Relative contribution of various airway protective mechanisms to prevention of aspiration during swallowing

2003 ◽  
Vol 284 (6) ◽  
pp. G933-G939 ◽  
Author(s):  
Bidyut K. Medda ◽  
Mark Kern ◽  
Junlong Ren ◽  
Pengyan Xie ◽  
Seckin O. Ulualp ◽  
...  
Keyword(s):  
Airway Protection ◽  
Protective Mechanisms ◽  
Laryngeal Elevation ◽  
Glottal Closure ◽  
Relative Contribution ◽  
Primary Mechanism ◽  
Before And After ◽  
Ues Opening ◽  
Pharyngeal Clearance ◽  
Risk Of Aspiration

Deglutitive airway protective mechanisms include glottal closure, epiglottal descent, and anterosuperior displacement of the larynx. Aspiration of swallowed material may occur during the pre-, intra-, or postpharyngeal phase of swallowing. Our objectives were to determine the relative contribution of the airway protective mechanisms during each phase of swallow in 14 decerebrated cats before and after suprahyoid myotomy, epiglottectomy, and unilateral cordectomy. After myotomy, superior excursions of the hyoid, thyroid, and cricoid cartilages and anteroposterior diameter of maximum upper esophageal spincter (UES) opening were significantly diminished, but the incidence of pharyngeal residue significantly increased ( P < 0.05). No aspiration was observed in the predeglutitive period. After myotomy, the incidence of aspiration significantly increased in both intra- and postdeglutitive periods. Epiglottectomy did not alter aspiration incidence, but unilateral cordectomy resulted in a 100% incidence of intra- and postdeglutitive aspiration. In conclusion, glottal closure constitutes the primary mechanism for prevention of intra- and postdeglutitive aspiration, but laryngeal elevation may assist this function. Bolus pulsion without laryngeal distraction can open the UES, but at risk of aspiration due to decreased pharyngeal clearance. The epiglottis provides no apparent airway protection during any phase of swallowing.

Mechanisms of airway protection during retching, vomiting, and swallowing

2002 ◽  
Vol 283 (3) ◽  
pp. G529-G536 ◽  
Author(s):  
Ivan M. Lang ◽  
Nicole Dana ◽  
Bidyut K. Medda ◽  
Reza Shaker
Keyword(s):  
Muscle Activation ◽  
Smooth Muscles ◽  
Upper Esophageal Sphincter ◽  
Striated Muscles ◽  
Airway Protection ◽  
Laryngeal Elevation ◽  
Glottal Closure ◽  
Adductor Muscles ◽  
Pharyngeal Muscles ◽  
Subglottal Pressure

We investigated the mechanisms of airway protection and bolus transport during retching and vomiting by recording responses of the pharyngeal, laryngeal, and hyoid muscles and comparing them with responses during swallowing and responses of the gastrointestinal tract. Five dogs were chronically instrumented with electrodes on the striated muscles and strain gauges on smooth muscles. Retching and vomiting were stimulated by apomorphine (5–10 ug/kg iv). During retching, the hyoid and thyroid descending and laryngeal abductor muscles were activated; between retches, the hyoid, thyroid, and pharyngeal elevating, and laryngeal adductor muscles were activated. Vomiting always occurred during the ascending phase of retching and consisted of three sequential phases of hyoid and pharyngeal muscle activation culminating in simultaneous activation of all recorded elevating and descending laryngeal, hyoid, and pharyngeal muscles. Retrograde activation of esophagus and pharyngeal muscles occurred during the later phases, and laryngeal adductor was maximally activated in all phases of the vomit. During swallowing, the laryngeal adductor activation was followed immediately by brief activation of the laryngeal abductor. We concluded that retching functions to mix gastric contents with refluxed intestinal secretions and to impart an orad momentum to the bolus before vomiting. During retches, the airway is protected by glottal closure, and between retches, it is protected by ascent of the larynx and closure of the upper esophageal sphincter. The airway is protected by maximum glottal closure during vomiting. During swallowing, the airway is protected by laryngeal elevation and glottal closure followed by brief opening of the glottis, which may release subglottal pressure expelling material from the laryngeal vestibule.

Mechanisms of airway protection and upper esophageal sphincter opening during belching

1992 ◽  
Vol 262 (4) ◽  
pp. G621-G628 ◽  
Author(s):  
R. Shaker ◽  
J. Ren ◽  
M. Kern ◽  
W. J. Dodds ◽  
W. J. Hogan ◽  
...  
Keyword(s):  
Vocal Cord ◽  
Hyoid Bone ◽  
Upper Esophageal Sphincter ◽  
Air Injection ◽  
Distinctive Pattern ◽  
Airway Protection ◽  
Glottal Closure ◽  
Closure Mechanism ◽  
Esophageal Sphincter ◽  
Ues Opening

The mechanisms of airway protection, upper esophageal sphincter (UES) opening, and their coordination during belching were studied with a concurrent videoendoscopic, videofluoroscopic, and manometric technique. Analysis of videoendoscopic recordings revealed that glottal function during gastric and esophageal belching was similar and consisted of vocal cord adduction resulting in closure of intoitus to trachea, followed by anterior-caudad movement of the glottis, followed by slitlike or triangular UES opening. When a belch episode was associated with an intragastric pressure increase, in addition to the above features, there was approximation of arytenoids to the base of the epiglottis before the UES opened. Duration of vocal cord closure during belches induced by 40 ml intraesophageal air injection was significantly longer than belches induced by 20 ml (P less than 0.01). Vocal cord closure preceded the UES opening invariably. Analysis of videofluoroscopic recordings showed that hyoid bone movement during belching had a distinctive pattern different from its movement during swallowing. UES opening started generally when the hyoid bone was pulled anteriorly. Anterior hyoid excursion of 0.78 +/- 0.1 cm during belching was significantly shorter than its excursion of 1.8 +/- 0.09 cm during swallowing (P less than 0.01). We conclude that glottal closure is an integral component of both esophageal and gastric belch reflexes that prevents aspiration of regurgitated material into the airway. Glottal closure mechanism during belching has two tiers of closure: 1) vocal cord closure and 2) aryepiglottic approximation. Glottal and UES functions are closely coordinated during belching, and finally, during belching, UES is pulled open after its relaxation.

Parathyroid gland before and after cisplatin treatment

1987 ◽  
Vol 45 ◽  
pp. 860-861
Author(s):  
S.K. Aggarwal ◽  
J.M. Fadool
Keyword(s):  
Parathyroid Gland ◽  
Wistar Rats ◽  
Antitumor Agent ◽  
The Body ◽  
Cross Linking ◽  
Limiting Factor ◽  
Hormonal Changes ◽  
Primary Mechanism ◽  
Before And After ◽  
Dna Strands

Cisplatin (CDDP) a potent antitumor agent suffers from severe toxic side effects with nephrotoxicity being the major dose-limiting factor, The primary mechanism of its action has been proposed to be through its cross-linking DNA strands. It has also been shown to inactivate various transport enzymes and induce hypocalcemia and hypomagnesemia that may be the underlying cause for some of its toxicities. The present is an effort to study its influence on the parathyroid gland for any hormonal changes that control calcium levels in the body.Male Swiss Wistar rats (Crl: (WI) BR) weighing 200-300 g and of 60 days in age were injected (ip) with cisplatin (7mg/kg in normal saline). The controls received saline injections only. The animals were injected (iv) with calcium (0.5 ml of 10% calcium gluconate/day) and were killed by decapitation on day 1 through 5. Trunk blood was collected in heparinized tubes.

Motor projection patterns to the hind limb of normal and paralysed chick embryos

Development ◽  
1982 ◽  
Vol 72 (1) ◽  
pp. 269-286
Author(s):  
N. G. Laing
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
Hind Limb ◽  
Muscle Volume ◽  
Chick Embryos ◽  
Relative Contribution ◽  
Hind Limbs ◽  
Lateral Motor Column ◽  
Before And After ◽  
Major Period

Counts were made of the number of motoneurons innervating the hind limbs of 10-day normal and paralysed chick embryos whose right hind limb buds had been subjected to varying degrees of amputation prior to innervation. The number of motoneurons on the intact sides of the paralysed embryos was found to be similar to the number present in normal embryos prior to the major period of motoneuron death. Since it has previously been shown that paralysis does not increase the number of motoneurons generated, this means that normal motoneuron death was largely prevented in the paralysed embryos. There were differences in the distributions of motoneurons in the rostrocaudal axis of the spinal cord between normal and paralysed embryos. Therefore, cell death does not eliminate a uniform fraction of motoneurons throughout the rostrocaudal extent of the chick embryo lumbar lateral motor column. It is also argued that there are differences in the relative contribution of the various lumbosacral levels to different parts of the limb, e.g. the shank, before and after the period of cell death. In both normal and paralysed embryos there was a linear relationship between the volume of limb muscle which developed after amputation and the number of motoneurons surviving in the spinal cord. There was no evidence of a ‘compression’ of motoneurons into the remaining muscle either after amputation alone or after amputation combined with paralysis. Motoneurons are therefore rigidly specified for certain parts of the limb. The relationship between motoneuron number and muscle volume on the amputated side differed from that of the intact side. For a similar increase in muscle volume there was a smaller increase in motoneuron number on the intact sides. This suggested a parallel to the paradoxically small increase in motoneuron number that occurs on the addition of a supernumerary limb.

Relative peripheral and central chemosensory responses to metabolic alkalosis

1983 ◽  
Vol 245 (6) ◽  
pp. R873-R880 ◽  
Author(s):  
M. Pokorski ◽  
S. Lahiri
Keyword(s):  
Steady State ◽  
Metabolic Alkalosis ◽  
Central Effect ◽  
Co2 Partial Pressure ◽  
Ventilatory Responses ◽  
Relative Contribution ◽  
Before And After ◽  
Ventilatory Effect ◽  
Peripheral Effect ◽  
Steady State Levels

We investigated the relative contribution of peripheral and central chemosensory mechanisms to ventilatory responses to metabolic alkalosis in anesthetized cats by simultaneously measuring steady-state carotid body chemosensory activity and ventilation. The effects of graded steady-state levels of metabolic alkalosis at constant levels of arterial O2 and CO2 partial pressure (PaO2 and PaCO2, respectively) were studied first. Then the responses to isocapnic hypoxia and hyperoxic hypercapnia before and after the induction of a given level of metabolic alkalosis were studied. From the relationship between the carotid chemosensory activity and ventilation, the contribution of the two chemosensory mechanisms was estimated. The depression of ventilation that could not be accounted for by a decrease in the carotid chemosensory activity is attributed to the central effect. We found that metabolic alkalosis decreased both carotid chemosensory activity and ventilation at all levels of PaO2 or PaCO2. The ventilatory effect of alkalosis increased during hypoxia due to suppression of both peripheral chemosensory input and its interaction with the central CO2-H+ drive. During hyperoxia the central effect of alkalosis was predominant, although the peripheral effect increased with hypercapnia. We conclude that acute metabolic alkalosis suppresses both peripheral and central chemosensory drives, and its ventilatory effect grows larger with decreasing PaO2.

scholarly journals Pre- and intraoperative acoustic and functional assessment of the novel APrevent® VOIS implant during routine medialization thyroplasty

2019 ◽  
Vol 277 (3) ◽  
pp. 809-817
Author(s):  
Guan-Yuh Ho ◽  
Matthias Leonhard ◽  
Doris-Maria Denk-Linnert ◽  
Berit Schneider-Stickler
Keyword(s):  
Vocal Fold ◽  
Type I ◽  
The Novel ◽  
Glottal Closure ◽  
Medialization Thyroplasty ◽  
Before And After ◽  
Glottal Insufficiency ◽  
The Mean ◽  
Acoustic Analyses ◽  
Short Time

Abstract Purpose Persistent unilateral vocal fold paralysis (UFVP) with glottal insufficiency often requires type I medialization thyroplasty (MT). Previous implants cannot be adjusted postoperatively if necessary. The newly developed APrevent® VOIS implant (VOIS) can provide postoperative re-adjustment to avoid revision MT. The objective of this pilot study is to evaluate the VOIS intraoperatively concerning voice improvement, surgical feasibility and device handling. Methods During routine MT, VOIS was applied short time in eight patients before the regular implantation of the Titanium Vocal Fold Medialization Implant (TVFMI™). In all patients, perceptual voice sound analysis using R(oughness)–B(reathiness)–H(oarseness)-scale, measurement of M(aximum)–P(honation)–T(ime) and glottal closure in videolaryngoscopy were performed before and after implanting VOIS/TVFMI™. Acoustic analyses of voice recordings were performed using freeware praat. Surgical feasibility, operative handling and device fitting of VOIS and TVFMI™ were assessed by the surgeon using V(isual)-A(nalog)-S(cale). Data were statistically analyzed with paired t test. Result All patients showed significant improvement of voice sound parameters after VOIS/TVFMI™ implantation. The mean RBH-scale improved from preoperative R = 2.1, B = 2.3, H = 2.5 to R = 0.6, B = 0.3, H = 0.8 after VOIS and R = 0.5, B = 0.3, H = 0.8 after TVFMI™ implantation. The mean MPT increased from preoperative 7.9 to 14.6 s after VOIS and 13.8 s after TVFMI™ implantation. VOIS/TVFMI™ achieved complete glottal closure in 7/8 patients. The satisfaction with intraoperative device fitting and device handling of VOIS was as good as that of TVFMI™. Conclusion The novel APrevent® VOIS implant showed similar intraoperative voice improvement compared to routinely used TVFMI™ without adverse device events and with safe device fitting.

Effects of atropine on potentiation of exercise-induced bronchospasm by cold air

1978 ◽  
Vol 45 (2) ◽  
pp. 238-243 ◽  
Author(s):  
E. C. Deal ◽  
E. R. McFadden ◽  
R. H. Ingram ◽  
J. J. Jaeger
Keyword(s):  
Ambient Air ◽  
Small Airways ◽  
Flow Limitation ◽  
Ambient Conditions ◽  
Cold Air ◽  
Relative Contribution ◽  
Maximal Expiratory Flow ◽  
Before And After ◽  
Expiratory Flow ◽  
Exercise Induced

The role of vagal efferent activity in the cold air potentiation of exercise-induced asthma was assessed by exercising nine subjects who breathed air at ambient and subfreezing temperatures before and after cholinergic blockade. Lung volumes and maximal expiratory flow volume curves with air and with 80% helium-20% oxygen were obtained before and 5--10 min after each challenge. Isovolume comparisons of maximal expiratory flow rates with the two gases were used to assess relative contributions of large and small airways to flow limitation. Exercise under ambient conditions resulted in the expected airway obstruction and cold air exaggerated the response. Atropine pretreatment had no effect on the cold air potentiation. After atropine with ambient air exercise, there was an increase in the relative contribution of large airways to flow limitation, whereas exercise with cold air resulted in an increase in the contribution of small airways. We concluded that the potentiating effects of cold air are local and suggest that the immediate stimulus is related to cooling of intrathoracic airways.

scholarly journals Sildenafil (Viagra®) Prevents Cox-1/ TXA2 Pathway-Mediated Vascular Hypercontractility in ApoE-/- Mice

2017 ◽  
Vol 44 (5) ◽  
pp. 1796-1809 ◽  
Author(s):  
Marcos A.S. Leal ◽  
Ananda T. Dias ◽  
Marcella L. Porto ◽  
Bruna F. Brun ◽  
Agata L. Gava ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Proinflammatory Cytokines ◽  
Contractile Response ◽  
Wild Type ◽  
Beneficial Effects ◽  
Relative Contribution ◽  
Before And After ◽  
Cox 2 ◽  
Phosphodiesterase 5 ◽  
Cox 1

Background/Aims: The atherosclerotic apolipoprotein E-deficient (apoE-/-) mouse exhibits impaired vasodilation and enhanced vasoconstriction responsiveness. The objectives of this study were: a) to determine the relative contribution of cyclooxygenases (Cox-1 and Cox-2), thromboxane A2 (TXA2) and endothelin-1 (ET-1) to enhancing vascular hyperresponsiveness in this model of atherosclerosis and b) to investigate the beneficial effects of the phosphodiesterase 5 inhibitor sildenafil on this endothelial dysfunction. Methods: Adult male apoE-/- mice were treated with sildenafil (40 mg/kg/day, for 3 weeks) and compared with non-treated ApoE-/- and wild-type mice. The beneficial effects of sildenafil on vascular contractile response to phenylephrine (PE) in aortic rings were evaluated before and after incubation with Cox-1 (SC-560) or Cox-2 (NS-398) inhibitors or the TP antagonist SQ-29548, and on contractile responsiveness to ET-1. Results: ApoE-/- mice exhibited enhanced vasoconstriction to PE (Rmax ∼35%, p<0.01), which was prevented by treatment with sildenafil. The enhanced PE-induced contractions were abolished by both Cox-1 inhibition and TP antagonist, but were not modified by Cox-2 inhibition. Aortic rings from ApoE-/- mice also exhibited enhanced contractions to ET-1 (Rmax ∼30%, p<0.01), which were attenuated in sildenafil-treated ApoE-/- mice. In addition, we observed augmented levels of vascular proinflammatory cytokines in ApoE-/- mice, which were partially corrected by treatment with sildenafil (IL-6, IL-10/IL-6 ratio and MCP-1). Conclusion: The present data show that the Cox-1/TXA2 pathway prevails over the Cox-2 isoform in the mediation of vascular hypercontractility observed in apoE-/-mice. The results also show a beneficial effect of sildenafil on this endothelial dysfunction and on the proinflammatory cytokines in atherosclerotic animals, opening new perspectives for the treatment of other endothelium-related cardiovascular abnormalities.

Capsaicin-induced activation of pulmonary vagal C fibers produces reflex laryngeal closure in the rat

2006 ◽  
Vol 101 (4) ◽  
pp. 1104-1112 ◽  
Author(s):  
I-Jung Lu ◽  
Kun-Ze Lee ◽  
Ji-Chuu Hwang
Keyword(s):  
Intravenous Administration ◽  
Digital Camera ◽  
Vocal Folds ◽  
Emg Activity ◽  
Glottal Closure ◽  
C Fibers ◽  
Before And After ◽  
Subglottal Pressure ◽  
Male Wistar Rats ◽  
The Right

Our recent studies show that intravenous administration of capsaicin induces enhancement of the intralaryngeal thyroarytenoid (TA) branch but a reduction of the intralaryngeal abducent branch, suggesting that the glottis is likely closed by capsaicin. The aim of the present study was to examine whether the glottis is adducted by intravenous administration of capsaicin. Electromyographic (EMG) activity of the TA muscle, subglottal pressure (SGP), and glottal behavior were evaluated before and after intravenous administration of capsaicin in male Wistar rats that were anesthetized and tracheostomized. Catheters were placed in the femoral artery and vein, as well as in the right jugular vein. Low and high doses of capsaicin (0.625 and 1.25 μg/kg) produced apnea and increases in the amplitude of the TA EMG. This enhancement of the TA EMG was observed during apnea as well as during recovery from apnea. Moreover, the onset of the TA EMG was advanced such that it commenced earlier during inspiration. Concomitantly, the SGP substantially increased. Increases in both the TA EMG and SGP were abolished after bilateral sectioning of the recurrent laryngeal nerve. In some animals, movement of the vocal folds was recorded by taking a motion picture with a digital camera under a surgical microscope. With intravenous administration of capsaicin, a tight glottal closure, decreases in blood pressure, and bradycardia were observed. These results strongly suggest that glottal closure is reflexively induced by intravenous administration of capsaicin and that closure of the glottis is beneficial for the defense of the airway and lungs when an animal is exposed to environmental irritants.

Relative contribution of vasodilator prostanoids and NO to metabolic vasodilation in the human forearm

1999 ◽  
Vol 276 (2) ◽  
pp. H663-H670 ◽  
Author(s):  
Stephen J. Duffy ◽  
Gishel New ◽  
Binh T. Tran ◽  
Richard W. Harper ◽  
Ian T. Meredith
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Venous Occlusion ◽  
Healthy Humans ◽  
Relative Contribution ◽  
Prostanoid Production ◽  
Before And After ◽  
Forearm Exercise ◽  
Exercise Induced ◽  
Metabolic Vasodilation

Although many factors are thought to contribute to the regulation of metabolic vasodilation in skeletal muscle vasculature, recent interest has focused on the role of the endothelium. We examined the relative roles of nitric oxide (NO) and of vasodilator prostanoids in the control of metabolically induced functional hyperemia in the forearm of humans. In 43 healthy volunteers [24 ± 5 (SD) yr] we assessed resting and functional hyperemic blood flow (FHBF) in response to 2 min of isotonic forearm exercise before and after inhibition of NO and/or vasodilator prostanoid production with intra-arterial N G-monomethyl-l-arginine (l-NMMA, 2 mg/min) and aspirin (ASA, 3 mg/min), respectively. Blood flow was measured using venous occlusion plethysmography.l-NMMA and ASA decreased resting forearm blood flow by 42% ( P < 0.0001) and 23% ( P < 0.0001), respectively, whereas infusion of ASA followed byl-NMMA reduced flow by a further 24% ( P < 0.05).l-NMMA reduced peak FHBF by 18% [from 13.9 ± 1.0 to 11.4 ± 1.1 (SE) ml ⋅ 100 ml forearm−1 ⋅ min−1, P = 0.003] and the volume “repaid” after 1 and 5 min by 25% (8.9 ± 0.7 vs. 6.7 ± 0.7 ml/100 ml, P < 0.0001) and 37% (26.6 ± 1.8 vs. 16.8 ± 1.6 ml/100 ml, P < 0.0001). ASA similarly reduced peak FHBF by 19% (from 14.5 ± 1.1 to 11.8 ± 0.9 ⋅ 100 ml forearm−1 ⋅ min−1, P < 0.001) and the volume repaid after 1 and 5 min by 14% (7.5 ± 0.6 vs. 6.4 ± 0.6 ml/100 ml, P = 0.0001) and 20% (21.2 ± 1.5 vs. 16.9 ± 1.5 ml/100 ml, P < 0.0001), respectively. The coinfusion of ASA andl-NMMA did not decrease FHBF to a greater extent than either agent alone. These data suggest that endothelium-derived NO and vasodilator prostanoids contribute to resting blood flow and metabolic vasodilation in skeletal muscle vasculature in healthy humans. Although these vasodilator mechanisms operate in parallel in exercise-induced hyperemia, they appear not to be additive. Other mechanisms must also be operative in metabolic vasodilation.

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