Effect of Almitrine on Ventilation and on Diaphragm and Geniohyoid Muscle Activity in the Rat

1996 ◽  
Vol 91 (3) ◽  
pp. 337-345 ◽  
Author(s):  
Ken D. O'halloran ◽  
Aidan K. Curran ◽  
Aidan Bradford

1. Ventilation was measured during normoxia, hypoxia and hypercapnia before and after administration of almitrine in conscious, unrestrained, tracheostomized rats with the superior laryngeal nerves intact or cut. In superior laryngeal nerve-intact animals breathing air, almitrine increased minute ventilation due to an increase in respiratory frequency with no change in tidal volume. In superior laryngeal nerve-sectioned animals, the minute ventilatory response to almitrine was reduced due to a reduced tidal volume component of the response. Almitrine increased the ventilatory response to hypercapnia in superior laryngeal nerve-intact but not in sectioned animals. 2. In anaesthetized, vagotomized rats breathing spontaneously through a low-cervical tracheostomy, diaphragm and geniohyoid electromyographic activities were recorded. Arterial blood pressure and rectal temperature were continuously monitored. A single dose of almitrine was administered intravenously. In all animals, the geniohyoid muscle had phasic inspiratory activity which slightly preceded diaphragm activity. Almitrine had no effect on respiratory frequency or inspiratory and expiratory duration but increased mean peak integrated diaphragm (+29.3 ±13.6%) and geniohyoid (+ 132.0 ±21.3%) muscle activity. 3. These results show that almitrine exerts part of its ventilatory effects through superior laryngeal nerve afferents. Almitrine preferentially excites upper airway compared with diaphragm muscle activity, suggesting a potential role in the alleviation of obstructive apnoea.

1997 ◽  
Vol 83 (3) ◽  
pp. 768-775 ◽  
Author(s):  
Aidan K. Curran ◽  
Peter R. Eastwood ◽  
Craig A. Harms ◽  
Curtis A. Smith ◽  
Jerome A. Dempsey

Curran, Aidan K., Peter R. Eastwood, Craig A. Harms, Curtis A. Smith, and Jerome A. Dempsey. Superior laryngeal nerve section alters responses to upper airway distortion in sleeping dogs. J. Appl. Physiol. 83(3): 768–775, 1997.—We investigated the effect of superior laryngeal nerve (SLN) section on expiratory time (Te) and genioglossus electromyogram (EMGgg) responses to upper airway (UA) negative pressure (UANP) in sleeping dogs. The same dogs used in a similar intact study (C. A. Harms, C. A., Y.-J. Zeng, C. A. Smith, E. H. Vidruk, and J. A. Dempsey. J. Appl. Physiol. 80: 1528–1539, 1996) were bilaterally SLN sectioned. After recovery, the UA was isolated while the animal breathed through a tracheostomy. Square waves of negative pressure were applied to the UA from below the larynx or from the mask (nares) at end expiration and held until the next inspiratory effort. Section of the SLN increased eupneic respiratory frequency and minute ventilation. Relative to the same dogs before SLN section, sublaryngeal UANP caused less Te prolongation while activation of the genioglossus required less negative pressures. Mask UANP had no effect on Te or EMGgg activity. We conclude that the SLN 1) is not obligatory for the reflex prolongation of Te and activation of EMGgg activity produced by UANP and 2) plays an important role in the maintenance of UA stability and the pattern of breathing in sleeping dogs.


1988 ◽  
Vol 64 (6) ◽  
pp. 2544-2551 ◽  
Author(s):  
H. Rigatto ◽  
C. Wiebe ◽  
C. Rigatto ◽  
D. S. Lee ◽  
D. Cates

We studied the ventilatory response to hypoxia in 11 unanesthetized newborn kittens (n = 54) between 2 and 36 days of age by use of a flow-through system. During quiet sleep, with a decrease in inspired O2 fraction from 21 to 10%, minute ventilation increased from 0.828 +/- 0.029 to 1.166 +/- 0.047 l.min-1.kg-1 (P less than 0.001) and then decreased to 0.929 +/- 0.043 by 10 min of hypoxia. The late decrease in ventilation during hypoxia was related to a decrease in tidal volume (P less than 0.001). Respiratory frequency increased from 47 +/- 1 to 56 +/- 2 breaths/min, and integrated diaphragmatic activity increased from 14.9 +/- 0.9 to 20.2 +/- 1.4 arbitrary units; both remained elevated during hypoxia (P less than 0.001). Younger kittens (less than 10 days) had a greater decrease in ventilation than older kittens. These results suggest that the late decrease in ventilation during hypoxia in the newborn kitten is not central but is due to a peripheral mechanism located in the lungs or respiratory pump and affecting tidal volume primarily. We speculate that either pulmonary bronchoconstriction or mechanical uncoupling of diaphragm and chest wall may be involved.


1984 ◽  
Vol 56 (3) ◽  
pp. 746-752 ◽  
Author(s):  
E. van Lunteren ◽  
W. B. Van de Graaff ◽  
D. M. Parker ◽  
J. Mitra ◽  
M. A. Haxhiu ◽  
...  

The effects of negative pressure applied to just the upper airway on nasal and laryngeal muscle activity were studied in 14 spontaneously breathing anesthetized dogs. Moving average electromyograms were recorded from the alae nasi (AN) and posterior cricoarytenoid (PCA) muscles and compared with those of the genioglossus (GG) and diaphragm. The duration of inspiration and the length of inspiratory activity of all upper airway muscles was increased in a graded manner proportional to the amount of negative pressure applied. Phasic activation of upper airway muscles preceded inspiratory activity of the diaphragm under control conditions; upper airway negative pressure increased this amount of preactivation. Peak diaphragm activity was unchanged with negative pressure, although the rate of rise of muscle activity decreased. The average increases in peak upper airway muscle activity in response to all levels of negative pressure were 18 +/- 4% for the AN, 27 +/- 7% for the PCA, and 122 +/- 31% for the GG (P less than 0.001). Rates of rise of AN and PCA electrical activity increased at higher levels of negative pressure. Nasal negative pressure affected the AN more than the PCA, while laryngeal negative pressure had the opposite effect. The effects of nasal negative pressure could be abolished by topical anesthesia of the nasal passages, while the effects of laryngeal negative pressure could be abolished by either topical anesthesia of the larynx or section of the superior laryngeal nerve. Electrical stimulation of the superior laryngeal nerve caused depression of AN and PCA activity, and hence does not reproduce the effects of negative pressure.(ABSTRACT TRUNCATED AT 250 WORDS)


PEDIATRICS ◽  
1983 ◽  
Vol 71 (4) ◽  
pp. 634-638
Author(s):  
Manuel Durand ◽  
Ellen McCann ◽  
June P. Brady

The effect of continuous positive airway pressure (CPAP) on the ventilatory response to CO2 in newborn infants is unknown. The CO2 response to 4% CO2 in air was studied in nine preterm infants without lung disease before and during administration of CPAP (4 to 5 cm H2O) delivered by face mask. Minute ventilation, tidal volume, respiratory frequency, and end-tidal Pco2 were measured, and the slope and intercept of the CO2 response were calculated. Respiratory pattern and changes in oxygenation were also analyzed by measuring inspiratory and expiratory time, mean inspiratory flow, mean expiratory flow, effective respiratory timing, endtidal Po2, and transcutaneous Po2. CPAP significantly decreased minute ventilation from 278.7 to 197.6 mL/mm/kg (P < .001). Tidal volume and respiratory frequency were also significantly decreased. The slope of the CO2 response during CPAP was not significantly different from the slope before CPAP (36 v 33 mL/min/kg/mm Hg, P > .1), but the intercept was shifted to the right (P < .001). The decrease in respiratory frequency was primarily due to a prolongation of expiratory time (P < .05). In addition, transcutaneous Po2 increased during administration of CPAP (P < .001). These findings indicate that: (1) CPAP significantly decreases ventilation in preterm infants without lung disease, affecting both tidal volume and respiratory frequency; (2) CPAP does not appreciably alter the ventilatory response to CO2; (3) the changes in respiratory frequency are primarily accounted for by a prolongation of expiratory time; (4) CPAP improves oxygenation.


1993 ◽  
Vol 75 (4) ◽  
pp. 1552-1558 ◽  
Author(s):  
S. Okabe ◽  
W. Hida ◽  
Y. Kikuchi ◽  
H. Kurosawa ◽  
J. Midorikawa ◽  
...  

To examine the effects of sustained hypoxia on upper airway and chest wall muscle activity in humans, we measured genioglossus muscle (GG) activity, inspiratory intercostal muscle (IIM) activity, and ventilation during sustained hypoxia in 17 normal subjects and 17 patients with obstructive sleep apnea (OSA). The trial of sustained hypoxia was performed as follows: after an equilibration period of 3 min, isocapnic hypoxia (arterial O2 saturation = 80 +/- 2%) was maintained for 20 min. GG EMG was measured with a fine-wire electrode inserted percutaneously, and IIM EMG was measured with surface electrodes. Ventilatory response to sustained hypoxia was initially increased and subsequently decreased. Stable phasic GG activity during spontaneous tidal breathing was observed in 6 normal subjects and 10 patients with OSA. Responses of GG and IIM activities to sustained hypoxia showed a biphasic response qualitatively similar to the ventilatory response in these 16 subjects. The absolute value of the subsequent decline in GG activity was similar to that of the initial increase, whereas the subsequent decline in IIM activity was smaller than that of the initial increase. Percent GG activity was significantly lower than both percent IIM activity and percent minute ventilation during the decline and plateau phases. There were no significant differences in ventilatory and EMG responses between the normal subjects and the patients with OSA. We conclude that, during wakefulness, upper airway muscle activity declined to a greater extent than inspiratory pump muscle activity during sustained hypoxia.


1993 ◽  
Vol 75 (1) ◽  
pp. 416-423 ◽  
Author(s):  
J. A. Wozniak ◽  
A. A. Hutchison ◽  
P. C. Kosch

Term human newborns were challenged with a 2–3% CO2 gas mixture during quiet sleep. A common ventilatory response, consisting of increased tidal volume with no change in respiratory frequency or timing, was observed in all eight subjects. Minute ventilation and mean inspiratory and expiratory flow rates were elevated in all eight subjects [38 +/- 8 (SE), 38 +/- 22, and 39 +/- 9%, respectively]. Diaphragm, intercostal, and posterior cricoarytenoid (PCA) muscle activities during inspiration were increased in four of eight, six of eight, and seven of eight subjects, respectively Changes in intercostal and PCA muscle activities correlated with changes in inspiratory flow rates (r = 0.77 and 0.66, respectively). Diaphragmatic braking of expiratory airflow varied between subjects during room air breathing and did not change in six subjects with CO2 breathing. The remaining two subjects increased postinspiratory inspiratory diaphragmatic activity. Baseline expiratory PCA activity was augmented with CO2 breathing in six of eight subjects and correlated with increases in mean expiratory airflow (r = 0.76). The newborn infant is capable of using a variety of breathing strategies to augment tidal volume and minute ventilation, and control of the upper airway appears to be critical in modulating airflow during CO2 breathing.


2015 ◽  
Vol 27 (3) ◽  
pp. 791-794 ◽  
Author(s):  
Hidetaka Imagita ◽  
Akira Nishikawa ◽  
Susumu Sakata ◽  
Yasue Nishii ◽  
Akira Minematsu ◽  
...  

2019 ◽  
Vol 126 (1) ◽  
pp. 111-123 ◽  
Author(s):  
Kun-Ze Lee

The present study was designed to investigate breathing patterns across the sleep-wake state following a high cervical spinal injury in rats. The breathing patterns (e.g., respiratory frequency, tidal volume, and minute ventilation), neck electromyogram, and electroencephalography of unanesthetized adult male rats were measured at the acute (i.e., 1 day), subchronic (i.e., 2 wk), and/or chronic (i.e., 6 wk) injured stages after unilateral contusion of the second cervical spinal cord. Cervical spinal cord injury caused a long-term reduction in the tidal volume but did not influence the sleep-wake cycle duration. The minute ventilation during sleep was usually lower than that during the wake period in uninjured animals due to a decrease in respiratory frequency. However, this sleep-induced reduction in respiratory frequency was not observed in contused animals at the acute injured stage. By contrast, the tidal volume was significantly lower during sleep in contused animals but not uninjured animals from the acute to the chronic injured stage. Moreover, the frequency of sigh and postsigh apnea was elevated in acutely contused animals. These results indicated that high cervical spinal contusion is associated with exacerbated sleep-induced attenuation of the tidal volume and higher occurrence of sleep apnea, which may be detrimental to respiratory functional recovery after cervical spinal cord injury. NEW & NOTEWORTHY Cervical spinal injury is usually associated with sleep-disordered breathing. The present study investigated breathing patterns across sleep-wake state following cervical spinal injury in the rat. Unilateral cervical spinal contusion significantly impacted sleep-induced alteration of breathing patterns, showing a blunted frequency response and exacerbated attenuated tidal volume and occurrence of sleep apnea. The result enables us to investigate effects of cervical spinal injury on the pathogenesis of sleep-disordered breathing and evaluate potential therapies to improve respiration.


2020 ◽  
Vol 10 (4) ◽  
Author(s):  
Parviz Amri ◽  
Novin Nikbakhsh ◽  
Seyed Reza Modaress ◽  
Ramin Nosrati

Background: Rigid bronchoscopy is often used to diagnose and treat the location of resection of the tracheal stenosis. It is a selective procedure for the dilatation of tracheal stenosis, especially when accompanied by respiratory distress. Objectives: We introduced patients who were diagnosed with tracheal stenosis and candidate for rigid bronchoscopy dilatation by the upper airway nerve blocks. Methods: This prospective observational study was conducted on 17 patients who underwent dilatation with rigid bronchoscopy in tracheal stenosis at Hospitals affiliated with Babol University of Medical Sciences from 2002 to 2017. The patients were given three nerve blocks, 6 bilateral superior laryngeal nerve block, bilateral glossopharyngeal nerve block, and recurrent laryngeal nerve block (transtracheal) before awake rigid bronchoscopy using 2% lidocaine. We evaluated the demographic data, the cause of tracheal stenosis, the quality of the airway nerve block (Intubation score), patients’ satisfaction from bronchoscopy and thoracic surgeons’ satisfaction. Complications of nerve blocks were recorded. Results: From 2002 to 2017, 17 patients (14 were male and 3 were) female with tracheal stenosis who were candidates for dilatation with bronchoscopy and accepted the upper nerve block were included. The quality of the block was acceptable in 16 (94%) patients. 15 patients received fentanyl, and only two patients did not need to intravenous sedation. The mean age of patients was 29.59 ± 11.59. The average satisfaction of the surgeon was 8.82 ± 1.13 and the satisfaction of patients with anesthesia was 8.89 ± 1.16. There was one serious complication (laryngospasm) in one patient. Conclusions: The upper airway nerve block method is a suitable anesthesia technique for patients with tracheal stenosis who are candidates for the tracheal dilatation with rigid bronoscopy, especially when the patient has respiratory distress and has not been evaluated before surgery.


PEDIATRICS ◽  
1984 ◽  
Vol 73 (5) ◽  
pp. 652-655
Author(s):  
Jonathan M. Couriel ◽  
Anthony Olinsky

The ventilatory response to acute hypercapnia was studied in 68 parents of victims of sudden infant death syndrome and 56 control subjects. Tidal volume, inspiratory time, and total respiratory cycle time were measured before and immediately after a vital capacity breath of 13% CO2 in oxygen. Instantaneous minute ventilation, mean inspiratory flow (tidal volume/inspiratory time), and respiratory timing (inspiratory time/total respiratory cycle time) were calculated. Both groups of subjects showed a marked increase in tidal volume (48.4% ± 26.5%), instantaneous minute ventilation (56% ± 35%), and tidal volume/inspiratory time (56.8% ± 33.5%) after inhalation of the test gas, with little change in inspiratory time/total respiratory cycle time. There were no significant differences between the two groups for ventilation before or after inhalation of the test gas. The ventilatory response to acute hypercapnia is mediated by the peripheral chemoreceptors. These results suggest that an inherited abnormality of peripheral chemoreceptor function is unlikely to be a factor leading to sudden infant death syndrome.


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