Breathing and upper airway CO2 in reptiles: role of the nasal and vomeronasal systems

1989 ◽  
Vol 256 (1) ◽  
pp. R91-R97
Author(s):  
E. L. Coates ◽  
G. O. Ballam
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Olfactory Nerve ◽  
Pause Duration ◽  
Thamnophis Sirtalis ◽  
Nerve Transection ◽  
Vomeronasal System ◽  
Upper Airways ◽  
Before And After

The ventilatory response of the garter snake, Thamnophis sirtalis, to 2% CO2 delivered to the upper airways (UA) was measured before and after the olfactory or vomeronasal nerves were transected. The UA (nasal cavities and mouth) were isolated from the gas source inspired into the lungs by inserting an endotracheal T tube into the glottis. CO2 was administered to the UA via a head chamber. The primary ventilatory response to UA CO2 was a significant decrease in ventilatory frequency (f) and minute ventilation. The decrease in f was caused by a significant increase in the pause duration. Tidal volume, expiratory duration, and inspiratory duration were not altered with UA CO2. The f response to UA CO2 was abolished with olfactory nerve transection, whereas vomeronasal nerve transection significantly increased the magnitude of the f depression. These results indicate that CO2-sensitive receptors are located in the nasal epithelium and that the olfactory nerves must be intact for the UA CO2 f response to be observed. In addition, the vomeronasal system appears to modulate the ventilatory response to UA CO2.

Ventilatory responses to carbon dioxide at low and high levels of oxygen are elevated after episodic hypoxia in men compared with women

2004 ◽  
Vol 97 (5) ◽  
pp. 1673-1680 ◽  
Author(s):  
Chris Morelli ◽  
M. Safwan Badr ◽  
Jason H. Mateika
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
High Oxygen ◽  
Set Point ◽  
Ventilatory Responses ◽  
Episodic Hypoxia ◽  
Before And After ◽  
Oxygen Gas ◽  
End Tidal

We hypothesized that the acute ventilatory response to carbon dioxide in the presence of low and high levels of oxygen would increase to a greater extent in men compared with women after exposure to episodic hypoxia. Eleven healthy men and women of similar race, age, and body mass index completed a series of rebreathing trials before and after exposure to eight 4-min episodes of hypoxia. During the rebreathing trials, subjects initially hyperventilated to reduce the end-tidal partial pressure of carbon dioxide (PetCO2) below 25 Torr. Subjects then rebreathed from a bag containing a normocapnic (42 Torr), low (50 Torr), or high oxygen gas mixture (150 Torr). During the trials, PetCO2 increased while the selected level of oxygen was maintained. The point at which minute ventilation began to rise in a linear fashion as PetCO2 increased was considered to be the carbon dioxide set point. The ventilatory response below and above this point was determined. The results showed that the ventilatory response to carbon dioxide above the set point was increased in men compared with women before exposure to episodic hypoxia, independent of the oxygen level that was maintained during the rebreathing trials (50 Torr: men, 5.19 ± 0.82 vs. women, 4.70 ± 0.77 l·min−1·Torr−1; 150 Torr: men, 4.33 ± 1.15 vs. women, 3.21 ± 0.58 l·min−1·Torr−1). Moreover, relative to baseline measures, the ventilatory response to carbon dioxide in the presence of low and high oxygen levels increased to a greater extent in men compared with women after exposure to episodic hypoxia (50 Torr: men, 9.52 ± 1.40 vs. women, 5.97 ± 0.71 l·min−1·Torr−1; 150 Torr: men, 5.73 ± 0.81 vs. women, 3.83 ± 0.56 l·min−1·Torr−1). Thus we conclude that enhancement of the acute ventilatory response to carbon dioxide after episodic hypoxia is sex dependent.

Ventilatory responses to hypoxia in rats pretreated with nonpeptide NK1 receptor antagonist CP-96,345

1994 ◽  
Vol 76 (4) ◽  
pp. 1528-1532 ◽  
Author(s):  
G. T. De Sanctis ◽  
F. H. Green ◽  
X. Jiang ◽  
M. King ◽  
J. E. Remmers
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Frequency Component ◽  
Nk1 Receptor ◽  
Adult Rats ◽  
Nk1 Receptors ◽  
Before And After ◽  
Sites Of Action

This study reports experiments designed to evaluate the role of neurokinin-1 (NK1) receptors for substance P (SP) in the ventilatory response to acute hypoxia. Ventilation was measured by indirect plethysmography in eight unanesthetized unrestrained adult rats before and after bolus injection of 1, 5, or 10 mg/kg (ip) of CP-96,345 (Pfizer), a potent nonpeptide competitive antagonist of the SP NK1 receptor. Ventilation was measured while the rats breathed air or 8% O2–92% N2 with and without administration of SP antagonist. Pretreatment with CP-96,345 decreased the magnitude of the hypoxic response in a dose-dependent fashion. Minute ventilation in rats pretreated with CP-96,345 was reduced by 22.1% (P < 0.05) at the highest dose (10 mg/kg), largely because of an attenuation of the frequency component. Although both control and treated rats responded to hypoxia with a decrease in duration of inspiration and expiration rats pretreated with CP-96,345 displayed a smaller decrease in inspiration and expiration than control rats (P < 0.05). We have recently shown that neuropeptide-containing fibers are important for mediating the tachypnic response during acute isocapnic hypoxia in rats. The attenuation in minute ventilation at the highest dose (10 mg/kg) is comparable in magnitude to the attenuation observed with neonatal capsaicin treatment, which permanently ablates neuropeptide-containing unmyelinated fibers. Accordingly, this previously reported role of capsaicin-sensitive nerves in the hypoxic ventilatory response of rats is probably attributable to released SP acting at NK1 receptors. One of the likely sites of action of SP antagonists is the carotid body.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory response to moderate and severe hypoxia in adult dogs: role of endorphins

1988 ◽  
Vol 65 (3) ◽  
pp. 1383-1388 ◽  
Author(s):  
J. I. Schaeffer ◽  
G. G. Haddad
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Severe Hypoxia ◽  
Moderate Hypoxia ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Before And After ◽  
The Relationship ◽  
Arterial Po2

To determine the role of opioids in modulating the ventilatory response to moderate or severe hypoxia, we studied ventilation in six chronically instrumented awake adult dogs during hypoxia before and after naloxone administration. Parenteral naloxone (200 micrograms/kg) significantly increased instantaneous minute ventilation (VT/TT) during severe hypoxia, (inspired O2 fraction = 0.07, arterial PO2 = 28-35 Torr); however, consistent effects during moderate hypoxia (inspired O2 fraction = 0.12, arterial PO2 = 40-47 Torr) could not be demonstrated. Parenteral naloxone increased O2 consumption (VO2) in severe hypoxia as well. Despite significant increases in ventilation post-naloxone during severe hypoxia, arterial blood gas tensions remained the same. Control studies revealed that neither saline nor naloxone produced a respiratory effect during normoxia; also the preservative vehicle of naloxone induced no change in ventilation during severe hypoxia. These data suggest that, in adult dogs, endorphins are released and act to restrain ventilation during severe hypoxia; the relationship between endorphin release and moderate hypoxia is less consistent. The observed increase in ventilation post-naloxone during severe hypoxia is accompanied by an increase in metabolic rate, explaining the isocapnic response.

scholarly journals Endotracheal and upper airways suctioning: changes in newborns’ physiological parameters

2011 ◽  
Vol 19 (6) ◽  
pp. 1369-1376 ◽  
Author(s):  
Andréa Lopes Barbosa ◽  
Maria Vera Lúcia Moreira Leitão Cardoso ◽  
Thays Bezerra Brasil ◽  
Carmen Gracinda Silvan Scochi
Keyword(s):  
Neonatal Intensive Care ◽  
Upper Airway ◽  
Physiological Parameters ◽  
Public Institution ◽  
Pharmacological Interventions ◽  
Upper Airways ◽  
Nasal Cpap ◽  
Before And After ◽  
The City ◽  
Airway Suctioning

This study investigated which physiological parameters change when endotracheal and upper airway suctioning is performed immediately before, immediately after and five minutes after this procedure is performed in newborns hospitalized in a Neonatal Intensive Care Unit (NICU). This is a quantitative and longitudinal study, before and after type, performed in the NICU of a public institution in the city of Fortaleza, CE, Brazil. The sample was composed of 104 newborns using oxigenotherapy and who needed endotracheal and upper airway suctioning. The results showed significant alterations in respiratory and heart rates (p<0.05) in neonates using Oxyhood and nasal CPAP while the pulse significantly changed (p<0.05) in newborns placed in oxyhood, using nasal CPAP and Mechanical Ventilation; oxygen saturation was the only parameter that did not alter significantly. We propose that nurses develop non-pharmacological interventions to reduce potential alterations caused in newborns’ physiological parameters due to this procedure.

Respiratory effects of airflow through the upper airways in newborn kittens and puppies

1982 ◽  
Vol 53 (4) ◽  
pp. 805-814 ◽  
Author(s):  
S. F. Al-Shway ◽  
J. P. Mortola
Keyword(s):  
Airway Pressure ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Steady Flows ◽  
Breathing Frequency ◽  
Upper Airways ◽  
Respiratory Effects ◽  
Pentobarbital Sodium ◽  
Ventilatory Pattern ◽  
Stimulation Of

Kittens, puppies, cats, and dogs were anesthetized with pentobarbital sodium and tracheotomized. The ventilatory pattern was recorded before, during, and after the delivery of steady flows of room air of 20 or 50 ml X s-1 X kg-1 in the expiratory direction through a cannula inserted just below the larynx. In the newborn, a reduction in breathing frequency, mainly due to a prolongation of the expiratory time, and a decrease in tidal volume contributed to a reduction in minute ventilation particularly with the higher flows; in some instances apnea resulted. Small or no effects were observed in the adult. The ventilatory inhibition was still present when humidified 37 degrees C warmed airstreams were delivered, and it was unchanged when airflows of 4.9% CO21.5% O2–82.6% N2 were applied. After local anesthesia of the laryngeal region or after bypassing the larynx, the ventilatory inhibition disappeared. By closure of a nostril at any given airflow, the upper airway pressure was substantially increased; however, this maneuver did not enhance the respiratory depression. We conclude that airflow through the upper airways can inhibit ventilation in newborn kittens and puppies presumably through the stimulation of airflow-sensitive laryngeal receptors.

Increased chemoreceptor output and ventilatory response to sustained hypoxia

1989 ◽  
Vol 67 (3) ◽  
pp. 1157-1163 ◽  
Author(s):  
D. Georgopoulos ◽  
S. Walker ◽  
N. R. Anthonisen
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Base Line ◽  
Breathing Patterns ◽  
Peripheral Chemoreceptor ◽  
Depressant Action ◽  
Before And After ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
Sustained Hypoxia

In adult humans the ventilatory response to sustained hypoxia (VRSH) is biphasic, characterized by an initial brisk increase, due to peripheral chemoreceptor (PC) stimulation, followed by a decline attributed to central depressant action of hypoxia. To study the effects of selective stimulation of PC on the ventilatory response pattern to hypoxia, the VRSH was evaluated after pretreatment with almitrine (A), a PC stimulant. Eight subjects were pretreated with A (75 mg po) or placebo (P) on 2 days in a single-blind manner. Two hours after drug administration, they breathed, in succession, room air (10 min), O2 (5 min), room air (5 min), hypoxia [25 min, arterial O2 saturation (SaO2) = 80%], O2 (5 min), and room air (5 min). End-tidal CO2 was kept constant at the normoxic base-line values. Inspiratory minute ventilation (VI) and breathing patterns were measured over the last 2 min of each period and during minutes 3–5 of hypoxia, and nadirs in VI were assessed just before and after O2 exposure. Independent of the day, the VRSH was biphasic. With P and A pretreatment, early hypoxia increased VI 4.6 +/- 1 and 14.2 +/- 1 (SE) l/min, respectively, from values obtained during the preceding room-air period. On A day the hypoxic ventilatory decline was significantly larger than that on P day, and on both days the decline was a constant fraction of the acute hypoxic response.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of testosterone on the apneic threshold in women during NREM sleep

2003 ◽  
Vol 94 (1) ◽  
pp. 101-107 ◽  
Author(s):  
X. S. Zhou ◽  
J. A. Rowley ◽  
F. Demirovic ◽  
M. P. Diamond ◽  
M. S. Badr
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Premenopausal Women ◽  
Nrem Sleep ◽  
Central Apnea ◽  
Rapid Eye Movement Sleep ◽  
A Value ◽  
Before And After ◽  
Testosterone Administration ◽  
End Tidal

The hypocapnic apneic threshold (AT) is lower in women relative to men. To test the hypothesis that the gender difference in AT was due to testosterone, we determined the AT during non-rapid eye movement sleep in eight healthy, nonsnoring, premenopausal women before and after 10–12 days of transdermal testosterone. Hypocapnia was induced via nasal mechanical ventilation (MV) for 3 min with tidal volumes ranging from 175 to 215% above eupneic tidal volume and respiratory frequency matched to eupneic frequency. Cessation of MV resulted in hypocapnic central apnea or hypopnea depending on the magnitude of hypocapnia. Nadir minute ventilation as a percentage of control (%V˙e) was plotted against the change in end-tidal CO2(Pet CO2 ); %V˙e was given a value of zero during central apnea. The AT was defined as the Pet CO2 at which the apnea closest to the last hypopnea occurred; hypocapnic ventilatory response (HPVR) was defined as the slope of the linear regression V˙e vs. Pet CO2 . Both the AT (39.5 ± 2.9 vs. 42.1 ± 3.0 Torr; P = 0.002) and HPVR (0.20 ± 0.05 vs. 0.33 ± 0.11%V˙e/Torr; P = 0.016) increased with testosterone administration. We conclude that testosterone administration increases AT in premenopausal women, suggesting that the increased breathing instability during sleep in men is related to the presence of testosterone.

scholarly journals Permeabilization surgery of the upper respiratory tract and its effects on sleep fragmentation and REM sleep

2017 ◽  
Vol 7 (25) ◽  
pp. 47-56 ◽  
Author(s):  
Ionut Tanase ◽  
Claudiu Manea ◽  
Codrut Sarafoleanu
Keyword(s):  
Sleep Disorders ◽  
Surgical Procedures ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Upper Airway ◽  
Sleep Fragmentation ◽  
Upper Respiratory Tract ◽  
Upper Airways ◽  
Falling Asleep ◽  
Before And After

AbstractUsually, patients with sleep disorders may complain of tiredness, fatigue, daytime sleepiness, difficulty in concentrating, and can reach up to falling asleep in inappropriate situations – condition known as the Pickwick syndrome. To avoid these unpleasant symptoms, a series of surgical procedures regarding the anatomical structures involved in sleep apnea were developed.The article is a general review regarding the sleep disorders and the influence of upper airways permeability on the quality of sleep and the sleep staging distribution. Also, we present some preliminary data obtained in a clinical study underwent in CESITO Centre “Sfanta Maria” Hospital, Bucharest, involving patients with sleep pathology that had polysomnographic evaluations before and after various surgical procedures of nasal and pharyngeal permeabilization.AIMS.To determine that permeabilization surgery of the upper airway tract may be used successfully in order to decrease the sleep fragmentation and increase the time of slow-wave sleep.CONCLUSION.6 months after the permeabilization surgery of the upper airway tract, the polysomnography reveals that the arousals index decreased and the sleep architecture undergoes changes that consist in decreasing the Stage 1 and Stage 2 sleep, therefore REM sleep reaches a better score.

Acute mountain sickness, chemosensitivity, and cardiorespiratory responses in humans exposed to hypobaric and normobaric hypoxia

2014 ◽  
Vol 116 (7) ◽  
pp. 945-952 ◽  
Author(s):  
Normand A. Richard ◽  
Inderjeet S. Sahota ◽  
Nadia Widmer ◽  
Sherri Ferguson ◽  
A. William Sheel ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Acute Mountain Sickness ◽  
Blood Oxygenation ◽  
Normobaric Hypoxia ◽  
Hypoxic Exposure ◽  
Hypoxic Ventilatory Response ◽  
Before And After ◽  
Mountain Sickness ◽  
Normobaric Normoxia

We examined the control of breathing, cardiorespiratory effects, and the incidence of acute mountain sickness (AMS) in humans exposed to hypobaric hypoxia (HH) and normobaric hypoxia (NH), and under two control conditions [hypobaric normoxia (HN) and normobaric normoxia (NN)]. Exposures were 6 h in duration, and separated by 2 wk between hypoxic exposures and 1 wk between normoxic exposures. Before and after exposures, subjects ( n = 11) underwent hyperoxic and hypoxic Duffin CO2 rebreathing tests and a hypoxic ventilatory response test (HVR). Inside the environmental chamber, minute ventilation (V̇e), tidal volume (Vt), frequency of breathing ( fB), blood oxygenation, heart rate, and blood pressure were measured at 5 and 30 min and hourly until exit. Symptoms of AMS were evaluated using the Lake Louise score (LLS). Both the hyperoxic and hypoxic CO2 thresholds were lower after HH and NH, whereas CO2 sensitivity was increased after HH and NH in the hypoxic test and after NH in the hyperoxic test. Values for HVR were similar across the four exposures. No major differences were observed for V̇e or any other cardiorespiratory variables between NH and HH. The LLS was greater in AMS-susceptible than in AMS-resistant subjects; however, LLS was alike between HH and NH. In AMS-susceptible subjects, fB correlated positively and Vt negatively with the LLS. We conclude that 6 h of hypoxic exposure is sufficient to lower the peripheral and central CO2 threshold but does not induce differences in cardiorespiratory variables or AMS incidence between HH and NH.

Upper airway muscle activity during sustained hypoxia in awake humans

1993 ◽  
Vol 75 (4) ◽  
pp. 1552-1558 ◽  
Author(s):  
S. Okabe ◽  
W. Hida ◽  
Y. Kikuchi ◽  
H. Kurosawa ◽  
J. Midorikawa ◽  
...  
Keyword(s):  
Muscle Activity ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Normal Subjects ◽  
Initial Increase ◽  
Fine Wire ◽  
Obstructive Sleep ◽  
Arterial O2 Saturation ◽  
Sustained Hypoxia

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.

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