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Biomedical subjects

N E Robinson

Publications and source records attributed to N E Robinson.

At least 55 records · Page 3Linked to original sources
PubMed1999

Distribution of substance P binding sites in equine airways.

Autoradiography with [125I]-Bolton Hunter substance P ([I]-BHSP) was used to detect substance P binding sites in the equine lung. Specific [I]-BHSP binding sites were very dense over small bronchial vessels, tracheobronchial glands and airway epithelium in large and small airways. The density of [I]-BHSP binding sites over airway smooth muscle was much lower than in the preceding tissues. Competition with an excess of either a specific neurokinin 1 receptor agonist, or a specific neurokinin 2 receptor agonist indicated that most specific [I]-BHSP binding sites in the equine lung represent neurokinin 1 receptors. The receptor-mediated effects of substance P in the equine lung are most likely to involve regulation of vascular tone and airway secretions based upon the density of specific [I]-BHSP binding sites in these tissues. Activation of intrapulmonary afferent nerves containing Substance P by noxious stimuli such as inhaled allergens or irritants may lead to increased mucus secretion and decreased airway diameter due to vascular congestion.

Animals↗
PubMed1999

Pathophysiology of dorsal displacement of the soft palate in horses.

Dorsal displacement of the soft palate (DDSP) is an intermittent obstructive upper airway condition that occurs in athletic horses during high-intensity exercise. The pathogenesis of this condition is unknown, but may involve epiglottic hypoplasia, malformation, or neuromuscular dysfunction. In this paper, we report on investigations into the pathophysiology of DDSP. In 3 separate experiments, Standardbred horses were exercised on a high-speed treadmill at speeds corresponding to 50, 75 and 100% of maximum heart rate. The upper airway was evaluated by videoendoscopy and measurement of tracheal pressures. In experiment 1, we examined the effect of bilateral hypoglossal and glossopharyngeal nerve block on epiglottic function in exercising horses. This nerve block caused epiglottic retroversion and inspiratory upper airway obstruction. However, DDSP did not occur. In experiment 2, we evaluated the hypothesis that tensor veli palatini muscle dysfunction is involved in the pathogenesis of DDSP. Bilateral tensor veli palatini muscle tenectomy did not cause DDSP, but caused instability of the rostral half of the soft palate and a modest inspiratory upper airway obstruction. In experiment 3, we hypothesised that palatinus and palatopharyngeal dysfunction causes DDSP. The pharyngeal branch of the vagus nerve was blocked bilaterally in the guttural pouch. This block caused DDSP in all horses within 2-15 min after nerve block. Furthermore, DDSP created an expiratory nasopharyngeal obstruction. Because the pharyngeal branch of the vagus nerve is in close proximity to the retropharyngeal lymph node chain, we suggest that retropharyngeal lymphadenopathy may cause neural dysfunction and thereby be involved in the pathogenesis of clinical DDSP.

Animals↗
PubMed1999

Mediators of anaphylaxis but not activated neutrophils augment cholinergic responses of equine small airways.

Neutrophilic inflammation in small airways (SA) and bronchospasm mediated via muscarinic receptors are features of chronic obstructive pulmonary disease in horses (COPD). Histamine, serotonin, and leukotrienes (LTs) are reported to be involved in the exacerbation of COPD, and currently, histamine has been shown to increase tension response to electrical field simulation (EFS) in equine SA. We tested the effects of these mediators and the effects of activated neutrophils on the cholinergic responses in SA. Histamine, serotonin, and LTD4 had a synergistic effect on EFS responses and only an additive effect on the tension response to exogenous ACh or methacholine. Atropine and TTX entirely eliminated the EFS-induced tension response in the presence of all three inflammatory mediators, indicating that augmentation of the EFS response applies only to the endogenous cholinergic response. Neutrophils isolated from control and COPD-affected horses were activated by zymosan, producing 18.1 +/- 2.3 and 25.0 +/- 2.3 nmol superoxide. 10(6) cells-1. 30 min-1, respectively. However, in contrast to the profound effect of mediators, incubation of SA for over 1 h in a suspension of up to 30 x 10(6) zymosan-treated neutrophils/ml did not significantly affect EFS responses of SA isolated from either control or COPD-affected horses. We conclude that in equine SA 1) the endogenous cholinergic responses are subject to strong facilitation by inflammatory mediators; 2) activated neutrophils do not affect cholinergic responses in SA; and 3) in acute bouts of equine COPD, histamine, LTD4, and serotonin (mediators primarily associated with type I allergic reaction) rather than mediators derived from neutrophils most likely contribute to increased cholinergic airway tone.

Anaphylaxis↗
PubMed1999

Modulation of ACh release from airway cholinergic nerves in horses with recurrent airway obstruction.

To evaluate the functional status of neuronal alpha2-adrenoceptors (ARs) and beta2-ARs on ACh release in horses with recurrent airway obstruction (RAO), we examined the effects of the physiological agonists epinephrine (Epi) and norepinephrine (NE) and the beta2-agonists RR- and RR/SS-formoterol on ACh release from airway cholinergic nerves of horses with RAO. Because SS-formoterol, a distomer of the beta2-agonist, increases ACh release from airways of control horses only after the autoinhibitory muscarinic receptors are blocked by atropine, we also tested the hypothesis that if there is an M2-receptor dysfunction in equine RAO, SS-formoterol should increase ACh release even in the absence of atropine. ACh release was evoked by electrical field stimulation and measured by HPLC. Epi and NE caused less inhibition of ACh release in horses with RAO than in control horses. At the catecholamine concentration achieved during exercise (10(-7) M), the inhibition induced by Epi and NE was 10.8 +/- 13.2 and 3.4 +/- 6.8%, respectively, in equine RAO versus 41.0 +/- 6.4 and 27.1 +/- 5.6%, respectively, in control horses. RR- and RR/SS-formoterol (10(-8) to 10(-5) M) increased ACh release to a similar magnitude as that in control horses. These results indicate that neuronal beta2-ARs are functioning; however, the alpha2-ARs are dysfunctional in the airways of horses with RAO in response to circulating catecholamines. SS-formoterol (10(-8) to 10(-5) M) facilitated ACh release in horses with RAO even in the absence of atropine. Addition of atropine did not cause significantly more augmentation of ACh release over the effect of SS-formoterol alone. The magnitude of augmentation in horses with RAO in the absence of atropine was similar to that in control horses in the presence of atropine. The latter observations could be explained by neuronal muscarinic-autoreceptor dysfunction in equine RAO.

Acetylcholine↗
PubMed1999

Pre- and postjunctional effects of inflammatory mediators in horse airways.

In addition to their direct contractile effects, histamine (Hist), serotonin [5-hydroxytryptamine (5-HT)], and leukotriene (LT) D(4), in low concentrations, dramatically augment electrical field stimulation (EFS)-induced smooth muscle contractions in equine airways. To determine the mechanism of their action, we studied, in trachealis strips, the effect of these mediators on both cholinergically induced tension and the release of ACh from cholinergic nerves. All three mediators synergistically augmented the contraction of the trachealis that was due to release of endogenous ACh, i.e., EFS-induced contraction. These same mediators caused only a small but parallel shift of the ACh concentration-response curve. Comparison of the mediator effects on the responses to endogenous and exogenous ACh suggested a prejunctional effect. However, release of ACh was augmented only by Hist and 5-HT but not by LTD(4). Hist-induced contraction of trachealis was abolished by pyrilamine (H(1)-receptor antagonist) but not by ranitidine (H(2)-receptor antagonist), whereas thioperamide (H(3)-receptor antagonist) shifted the Hist response curve to the left. The augmenting effect of Hist on EFS-induced contraction was abolished by pyrilamine and unaffected by ranitidine or thioperamide. We conclude that inflammatory mediators can increase endogenous cholinergic responses of equine airways via both prejunctional and postjunctional mechanisms. LTD(4) acts solely on smooth muscle, whereas 5-HT and Hist additionally act on neuronal receptors to facilitate release of ACh. Excitatory effects of Hist, i.e., direct contractile effect, and augmentation of endogenous cholinergic response are both mediated via H(1) receptors, whereas the inhibitory H(3) receptors partially oppose the direct contractile effect of this mediator.

Acetylcholine↗
PubMed1999

Aerosolized albuterol sulfate used as a bronchodilator in horses with recurrent airway obstruction.

OBJECTIVE: To determine the dose of aerosolized albuterol sulfate required to cause bronchodilation in horses with recurrent airway obstruction (RAO) and duration of this effect. ANIMALS: 19 horses with RAO (10 in experiment 1; 9 in experiment 2). PROCEDURE: Horses were moved from pasture to stables, and airway obstruction was induced. Pulmonary function was measured in 10 horses before and 5, 10, and 30 minutes after administration of vehicle or 120, 240, 360, or 720 microg of the drug. Nine horses received vehicle or 360 or 720 microg of albuterol, and pulmonary function was measured at baseline and 5 minutes and 1, 2, 3, 4, 5, 6, and 7 hours later. Horses were evaluated for adverse drug effects. RESULTS: 360 microg of albuterol was required to cause significant bronchodilatation; 720 microg did not enhance bronchodilatation or increase duration of action. Depending on which pulmonary function parameter was evaluated, bronchodilatation achieved by use of albuterol lasted between 30 minutes and 1 hour. Because there was a significant vehicle effect, the combined effect of vehicle and drug lasted up to 3 hours. Adverse effects were not observed. CONCLUSIONS: Aerosolized albuterol, 360 or 720 microg, is a safe and effective bronchodilator in horses with RAO. Onset of action is rapid (5 minutes), and effects last from 30 minutes to 3 hours. CLINICAL RELEVANCE: Aerosolized albuterol is useful for treatment of bronchospasm in horses with RAO.

Administration, Inhalation↗
PubMed1998

Effects of enantiomers of beta 2-agonists on ACh release and smooth muscle contraction in the trachea.

The beta 2-agonists currently used as bronchodilators are racemic mixtures of R- and S-enantiomers. In the present study, we examined the effects of enantiomers of the beta 2-agonists albuterol and formoterol on acetylcholine (ACh) release from equine trachealis parasympathetic nerves. ACh release was evoked by electrical field stimulation (20 V, 0.5 ms, 0.5 Hz) and measured by high-performance liquid chromatography coupled with electrochemical detection. We also tested the effects of enantiomers of albuterol and formoterol on equine tracheal smooth muscle (TSM) contraction in response to exogenous ACh. R- and RS-albuterol (10(-8) to 10(-5) M) and RR- and RR/SS-formoterol (10(-8) to 10(-5) M) augmented ACh release in a concentration-dependent manner. Beginning at 10(-6) M, SS-formoterol significantly increased ACh release, and at 10(-5) M, release increased by 71.9 +/- 8.7% over baseline. This effect was only observed, however, when the prejunctional muscarinic autoinhibitory effect of ACh was prevented with atropine. Both the RR- and SS-formoterol-induced increases in ACh release were abolished by the beta 2-antagonist ICI-118551 (3 x 10(-7) M). The effect of S-albuterol on ACh release was variable, and the mean increase induced by 10(-5) M was 30.8 +/- 16.1% in the presence of atropine. In the muscle tension study, R- and RS-albuterol and RR- and RR/SS-formoterol (10(-8) to 10(-5) M) but not the S-enantiomers inhibited TSM contraction. Even though R-enantiomers augment ACh release, they potently inhibit TSM contraction. Because racemic beta 2-agonists are bronchodilators on acute administration, the postjunctional spasmolytic effects of R-enantiomers predominate over the spasmogenic effect evoked via increased ACh release. The S-enantiomers, in contrast, do not inhibit TSM contraction and therefore would not contribute to the observed bronchodilation of the racemate. The S-enantiomers do prejunctionally facilitate ACh release when prejunctional muscarinic autoreceptors are dysfunctional, suggesting a potentially deleterious effect.

Acetylcholine↗
PubMed1998

Role of cAMP and neuronal K+ channels on alpha 2-AR-induced inhibition of ACh release in equine trachea.

To investigate the effects of changes in intracellular cAMP on alpha 2-adrenoceptor (AR)-induced inhibition of airway acetylcholine (ACh) release, we examined the effects of the alpha 2-AR agonist clonidine on electrical field stimulation-evoked ACh release from equine tracheal parasympathetic nerves before and after treatment with 8-bromo-cAMP or forskolin. We also tested whether charybdotoxin (ChTX)- or iberiotoxin (IBTX)-sensitive Ca(2+)-activated K+ channels mediate alpha 2-AR-induced inhibition by examining the effect of clonidine in the absence and presence of ChTX or IBTX on ACh release. The amount of released ACh was measured by HPLC coupled with electrochemical detection. Clonidine (10(-7) to 10(-5) M) dose dependently inhibited ACh release before and after treatment with 8-bromo-cAMP (10(-3) M) or forskolin (3 x 10(-5) M). ChTX and IBTX, both at the concentration of 5 x 10(-7) M, significantly increased ACh release; however, they did not alter the magnitude of clonidine-induced inhibition. These results indicated that in equine tracheal parasympathetic nerves, alpha 2-AR-induced inhibition of ACh release is via an intracellular cAMP-independent pathway. Activation of both ChTX- and IBTX-sensitive Ca(2+)-activated K+ channels inhibits the electrical field stimulation-evoked ACh release, but these channels are not involved in the alpha 2-AR-induced inhibition of ACh release.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1998

Regional differences in endothelial function in horse lungs: possible role in blood flow distribution?

We investigated regional differences of in vitro responses of pulmonary arteries (6-mm OD) from the dorsocaudal (top) and cranioventral (bottom) lung regions to endothelium-dependent vasodilators (methacholine, bradykinin, and calcium ionophore A-23187). Methacholine relaxed endothelium-intact top vessels; however, in bottom vessels, a small relaxation preceded a profound contraction. In top vessels, removal of endothelial cells converted relaxation to contraction, and in bottom vessels it abolished relaxation and enhanced contraction. Bradykinin and A-23187 were more potent and caused greater endothelium-mediated relaxation in top than in bottom arteries. The endothelium-independent vasodilator sodium nitroprusside caused similar relaxations in all rings. Nomega-nitro-L-arginine and NG-monomethyl-L-arginine and methylene blue abolished relaxation of top and bottom arteries to methacholine; meclofenamate had little effect. We conclude that regional differences in endothelium-mediated relaxation are caused by differences in the magnitude of the endothelial release of nitric oxide. Similar differences in endothelium-dependent flow-mediated vasodilation and endothelial nitric oxide release may result in preferential perfusion of caudodorsal lung regions.

Animals↗
PubMed1998

Effect of bilateral blockade of the pharyngeal branch of the vagus nerve on soft palate function in horses.

OBJECTIVE: To determine the effect of bilateral blockade of the pharyngeal branch of the vagus nerve on soft palate function in horses. ANIMALS: 5 Standardbreds. PROCEDURE: Peak tracheal inspiratory and expiratory pressures and airflow were measured while horses exercised at the speeds corresponding to 75 and 100% of the speed that resulted in maximal heart rate, with and without pharyngeal branch of the vagus nerve blockade. Respiratory frequency-to-stride frequency coupling ratio was measured by correlating foot fall measurements with respiratory frequency. The pharyngeal branch of the vagus nerve was blocked bilaterally as the nerve coursed through the auditory tube diverticulum (guttural pouch) across the longus capitus muscle. RESULTS: Persistent, reversible dorsal displacement of the soft palate (DDSP) occurred in all horses after nerve blockade, and lasted from 1 to 3 hours; normal nasopharyngeal function returned within 3 hours. Compared with control values, peak expiratory tracheal pressure increased (P = 0.001), expiratory impedance increased (P = 0.007), and minute ventilation decreased (P = 0.04). Respiratory frequency-to-stride frequency coupling ratio decreased (P = 0.009) so that horses took 1 breath/stride without the nerve block and, approximately, 1 breath/2 strides with the block. CONCLUSION: DDSP creates flow-limiting expiratory obstruction and may be caused by neuromuscular dysfunction involving the pharyngeal branch of the vagus nerve. It may alter performance by causing expiratory obstruction and by altering breathing strategy in horses. CLINICAL RELEVANCE: A repeatable, reversible model of DDSP exists that allows further study of the disease. Dysfunction of the neuromuscular group, pharyngeal branch of the vagus nerve and palatinus and palatopharyngeus muscles, may be implicated in the pathogenesis of clinical DDSP.

Animals↗
PubMed1997

In vitro responses of equine small airways and lung parenchyma.

In vitro responses of equine small peripheral airways (SA) and lung parenchyma (LP) were studied. We examined their contractile and relaxant responses and investigated effects of histamine, and endogenous prostanoids as these mediators may play a role in development or recurrent airway obstruction in horses (heaves). SA and LP electrical field stimulation (EFS) induced nearly maximal and partial frequency-dependent contractions, respectively. These contractions were virtually abolished in SA but only partially inhibited in LP by atropine (ATR) and tetrodotoxin (TTX). Methacholine (MCh) contracted SA with a 5-fold higher potency and greater maximal tension than LP. In SA but not in LP, a large augmentation of EFS responses at 1-4 Hz was produced by both meclofenamate, a cyclooxygenase blocker and 3 microM histamine. We conclude that: (1) excitatory input from cholinergic nerves largely determines SA tone, but has minor effect in LP; (2) in SA endogenous inhibitory prostanoids modulate contractile response to nerve stimulation; and (3) inhibition of cyclooxygenase and histamine greatly potentiate responses to nerve stimulation in SA. These data are consistent with the hypothesis that, in horses with heaves, histamine release and an altered prostanoid profile contribute to cholinergically mediated SA obstruction.

Animals↗
PubMed1997

Tachykinin receptors in the equine pelvic flexure.

Tachykinins, of which substance P (SP) is the prototype, are neuropeptides which are widely distributed in the nervous systems. In the equine gut, SP is present in enteric nerves and is a powerful constrictor of enteric muscle; in other species, SP is also known to have potent vasodilatory and pro-inflammatory effects. The specific effects of SP are determined by the subtype of receptor present in the target tissue. There are 3 known subtypes of tachykinin receptors, distinguished by their relative affinities for SP and other tachykinins. The distribution of SP binding sites in the equine pelvic flexure was determined using 125I-Bolton Hunter SP (I-BHSP) autoradiography. Most I-BHSP binding sites were determined to be saturable and specific, therefore presumably representing tachykinin receptors. The greatest degree of I-BHSP binding occurred over very small vessels, and over the muscularis mucosae; I-BHSP binding was also intense over the circular muscle of the muscularis externa and mucosa, and present, although less intense, over the longitudinal muscle of the muscularis externa. Competition of I-BHSP with specific receptor agonists for binding sites in the equine pelvic flexure were used to determine the subtypes of tachykinin receptors present. The neurokinin-1 receptor subtype predominated in the equine pelvic flexure, followed by the neurokinin-3 receptor subtype.

Animals↗
PubMed1997

Origin and modulation of ACh release from rat airway cholinergic nerves.

The release of acetylcholine (ACh) from airway parasympathetic nerves was studied in rat trachea. We established stimulus parameters, examined the role of extracellular Ca2+, and investigated the origin of the released ACh by use of vesamicol, an inhibitor of ACh uptake in synaptic vesicles. The role of muscarinic autoreceptors and prostanoids on ACh release was also studied. Tracheal rings were incubated in Krebs-Henseleit solution containing neostigmine and guanethidine with or without atropine. ACh release was measured by high-performance liquid chromatography with electrochemical detection. ACh release was dependent on frequency (0.5-16 Hz), voltage (10-25 V), and pulse duration (0.5-4 ms). At 4 Hz, one-fifth of electrical field stimulation-induced ACh release was extracellular Ca2+ independent and vesamicol resistant, indicating its nonvesicular origin. Three-fifths were Ca2+ dependent and vesamicol sensitive, indicating that it was newly synthesized, and one-fifth was Ca2+ dependent but vesamicol resistant, indicating its origin from prestored vesicles. At 16 Hz, two-fifths were nonvesicular and three-fifths were newly synthesized. Blockade of the muscarinic autoreceptor by atropine potentiated the release of ACh four- to fivefold. Neither of the cyclooxygenase inhibitors indomethacin or meclofenamate nor exogenous prostaglandin E2 affected ACh release, indicating that inhibitory prostanoids do not modulate ACh release.

Acetylcholine↗
PubMed1997

Mechanism of capsaicin-induced relaxation in equine tracheal smooth muscle.

The effects of capsaicin and neuropeptides were examined in equine tracheal smooth muscle (TSM). Neither capsaicin nor substance P (SP) contracted TSM. Capsaicin (100 microM) elicited relaxation in TSM contracted with methacholine. This relaxation was not mimicked by SP or calcitonin gene-related peptide (CGRP). Relaxation was not attenuated by removal of the epithelium or by pretreatment of tissue with meclofenamate or the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine. Previous exposure of TSM to capsaicin did not eliminate the relaxation responses to subsequent capsaicin. Although vasoactive intestinal peptide (VIP) elicited marked relaxation that was attenuated by alpha-chymotrypsin, alpha-chymotrypsin did not affect the capsaicin-induced relaxation. Capsaicin-induced relaxation was abolished by charybdotoxin, a blocker of large-conductance Ca(2+)-activated K+ channels. These results indicate that capsaicin-induced equine TSM relaxation is not mediated either by neuropeptides such as SP or CGRP released from capsaicin-sensitive sensory nerves or by prostanoids, NO, or VIP. Relaxation is due to the effect of capsaicin on large-conductance Ca(2+)-activated K+ channels. The peptidergic nerves play no important role in the regulation of TSM tone in horse airways.

Animals↗
PubMed1997

Effect of bilateral tenectomy of the tensor veli palatini muscle on soft palate function in horses.

OBJECTIVE: To determine the effect of bilateral tenectomy of the tensor veli palatini muscle on soft palate and nasopharyngeal function in exercising horses. ANIMALS: 5 Standardbreds. PROCEDURE: Treadmill videoendoscopy was performed on 5 Standardbreds exercising at 50, 75, and 100% of the speed that produced maximum heart rate; tracheal and pharyngeal pressures were measured before and after surgery. Tenectomy of the tensor veli palatini muscle was performed bilaterally on each horse while under general anesthesia, using a transoral approach. RESULTS: Peak inspiratory tracheal pressures were significantly (P = 0.016) more negative and there was a trend (P = 0.06) for peak pharyngeal inspiratory pressure to be less negative following bilateral tenectomy of the tensor veli palatini muscle, compared with preoperative values. The rostral half of the soft palate was unstable and collapsed dorsally into the nasopharynx during inspiration, causing partial obstruction of the nasopharynx. The caudal free margin of the soft palate remained ventral to the epiglottis, and dorsal displacement of the soft palate did not occur in any horse. CONCLUSIONS: Bilateral tenectomy of the tensor veli palatini muscle did not cause dorsal displacement of the soft palate in horses while exercising at maximum heart rate, but resulted in collapse of the nasopharynx during inspiration. CLINICAL RELEVANCE: Results of our study indicate that the tensor veli palatini muscle functions to support and dilate the nasopharynx during intense inspiratory efforts in horses by tensing the palatine aponeurosis.

Anesthesia, General↗
PubMed1997

Effects of bilateral hypoglossal and glossopharyngeal nerve blocks on epiglottic and soft palate position in exercising horses.

OBJECTIVE: To determine the effect of bilateral hypoglossal and and glossopharyngeal nerve block on epiglottic and soft palate position and tracheal and pharyngeal pressures in exercising horses. ANIMALS: 5 Standardbreds. PROCEDURE: Tracheal and pharyngeal pressures were measured in 5 Standardbreds exercising at the speed at which the horses achieved 50, 75, and 100% of maximal heart rate after bilateral hypoglossal and glossopharyngeal nerve block and without nerve block. Nerve block was achieved by injection of 1 to 2 ml of 2% mepivicaine hydrochloride between the glossopharyngeal and hypoglossal nerves, as they coursed through the medial compartment of the diverticulum of the auditory tube (guttural pouch), using videoendoscopic guidance and an injection apparatus. RESULTS: Compared with control values, peak inspiratory tracheal pressure was significantly (P = 0.02) more negative, and peak pharyngeal inspiratory pressure was less negative (P = 0.004) after bilateral hypoglossal and glossopharyngeal nerve block. Respiratory frequency was significantly (P = 0.024) lower after nerve block, compared with control values. The epiglottis was unstable and retroflexed through the rima glottis during inspiration after bilateral hypoglossal and glossopharyngeal nerve block. Despite loss of contact between the epiglottis and the caudal free margin of the soft palate, dorsal displacement of the soft palate did not occur. CONCLUSIONS AND CLINICAL RELEVANCE: Loss of contact of the epiglottis with the soft palate did not affect soft palate position, suggesting that when the soft palate is normal, the epiglottis does not function as a support, holding the soft palate in a ventral position. Therefore, epiglottic dysfunction is not solely responsible for intermittent dorsal displacement of the soft palate in horses, and neuromuscular dysfunction involving the hyoepiglotticus muscle, geniohyoideus muscle, or the hypoglossal nerve may cause epiglottic retroflexion in horses.

Animals↗