Response of Laryngeal Airway Resistance to Chemoreceptor Stimulation: Effect of Pulmonary Afferent Denervation

1982 ◽  
Vol 90 (6) ◽  
pp. 723-727
Author(s):  
Thomas V. McCaffrey

The response of laryngeal airway resistance to chemoreceptor stimulation was measured before and after vagotomy in ten anesthetized dogs. With the vagus nerves intact, stimulation of chemoreceptors produced a decrease in both inspiratory and expiratory laryngeal resistance. After bilateral vagotomy below the origin of the recurrent laryngeal nerves, stimulation of chemoreceptors produced a smaller decrease in inspiratory laryngeal resistance and an increase in expiratory laryngeal resistance. We concluded that pulmonary afferent input to the respiratory neurons maintains a low airway resistance during chemoreceptor stimulation.

1980 ◽  
Vol 89 (5) ◽  
pp. 462-466 ◽  
Author(s):  
Thomas V. McCaffrey ◽  
Eugene B. Kern

The response of laryngeal airway resistance to pulmonary receptor stimulation was studied in 20 mongrel dogs anesthetized with α-chloralose (80 mg/kg). Stimulation of pulmonary stretch receptors by lung inflation inhibited the phasic variation of laryngeal resistance during respiration and produced a sustained reduction of laryngeal resistance, which was related to lung inflation pressure. Stimulation of pulmonary J-receptors with capsaicin produced apnea and a large increase in laryngeal resistance. Capsaicin produced this reflex when injected into the pulmonary circulation but not when injected into the systemic circulation. Irritant receptor stimulation with histamine hydrochloride produced tachypnea and a reduction in inspiratory laryngeal resistance. Pulmonary receptor reflexes were abolished by dividing the vagus nerves distal to the origin of the recurrent laryngeal nerves. Laryngeal reflexes may be important in the regulation of respiration and the production of physiologic and pathologic alterations in pulmonary function.


1980 ◽  
Vol 87 (1) ◽  
pp. 229-236
Author(s):  
G. Benchetrit ◽  
P. Dejours

1. Ventilation was recorded by pneumotachography, before and after bilateral vagotomy, in conscious tortoises (Testudo horsfieldi) (breathing 0, 2, 3 or 4% CO2 in air or oxygen). 2. Each breath consists of expiratory and inspiratory phases and an apneic plateau (absence of air flow). Inhalation of hypercapnic mixtures led to increased ventilatory flow, augmentation of tidal volume, and an increase in respiratory frequency through the shortening of the apneic plateau. 3. Intact tortoises breathing hypercapnic-hyperoxic mixtures hyperventilated less than with hypercapnic-normoxic mixtures. 4. In bivagotomized animals, the respiratory frequency decreased, the expiratory and inspiratory durations lengthened, and the apneic plateau was prolonged. The tidal volume was increased, but ventilation, nevertheless, decreased slightly. 5. Bivagotomized animals breathing hypercapnic-normoxic or hypercapnic-hyperoxic mixtures hyperventilated, but less than intact animals under the same conditions. 6. It is concluded that in tortoises there are: (1) peripheral chemoreceptors which are innervated by branches of the vagus nerves, and are sensitive to CO2; and (2) an extrathoracic, probably central, ventilatory CO2 drive.


2001 ◽  
Vol 85 (4) ◽  
pp. 1522-1532 ◽  
Author(s):  
Chao Qin ◽  
Margaret J. Chandler ◽  
Kenneth E. Miller ◽  
Robert D. Foreman

Electrical stimulation of vagal afferents or cardiopulmonary sympathetic afferent fibers excites C1–C2spinal neurons. The purposes of this study were to compare the responses of superficial (depth <0.35 mm) and deeper C1–C2 spinal neurons to noxious chemical stimulation of cardiac afferents and determine the relative contribution of vagal and sympathetic afferent pathways for transmission of noxious cardiac afferent input to C1–C2 neurons. Extracellular potentials of single C1–C2 neurons were recorded in pentobarbital anesthetized and paralyzed male rats. A catheter was placed in the pericardial sac to administer a mixture of algogenic chemicals (0.2 ml) that contained adenosine (10− 3 M), bradykinin, histamine, serotonin, and prostaglandin E2(10− 5 M each). Intrapericardial chemicals changed the activity of 20/106 (19%) C1–C2 spinal neurons in the superficial laminae, whereas 76/147 (52%) deeper neurons responded to cardiac noxious input ( P < 0.01). Of 96 neurons responsive to cardiac inputs, 48 (50%) were excited (E), 41 (43%) were inhibited (I), and 7 were excited/inhibited (E-I) by intrapericardial chemicals. E or I neurons responsive to intrapericardial chemicals were subdivided into two groups: short-lasting (SL) and long-lasting (LL) response patterns. In superficial gray matter, excitatory responses to cardiac inputs were more likely to be LL-E than SL-E neurons. Mechanical stimulation of the somatic field from the head, neck, and shoulder areas excited 85 of 95 (89%) C1–C2 spinal neurons that responded to intrapericardial chemicals; 31 neurons were classified as wide dynamic range, 49 were high threshold, 5 responded only to joint movement, and no neuron was classified as low threshold. For superficial neurons, 53% had small somatic fields and 21% had bilateral fields. In contrast, 31% of the deeper neurons had small somatic fields and 46% had bilateral fields. Ipsilateral cervical vagotomy interrupted cardiac noxious input to 8/30 (6 E, 2 I) neurons; sequential transection of the contralateral cervical vagus nerve (bilateral vagotomy) eliminated the responses to intrapericardial chemicals in 4/22 (3 E, 1 I) neurons. Spinal transection at C6–C7 segments to interrupt effects of sympathetic afferent input abolished responses to cardiac input in 10/10 (7 E, 3 I) neurons that still responded after bilateral vagotomy. Results of this study support the concept that C1–C2 superficial and deeper spinal neurons play a role in integrating cardiac noxious inputs that travel in both the cervical vagal and/or thoracic sympathetic afferent nerves.


1961 ◽  
Vol 201 (1) ◽  
pp. 134-138 ◽  
Author(s):  
Richard H. Ulmer ◽  
Walter C. Randall

Pressures were recorded simultaneously from the four cardiac chambers in anesthetized, open-chest dogs during electrical stimulation of the stellate ganglion before and after bilateral vagotomy. Augmentation of atrial contraction was shown to accompany that in the ventricles by increased atrial pressures, as well as by the direct recording of atrial force. Fast-speed records revealed the augmentation was primarily in the a-wave. In some experiments mean atrial pressures increased slightly, in others they remained essentially unchanged, and, in still others, declined during stimulation. The particular response in any given animal was not predictable. There was no consistent relationship between the change in right and left mean atrial pressures, although they showed simultaneous augmentation in amplitude of the a-wave. The augmented a-wave resulted in a significant increment in the atrioventricular pressure gradient during late diastole, and thus contributed to increased ventricular filling. Mean pressures consistently increased in both right and left ventricles during stellate stimulation.


1971 ◽  
Vol 49 (5) ◽  
pp. 420-426 ◽  
Author(s):  
Paul F. Mercer

Renal function was studied in rats before and after section of the vagus nerves at the level of the common carotid arteries. In the control group of rats, sodium output and volume rate of urine flow increased following vagal section but glomerular filtration rate did not change. This response was not altered in other rats by desoxycorticosterone acetate, vasopressin, or renal nerve section. This response was similar to that seen in rats in which both common carotid arteries had been occluded. The natriuresis following bilateral vagotomy did not occur in rats in which the blood pressure was prevented from rising by means of aortic constriction. It is concluded that a natriuresis does occur following bilateral vagotomy. This natriuresis may be a result of the effect of arterial blood pressure following the vagotomy.


1980 ◽  
Vol 89 (3) ◽  
pp. 209-214 ◽  
Author(s):  
Thomas V. McCaffrey ◽  
Eugene B. Kern

The resistance of the larynx to airflow was measured during hypercapnia, hypoxemia, and stimulation of peripheral chemoreceptors by sodium cyanide and phenyl diguanide in 15 dogs anesthetized with α-chloralose (80 mg/kg). Laryngeal airway resistance (R1 x) was obtained by measuring the pressure difference between the subglottic region and the mouth while a constant flow of humidified air was passed through the larynx. During spontaneous respiration, R1 x varies with the phase of the respiratory cycle: R1 x is high during expiration (mean ± SEM = 0.79 ± 0.19 cm H2O/L/sec) and falls just before inspiration (0.49 ± 0.14 cm H2O/L/sec) and remains low until the end of inspiration. Hypercapnia, hypoxemia, and chemoreceptor stimulation each stimulated respiration and simultaneously decreased R1 x during both inspiration and expiration. Chemoreceptor stimulation with phenyl diguanide (100 μg/kg) and sodium cyanide (100 μg/kg) produced similar decreases in R1 x whether injected into the right atrium or left ventricle, indicating that these agents are not stimulating pulmonary receptors. The decrease in R1 x during stimulation of chemoreceptors will decrease the work of ventilation. This study suggests that the control of ventilation involves the active regulation of the resistance of the laryngeal airway.


1995 ◽  
Vol 32 (2) ◽  
pp. 138-144 ◽  
Author(s):  
David J. Zajac

Laryngeal airway resistance during vowel production was determined for 10 children without cleft palate and 14 children with cleft palate and adequate velopharyngeal function. The children with cleft palate were further grouped according to either complete or incomplete velopharyngeal closure. All children performed a syllable repetition task with nostrils occluded at self-determined effort and a targeted effort typical of adult speech. Results indicated that all children exhibited significantly greater laryngeal resistance at self-determined effort. No significant differences occurred among the groups of children at either effort level. Some children with incomplete velopharyngeal closure, however, tended to exhibit relatively increased laryngeal resistance at the targeted effort level when their nostrils were unoccluded. Implications for a regulation-control model of speech production and clinical assessment are discussed.


1983 ◽  
Vol 50 (1) ◽  
pp. 178-191 ◽  
Author(s):  
M. H. Droge ◽  
R. B. Leonard

Rhythmic motoneuronal activity was recorded from decerebrated, paralyzed stingrays and compared with electromyograms recorded from the same animals. Before and after paralysis, a rostral-to-caudal sequence of alternation occurred between dorsal (elevator) and ventral (depressor) efferents. The swimming pattern was thus observed in the absence of phasic afferent input, and this constitutes fictive locomotion. After paralysis, both the intersegmental delay (time between activation at progressively caudal recording sites) and the burst duration remained linearly related to the swim cycle period. In many instances, neither the slope nor the intercept was significantly altered by immobilization. The intercepts all fell near the origin, indicating that the fictive rhythm remains constant phase coupled. Although the swimming rhythm was obtained after paralysis, some differences occurred. These included fewer and shorter spontaneous sequences, a greater range of cycle periods, and longer burst durations. During fictive swimming, the burst duration:cycle period ratio usually increased to 0.53 from 0.39 observed before paralysis. Therefore, the silent periods seen between burst discharges in antagonist efferents during movement were often absent after paralysis. Mechanical stimulation of the tail reduced both cycle periods and burst durations; however, the burst:cycle ratio remained greater than or equal to 0.50. The linear relation between burst duration and cycle period found for spontaneous sequences was not changed by stimulation of the tail. During fictive swimming the inter- and intrasegmental coupling that characterizes stingray swimming becomes labile. Abnormal coupling appears more often during sequences with long swim cycles. Intrasegmental coupling is tighter than intersegmental coupling at any cycle period. Rhythmic activity at one segmental level can be independent of activity at other levels. This suggests that multiple oscillator circuits exist that are not dependent on propriospinal circuits interconnecting different segments. Rhythmicity in elevator and depressor motoneurons is not dependent on reciprocal connections between the circuitry driving the motor nuclei. Therefore, separate oscillators for elevators and depressors appear to be present within one spinal segment.


1976 ◽  
Vol 231 (4) ◽  
pp. 1279-1284 ◽  
Author(s):  
DR Kostreva ◽  
GL Hess ◽  
EJ Zuperku ◽  
J Neumark ◽  
RL Coon ◽  
...  

Excitatory cardiovascular responses to electrically stimulated upper thoracic sympathetic afferent nerves were observed in halothane-anesthetized mongrel dogs and monkeys. The central end of the transected ventral limb of the left ansa subclavia was stimulated before and after several types of denervation. Significant increases in right and left ventricular maximum systolic pressures, systolic and diastolic systemic blood pressures, and aortic flow were observed. The carotid sinuses were denervated bilaterally and stimulation of the ansa was repeated. The cardiovascular responses to stimulation of the ventral ansa after carotid sinus denervation were greater in magnitude than those observed prior to denervation. This carotid sinus modulation of cardiovascular responses was observed in dogs and monkeys. Cardiovascular responses to stimulation of the ventral ansa after bilateral vagotomy were significantly less than the responses observed after carotid sinus denervation prior to vagotomy. However, the responses after vagotomy were statistically identical to responses obtained while stimulating the ventral ansa when the carotid sinuses and vagi remained intact.


1991 ◽  
Vol 260 (4) ◽  
pp. H1353-H1358
Author(s):  
M. Hay ◽  
E. M. Hasser ◽  
K. P. Undesser ◽  
V. S. Bishop

Activation of the area postrema by either electrical stimulation or chemical application of L-glutamate has been shown to result in an enhancement of cardiovascular baroreflexes similar to that seen with systemic infusions of arginine vasopressin (AVP). In addition, it has been found that the effects of AVP on baroreflex inhibition of renal sympathetic nerve activity (RSNA) are similar to those observed with phenylephrine following lesions of the area postrema or after partial denervation of baroreceptor afferents. The present study was undertaken to determine the role of baroreceptor afferent input on area postrema stimulation-induced decreases in sympathetic activity. In anesthetized rabbits, the responses of arterial pressure, heart rate, and RSNA to area postrema electrical stimulation were obtained before and after progressive sinoaortic denervation and vagotomy. Stimulation of the area postrema in carotid sinus-denervated animals consistently decreased RSNA in a frequency-dependent manner. However, following bilateral removal of both the aortic nerves and the vagi, electrical stimulation of the area postrema had no effect on RSNA. These results suggest that the ability of area postrema stimulation to inhibit RSNA is dependent on the presence of baroreceptor afferent input.


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