309–13. http://dx.doi.org/10.1177/000348949910800316.

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25

Bauman, Nancy M., Deqiang Wang, Debra M. Jaffe, and Anthony D. Sandler. "The Role of Calcitonin Gene Related Peptide in the Laryngeal Chemoreflex." Otolaryngology–Head and Neck Surgery 113, no. 2 (August 1995): P120. http://dx.doi.org/10.1016/s0194-5998(05)80762-4.

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26

Xia, L., T. A. Damon, J. C. Leiter, and D. Bartlett. "Focal warming in the nucleus of the solitary tract prolongs the laryngeal chemoreflex in decerebrate piglets." Journal of Applied Physiology 102, no. 1 (January 2007): 54–62. http://dx.doi.org/10.1152/japplphysiol.00720.2006.

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The laryngeal chemoreflex (LCR), elicited by a drop of water in the larynx, is exaggerated by mild hyperthermia (body temperature = 40–41°C) in neonatal piglets. We tested the hypothesis that thermal prolongation of the LCR results from heating the nucleus of the solitary tract (NTS), where laryngeal afferents first form synapses in the brain stem. Three- to 13-day-old piglets were decerebrated and vagotomized and studied without anesthesia while paralyzed and ventilated. Phrenic nerve activity and rectal temperature were recorded. A thermode was placed in the medulla, and the brain tissue temperature was recorded with a thermistor ∼1 mm from the tip of the thermode. When the thermode was inserted into the brain stem, respiratory activity was arrested or greatly distorted in eight animals. However, the thermode was inserted in nine animals without disrupting respiratory activity, and in these animals, warming the medullary thermode (thermistor temperature = 40–41°C) while holding rectal temperature constant reversibly exaggerated the LCR. The caudal raphé was warmed focally by ∼2°C in four additional animals; this did not alter the duration of the LCR in these animals. Thermodes placed in the NTS did not disrupt respiratory activity, but they did prolong the LCR when warmed. Thermodes that were placed deep to the NTS in the region of the nucleus ambiguus disrupted respiratory activity, which precluded any analysis of the LCR. We conclude that prolongation of the laryngeal chemoreflex by whole body hyperthermia originates from the elevation of brain tissue temperature within in the NTS.

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27

Xia, L., J. C. Leiter, and D. Bartlett. "Gestational nicotine exposure exaggerates hyperthermic enhancement of laryngeal chemoreflex in rat pups." Respiratory Physiology & Neurobiology 171, no. 1 (April 2010): 17–21. http://dx.doi.org/10.1016/j.resp.2010.01.011.

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28

Rimell, Frank, George S. Goding, and Keri Johnson. "Cholinergic Agents in the Laryngeal Chemoreflex Model of Sudden Infant Death Syndrome." Laryngoscope 103, no. 6 (June 1993): 623???630. http://dx.doi.org/10.1288/00005537-199306000-00009.

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29

Diaz, Véronique, Dominique Dorion, Sylvain Renolleau, Patrick Létourneau, Irenej Kianicka, and Jean-Paul Praud. "Effects of capsaicin pretreatment on expiratory laryngeal closure during pulmonary edema in lambs." Journal of Applied Physiology 86, no. 5 (May 1, 1999): 1570–77. http://dx.doi.org/10.1152/jappl.1999.86.5.1570.

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The present study, performed in nonsedated, conscious lambs, consisted of two parts. In the first part, we 1) examined for the first time whether a respiratory response to pulmonary C-fiber stimulation could be elicited in nonsedated newborns and 2) determined whether this response could be abolished by capsaicin pretreatment. Then, by using capsaicin-desensitized lambs, we studied whether pulmonary C fibers were involved in the sustained, active expiratory upper airway closure previously observed during pulmonary edema. Airflow and thyroarytenoid and inferior pharyngeal constrictor muscle electromyographic activities were recorded. In the first set of experiments, a 5–10 μg/kg capsaicin bolus intravenous injection in seven intact lambs consistently led to a typical pulmonary chemoreflex, showing that C fibers are functionally mature in newborn lambs. In the second series of experiments, eight lambs pretreated with 25–50 mg/kg subcutaneous capsaicin did not exhibit any respiratory response to 10–50 μg/kg intravenous capsaicin injection, implicating C fibers in the response. Finally, in the above capsaicin-desensitized lambs, we observed that halothane-induced high-permeability pulmonary edema did not cause the typical response of sustained expiratory upper airway closure seen in the intact lamb. We conclude that functionally mature C fibers are present and responsible for a pulmonary chemoreflex in response to capsaicin intravenous injection in nonsedated lambs. Capsaicin pretreatment abolishes this reflex. Furthermore, the sustained expiratory upper airway closure observed during halothane-induced pulmonary edema in intact nonsedated lambs appears to be related to a reflex involving stimulation of pulmonary C fibers.

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30

Cummings, Kevin J. "Aspiring to inspire - serotonin, the laryngeal chemoreflex and the sudden infant death syndrome." Experimental Physiology 101, no. 7 (July 1, 2016): 790. http://dx.doi.org/10.1113/ep085834.

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31

Xia, Luxi, Mardi Crane-Godreau, James C. Leiter, and Donald Bartlett. "Gestational cigarette smoke exposure and hyperthermic enhancement of laryngeal chemoreflex in rat pups." Respiratory Physiology & Neurobiology 165, no. 2-3 (February 2009): 161–66. http://dx.doi.org/10.1016/j.resp.2008.11.004.

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32

Timmers, Henri J. L. M., John M. Karemaker, Wouter Wieling, Johannes H. A. M. Kaanders, Hans Th M. Folgering, Henri A. M. Marres, and Jacques W. M. Lenders. "Arterial baroreflex and peripheral chemoreflex function after radiotherapy for laryngeal or pharyngeal cancer." International Journal of Radiation Oncology*Biology*Physics 53, no. 5 (August 2002): 1203–10. http://dx.doi.org/10.1016/s0360-3016(02)02827-4.

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33

Heman-Ackah, Yolanda D. "Determinants of Fatal Apnea Responses to Acid Stimulation of the Larynx in Piglets." Annals of Otology, Rhinology & Laryngology 114, no. 7 (July 2005): 509–16. http://dx.doi.org/10.1177/000348940511400703.

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Objectives: This study explores the physiological determinants of laryngeal chemoreflex (LCR) response severity under hypoxic conditions. Methods: Thirty-four piglets underwent hypoxic laryngeal stimulation. Physiologic data were collected, and responses were graded as mild, moderate, or profound. Results: Prestimulation hypoxia caused respiratory depression and carbon dioxide retention in profound responders and respiratory stimulation in mild and moderate responders (p < .05). Resumption of respiration occurred in all animals when the Paco2 rose by a mean ± SD of 15.1 ± 6.5 mm Hg (p > .05). There was a significant difference between mild, moderate, and severe responders in change in arterial Pao2 and hydrogenated hemoglobin saturation during the LCR-induced response (p < .001 for both). Conclusions: Resumption of respiration is associated with accumulation of arterial Paco2. The respiratory response to hypoxia predicts the severity of the LCR response. The severity of the LCR-induced response is associated with changes in arterial Pao2 and hydrogenated hemoglobin saturation during the LCR-inducedapnea.

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Grogaard, J., A. Van den Abbeele, and H. Sundell. "Effect of alcohol on apnea reflexes in young lambs." Journal of Applied Physiology 59, no. 2 (August 1, 1985): 420–25. http://dx.doi.org/10.1152/jappl.1985.59.2.420.

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This study examined the effect of alcohol on two apnea reflexes considered to be protective mechanisms through which animals and humans preserve vital functions while they are submerged in water. The laryngeal chemoreflex and the trigeminal diving reflex were studied in unanesthetized 1- to 3-wk-old lambs. Reflex stimulation resulted in reduced ventilation or apnea, bradycardia, hypertension, and blood flow redistribution in the dive pattern. After alcohol, reflex stimulation resulted in increased apnea response, preserved blood flow redistribution, but less hypertension. The onset of regular breathing following laryngeal water stimulation was significantly delayed, after alcohol, and mechanical ventilation was used in three lambs to terminate the prolonged poststimulus apnea. Airway occlusion pressure, an index of neuromuscular inspiratory drive, decreased significantly after alcohol. The study demonstrates a potent effect of alcohol on apnea reflex responses. The effect of alcohol on respiratory drive and on the apnea reflex response should be considered when humans ingest alcohol, in particular by those participating in water sports.

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Donnelly, William T., Donald Bartlett, and J. C. Leiter. "Serotonin in the solitary tract nucleus shortens the laryngeal chemoreflex in anaesthetized neonatal rats." Experimental Physiology 101, no. 7 (June 12, 2016): 946–61. http://dx.doi.org/10.1113/ep085716.

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Storm, Hanne, Lauritz Stoltenberg, Ola D. Saugstad, Torleiv O. Rognum, and Karl L. Reichelt. "221 NALOXONE INHIBITS THE DURATION OF THE LARYNGEAL CHEMOREFLEX (LCR) ACTIVATED APNEA IN PIGLETS." Pediatric Research 36, no. 1 (July 1994): 39A. http://dx.doi.org/10.1203/00006450-199407000-00221.

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Grogaard, Jens, Elizabeth Kreuger, Daniel Lindstrom, and Hakan Sundell. "Effects of Carotid Body Maturation and Terbutaline on the Laryngeal Chemoreflex in Newborn Lambs." Pediatric Research 20, no. 8 (August 1986): 724–29. http://dx.doi.org/10.1203/00006450-198608000-00005.

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Bauman, Nancy M., Deqiang Wang, Debra A. Jaffe, Anthony D. Sandler, and Erich S. Luschei. "Effect of intravenous calcitonin gene-related peptide antagonist on the laryngeal chemoreflex in piglets." Otolaryngology–Head and Neck Surgery 121, no. 1 (July 1999): 1–6. http://dx.doi.org/10.1016/s0194-5998(99)70113-0.

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Lu, I.-Jung, Kun-Ze Lee, Jin-Tun Lin, and Ji-Chuu Hwang. "Capsaicin administration inhibits the abducent branch but excites the thyroarytenoid branch of the recurrent laryngeal nerves in the rat." Journal of Applied Physiology 98, no. 5 (May 2005): 1646–52. http://dx.doi.org/10.1152/japplphysiol.01133.2004.

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Our recent study showed that both inspiratory and expiratory activities of the recurrent laryngeal nerve (RLN) were enhanced by capsaicin administration in the rat (Lu IJ, Ku LC, Lin JT, Lee KZ, and Hwang JC. Chin J Physiol 45: 143–154, 2002). There are two intralaryngeal branches of the RLN: one innervates the thyroarytenoid (TA) muscle and the other innervates the abductor (Abd) muscles. To examine whether these two intralaryngeal branches respond similarly to capsaicin administration, their discharges as well as activities of the phrenic nerve (PNA) and the superior laryngeal nerve (SLNA) were monitored in anesthetized and ventilated rats at normocapnia in hyperoxia. The low dose of capsaicin (0.625 μg/kg) produced a cardiopulmonary chemoreflex, showing apnea, a decrease in PNA, hypotension, and bradycardia, and significant decreases in SLNA and the activity of the Abd branch. Concurrently, there was an increase in the intralaryngeal TA activity during both apnea and the recovery from apnea. The high dose of capsaicin (1.25 μg/kg) evoked larger chemoreflexive responses and laryngeal nerve activities. In addition, both doses of capsaicin initiated a similar delay in the onset of Abd activity and SLNA but an earlier onset for the TA branch to commence during inspiration. A bilateral vagotomy abolished the laryngeal responses to capsaicin administration. However, PNA and blood pressure were enhanced with capsaicin administration after the vagotomy. These results suggest that laryngeal adduction in response to capsaicin administration is vagal afferent dependent and that it may also represent reflexive protection for the airway and lungs.

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Storm, Hanne, Lauritz Stoltenberg, Stephanie Øyasaeter, Ola D. Saugstad, Torleiv O. Rognum, and Karl L. Reichelt. "β-Endorphin May Be a Mediator of Apnea Induced by the Laryngeal Chemoreflex in Piglets." Pediatric Research 38, no. 2 (August 1995): 205–10. http://dx.doi.org/10.1203/00006450-199508000-00012.

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Xia, Luxi, James C. Leiter, and Donald Bartlett. "Laryngeal apnea in rat pups: effects of age and body temperature." Journal of Applied Physiology 104, no. 1 (January 2008): 269–74. http://dx.doi.org/10.1152/japplphysiol.00721.2007.

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In neonatal mammals of many species, including human infants, apnea and other reflex responses frequently arise from stimulation of laryngeal receptors by ingested or regurgitated liquids. These reflexes, mediated by afferents in the superior laryngeal nerves (SLNs), are collectively known as the laryngeal chemoreflex (LCR) and are suspected to be responsible for some cases of the sudden infant death syndrome (SIDS). The LCR is strongly enhanced by mild increases in body temperature in decerebrate piglets, a finding that is of interest because SIDS victims are often found in overheated environments. Because of the experimental advantages of studying reflex development and mechanisms in neonatal rodents, we have developed methods for eliciting laryngeal apnea in anesthetized rat pups and have examined the influence of mild hyperthermia in animals ranging in age from 3 to 21 days. We found that apnea and respiratory disruption, elicited either by intralaryngeal water or by electrical stimulation of the SLN, occurred at all ages studied. Raising body temperature by 2–3°C prolonged the respiratory disturbance in response to either stimulus. This effect of hyperthermia was prominent in the youngest animals and diminished with age. We conclude that many studies of the LCR restricted to larger neonatal animals in the past can be performed in infant rodents using appropriate methods. Moreover, the developmental changes in the LCR and in the thermal modulation of the LCR seem to follow different temporal profiles, implying that distinct neurophysiological processes may mediate the LCR and thermal prolongation of the LCR.

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Xia, Luxi, Tracey Damon, Mary M. Niblock, Donald Bartlett, and J. C. Leiter. "Unilateral microdialysis of gabazine in the dorsal medulla reverses thermal prolongation of the laryngeal chemoreflex in decerebrate piglets." Journal of Applied Physiology 103, no. 5 (November 2007): 1864–72. http://dx.doi.org/10.1152/japplphysiol.00524.2007.

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The laryngeal chemoreflex (LCR) is elicited by water in the larynx and leads to apnea and respiratory disruption in immature animals. The LCR is exaggerated by the elevation of brain temperature within or near the nucleus of the solitary tract (NTS) in decerebrate piglets. Thermal prolongation of reflex apnea elicited by superior laryngeal nerve stimulation is reduced by systemic administration of GABAA receptor antagonists. Therefore, we tested the hypothesis that microdialysis within or near the NTS of gabazine, a GABAA receptor antagonist, would reverse thermal prolongation of the LCR. We examined this hypothesis in 21 decerebrate piglets (age 3–13 days). We elicited the LCR by injecting 0.1 ml of water into the larynx before and after each piglet's body temperature was elevated by ∼2.5°C and before and after 2–5 mM gabazine was dialyzed unilaterally and focally in the medulla. Elevated body temperature failed to prolong the LCR in one piglet, which was excluded from analysis. Elevated body temperature prolonged the LCR in all the remaining animals, and dialysis of gabazine into the region near the NTS ( n = 10) reversed the thermal prolongation of the LCR even though body temperature remained elevated. Dialysis of gabazine in other medullary sites ( n = 10) did not reverse thermal prolongation of the LCR. Gabazine had no consistent effect on baseline respiratory activity during hyperthermia. These findings are consistent with the hypothesis that hyperthermia activates GABAergic mechanisms in or near the NTS that are necessary for the thermal prolongation of the LCR.

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Heman-Ackah, Yolanda D., and George S. Goding. "Second Place—Resident Clinical Science Award 1999 Laryngeal Chemoreflex Severity and End-Apnea Pao2 and Paco2." Otolaryngology–Head and Neck Surgery 123, no. 3 (September 2000): 157–63. http://dx.doi.org/10.1067/mhn.2000.106710.

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Storm, Hanne, Lauritz Stoltenberg, Ola D. Saugstad, Torleiv O. Rognum, and Karl L. Reichelt. "Beta-endorphin immunoreactivity levels in CSF after laryngeal chemoreflex activation correlate with apnoea duration in piglets." Journal of Perinatal Medicine 24, no. 4 (January 1996): 363–72. http://dx.doi.org/10.1515/jpme.1996.24.4.363.

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Thach, Bradley T. "Some aspects of clinical relevance in the maturation of respiratory control in infants." Journal of Applied Physiology 104, no. 6 (June 2008): 1828–34. http://dx.doi.org/10.1152/japplphysiol.01288.2007.

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Two reflex mechanisms important for survival are discussed. Brain stem and cardiovascular mechanisms that are responsible for recovery from severe hypoxia (autoresuscitation) are important for survival in acutely hypoxic infants and adults. Failure of this mechanism may be important in sudden infant death syndrome (SIDS), because brain stem-mediated hypoxic gasping is essential for successful autoresuscitation and because SIDS infants appear to attempt to autoresuscitate just before death. A major function of another mechanism is to protect the airway from fluid aspiration. The various components of the laryngeal chemoreflex (LCR) change during maturation. The LCR is an important cause of prolonged apneic spells in infants. Consequently, it also may have a role in causing SIDS. Maturational changes and/or inadequacy of this reflex may be responsible for pulmonary aspiration and infectious pneumonia in both children and adults.

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Kuypers, Kristel, Tessa Martherus, Tereza Lamberska, Janneke Dekker, Stuart B. Hooper, and Arjan B. te Pas. "Reflexes that impact spontaneous breathing of preterm infants at birth: a narrative review." Archives of Disease in Childhood - Fetal and Neonatal Edition 105, no. 6 (April 29, 2020): 675–79. http://dx.doi.org/10.1136/archdischild-2020-318915.

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Some neural circuits within infants are not fully developed at birth, especially in preterm infants. Therefore, it is unclear whether reflexes that affect breathing may or may not be activated during the neonatal stabilisation at birth. Both sensory reflexes (eg, tactile stimulation) and non-invasive ventilation (NIV) can promote spontaneous breathing at birth, but the application of NIV can also compromise breathing by inducing facial reflexes that inhibit spontaneous breathing. Applying an interface could provoke the trigeminocardiac reflex (TCR) by stimulating the trigeminal nerve resulting in apnoea and a reduction in heart rate. Similarly, airflow within the nasopharynx can elicit the TCR and/or laryngeal chemoreflex (LCR), resulting in glottal closure and ineffective ventilation, whereas providing pressure via inflations could stimulate multiple receptors that affect breathing. Stimulating the fast adapting pulmonary receptors may activate Head’s paradoxical reflex to stimulate spontaneous breathing. In contrast, stimulating the slow adapting pulmonary receptors or laryngeal receptors could induce the Hering-Breuer inflation reflex or LCR, respectively, and thereby inhibit spontaneous breathing. As clinicians are most often unaware that starting primary care might affect the breathing they intend to support, this narrative review summarises the currently available evidence on (vagally mediated) reflexes that might promote or inhibit spontaneous breathing at birth.

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Donnelly, William T., Luxi Xia, Donald Bartlett, and J. C. Leiter. "Activation of serotonergic neurons in the medullary caudal raphe shortens the laryngeal chemoreflex in anaesthetized neonatal rats." Experimental Physiology 102, no. 8 (July 3, 2017): 1007–18. http://dx.doi.org/10.1113/ep086082.

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van der Velde, Liesbeth, Aidan K. Curran, James J. Filiano, Robert A. Darnall, Donald Bartlett, and J. C. Leiter. "Prolongation of the laryngeal chemoreflex after inhibition of the rostral ventral medulla in piglets: a role in SIDS?" Journal of Applied Physiology 94, no. 5 (May 1, 2003): 1883–95. http://dx.doi.org/10.1152/japplphysiol.01103.2002.

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We tested the hypothesis that inhibition of neurons within the rostral ventral medulla (RVM) would prolong the laryngeal chemoreflex (LCR), a putative stimulus in the sudden infant death syndrome (SIDS). We studied the LCR in 19 piglets, age 3–16 days, by injecting 0.05 ml of saline or water into the larynx during wakefulness, non-rapid eye movement (NREM) sleep, and REM sleep, before and after 1 or 10 mM muscimol dialysis in the RVM. Muscimol prolonged the LCR ( P < 0.05), and the prolongation was greater when the LCR was stimulated with water compared with saline ( P < 0.02). The LCR was longer during NREM sleep than during wakefulness and longest during REM sleep (REM compared with wakefulness). Muscimol had no effect on the likelihood of arousal from sleep after LCR stimulation. We conclude that the RVM provides a tonic facilitatory drive to ventilation that limits the duration of the LCR, and loss of this drive may contribute to the SIDS when combined with stimuli that inhibit respiration.

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Wang, Xiaolu, Ruichen Guo, and Wenjing Zhao. "Distribution of Fos-Like Immunoreactivity, Catecholaminergic and Serotoninergic Neurons Activated by the Laryngeal Chemoreflex in the Medulla Oblongata of Rats." PLOS ONE 10, no. 6 (June 18, 2015): e0130822. http://dx.doi.org/10.1371/journal.pone.0130822.

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Khurana, A., and B. T. Thach. "Effects of upper airway stimulation on swallowing, gasping, and autoresuscitation in hypoxic mice." Journal of Applied Physiology 80, no. 2 (February 1, 1996): 472–77. http://dx.doi.org/10.1152/jappl.1996.80.2.472.

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Severe hypoxia produces a state of neural depression known as hypoxic coma in which reflex activity is believed to be absent but from which spontaneous recovery (“autoresuscitation”) still can occur. We evaluated the swallowing reflex during hypoxic coma by employing mechanical and chemosensory stimuli. BALB/c mice were given 97% N2-3% CO2 to breathe. At onset of coma, a 0.05-ml bolus of saline or water was infused into the pharynx. Unlike mechanical stimulation (sham infusion), fluid infusion usually was followed by rapid swallowing, more so with water than with saline. This model allowed examination of interactions among swallowing, hypoxic gasping, airway fluid removal, and autoresuscitation. Compared with sham infusion, saline and water reduced gasping rate equally. Saline, however, prolonged the process of autoresuscitation more than did water, an effect possibly related to an observed increased retention of saline in the airway. Occasionally, mice failed to swallow after infusions, in which case airway obstruction during gasping and autoresuscitation failure was repeatedly observed. These studies suggest that the swallowing component of the laryngeal chemoreflex is present during hypoxic coma and that swallowing facilitates autoresuscitation when upper airway fluid is present.

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