Neurotransmitters and biphasic respiratory response to hypoxia

1984 ◽  
Vol 57 (1) ◽  
pp. 213-222 ◽  
Author(s):  
W. A. Long ◽  
E. E. Lawson
Keyword(s):  
Phrenic Nerve ◽  
Initial Increase ◽  
Base Line ◽  
Respiratory Response ◽  
Biphasic Response ◽  
Controlled System ◽  
Initial Exposure ◽  
End Tidal ◽  
Line Level ◽  
End Tidal Co2

Recent work from this laboratory (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 55:483–488, 1983) has shown that the biphasic respiratory response to hypoxia in piglets is due to changing central neural respiratory output. To test the hypothesis that either adenosine or opiatelike neurotransmitters mediate the failure to sustain hyperpnea in response to hypoxia, 12 piglets were studied ata mean age of 2.9 +/- 0.4 days (range 2–6 days). Animals were anesthetized, paralyzed, and ventilatedusing a servo-controlled system that maintained end-tidal CO2 constant. Electrical activity of the phrenic nerve was recorded as the index of breathing. An initial experimental trial of 6 min ventilation with 15% O2 was performed in all 12 piglets. Thereafter all 12 piglets were treated with aminophylline (n = 6), naloxone (n = 3), or naltrexone (n = 3) and again subjected to 15% O2. During initial exposure to hypoxia there was an initial increase in phrenic activity that was not sustained. During recovery ventilation with 100% O2, phrenic activity transiently declined below the base-line level and then gradually returned. Subsequent intravenous administration of aminophylline, naloxone, or naltrexone caused base-line phrenic activity to increase. Thereafter repeat exposures to 15% O2 were carried out. During these posttreatment trials of hypoxia, phrenic activity further increased, but the hyperventilation was again not sustained. These findings suggest it is unlikely that either adenosine or mu-endorphin neurotransmitters are the primary mediators of the biphasic response to hypoxia in newborns.

Control of breathing at the start of exercise as influenced by posture

1983 ◽  
Vol 55 (5) ◽  
pp. 1460-1466 ◽  
Author(s):  
D. Weiler-Ravell ◽  
D. M. Cooper ◽  
B. J. Whipp ◽  
K. Wasserman
Keyword(s):  
Stroke Volume ◽  
Phase I ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Initial Increase ◽  
Base Line ◽  
Co2 Output ◽  
End Tidal ◽  
Response To Exercise ◽  
Initial Change

It has been suggested that the initial phase of the ventilatory response to exercise is governed by a mechanism which responds to the increase in pulmonary blood flow (Q)--cardiodynamic hyperpnea. Because the initial change in stroke volume and Q is less in the supine (S) than in the upright (U) position at the start of exercise, we hypothesized that the increase in ventilation would also be less in the first 20 s (phase I) of S exercise. Ten normal subjects performed cycle ergometry in the U and S positions. Inspired ventilation (VI), O2 uptake (VO2), CO2 output (VCO2), corrected for changes in lung gas stores, and end-tidal O2 and CO2 tensions were measured breath by breath. Heart rate (HR) was determined beat by beat. The phase I ventilatory response was markedly different in the two positions. In the U position, VI increased abruptly by 81 +/- 8% (mean +/- SE) above base line. In the S position, the phase I response was significantly attenuated (P less than 0.001), the increase in VI being 50 +/- 6%. Similarly, the phase I VO2 and VO2/HR responses reflecting the initial increase in Q and stroke volume, were attenuated (P less than 0.001) in the S posture, compared with that for U; VO2 increased 49 +/- 5.3 and 113 +/- 14.7% in S and U, respectively, and VO2/HR increased 16 +/- 3.0 and 76 +/- 7.1% in the S and U, respectively. The increase in VI correlated well with the increase in VO2, (r = 0.80, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory response to moderate hypoxia in awake chemodenervated cats

1993 ◽  
Vol 74 (2) ◽  
pp. 805-810 ◽  
Author(s):  
W. Q. Long ◽  
G. G. Giesbrecht ◽  
N. R. Anthonisen
Keyword(s):  
Ventilatory Response ◽  
Systemic Blood Pressure ◽  
Initial Increase ◽  
Sham Operation ◽  
Biphasic Response ◽  
Peripheral Chemoreceptor ◽  
Moderate Hypoxia ◽  
Subsequent Decrease ◽  
End Tidal ◽  
Arterial Po2

In humans and cats the ventilatory response to 30 min of moderate hypoxia (arterial PO2 40–55 Torr) is biphasic: ventilation increases sharply for the first 5 min and then declines. In humans there is evidence that the decline is dependent on the initial increase. We therefore examined ventilatory responses to moderate isocapnic hypoxia in awake cats with and without carotid body denervation. Cats underwent denervation or a sham operation. Then they were studied in a Drorbaugh-Fenn plethysmograph while ventilation, arterial PO2, and end-tidal PO2 and PCO2 were measured. Three sham-operated and four denervated cats were studied with room air as the control. Sham animals demonstrated a biphasic response: ventilation rose to 211% of control at 5 min and fell to 114% of control at 25 min. Denervated animals showed neither the initial increase nor the subsequent decrease in ventilation. Three sham-operated and three denervated cats were studied with 2% CO2 added to the inspirate. Results were similar: intact cats showed a biphasic response to hypoxia, whereas denervated cats showed neither an increase nor a decrease in ventilation. Preliminary experiments showed that hypoxia was not associated with changes in CO2 output or systemic blood pressure in either denervated or intact animals. We conclude that depression of ventilation does not occur in awake denervated cats in response to moderate hypoxia and that the decline in ventilation that occurs in intact cats is in some way dependent on peripheral chemoreceptor output.

scholarly journals Evaluation of Protection Level, Respiratory Safety and Practical Aspects of Commercially Available Snorkel Masks as Personal Protection Devices against Aerosolized Contaminants and SARS-CoV2

2020 ◽  
Author(s):  
Peter Germonpre ◽  
Dirk Van Rompaey ◽  
Costantino Balestra
Keyword(s):  
Initial Increase ◽  
Personal Protection ◽  
Physiological Limits ◽  
Fit Testing ◽  
3D Printed ◽  
Protection Devices ◽  
Carbon Dioxide Co2 ◽  
End Tidal ◽  
Full Face ◽  
End Tidal Co2

Introduction: The SARS-CoV2 pandemic has led to an worldwide shortage of Personal Protection Devices (PPD) for medical and paramedical personnel. Adaptation of commercially available snorkel masks to serve as full face masks has been proposed. Even not formally approved as PPD, they are publicized on social media as suitable for this use. Concerns about actual protection levels and risk of carbon dioxide (CO2) accumulation while wearing them for extended periods made us perform a systematic testing of various brands, in order to verify whether they are as safe and effective as claimed. Methods: A ‘fit’ test was performed, analogous to gas mask testing. Respiratory safety was evaluated by measuring end-tidal CO2 and oxygen saturation while wearing the masks in rest and during physical exercise. Masks were tested with 3D adaptors to mount regular bacterial-viral ventilator filters when available, or with snorkel openings covered with N95/FFP2 cloth. Results: Modified masks performed reasonably well on the fit test, comparable to regular N95/FFP2 masks. Not all ventilator filters are equally protective. For all masks, a small initial increase in end-tidal CO2 was noted, remaining within physiological limits. Masks with specific adaptors (3D printed or provided by the manufacturer) are safer, have more flexibility and reliability than makeshift adaptations. Conclusions: These masks can offer benefit as a substitute for complete protective gear as they are easier to don and remove and offer full-face protection. They may be more comfortable to wear for extended periods. Proper selection of mask size, fit testing, quality of 3D printed parts and choice of filter are important.

Naloxone enhances respiratory output in cats

1979 ◽  
Vol 47 (5) ◽  
pp. 1105-1111 ◽  
Author(s):  
E. E. Lawson ◽  
T. G. Waldrop ◽  
F. L. Eldridge
Keyword(s):  
Phrenic Nerve ◽  
Opiate Receptors ◽  
Physiological Role ◽  
Opiate Antagonist ◽  
Nerve Activity ◽  
Phrenic Nerve Activity ◽  
End Tidal ◽  
Decerebrate Cats ◽  
End Tidal Co2

To investigate the physiological role of opiate receptors and opiatelike neurotransmitters, which are present in brain-stem respiratory centers, we administered naloxone to 10 cats by intravenous injection. These animals were vagotomized, paralyzed, and servo-ventilated to maintain constant end-tidal CO2; in addition, their carotid sinus nerves were sectioned bilaterally. Respiratory output was assessed by integration of phrenic nerve activity. Control saline infusions had no effect on respiratory output. However, administration of naloxone (0.4 mg/kg) caused phrenic minute output to increase significantly in each of five anesthetized cerebrate cats (control 7,272 +/- 1,615 U/min; 30 min postnaloxone 12,920 +/- 3,857 U/min; P less than 0.05) and five unanesthetized decerebrate cats (control 10,368 +/- 1,222 U/min; naloxone 14,648 +/- 3,225 U/min; P less than 0.05). In addition to the effect on phrenic minute output, naloxone infusion resulted in an increase of the inspiratory rate of rise of phrenic nerve activity in each cat. There was no change in the ratio of inspiratory duration to total respiratory period (TI/Ttot). Because naloxone is a specific opiate antagonist, we suggest that endogenous opiatelike neurotransmitters (endorphins) may modulate central inspiratory drive.

Effects of haloperidol and domperidone on ventilatory roll off during sustained hypoxia in cats

1992 ◽  
Vol 72 (5) ◽  
pp. 1945-1952 ◽  
Author(s):  
K. Tatsumi ◽  
C. K. Pickett ◽  
J. V. Weil
Keyword(s):  
Carotid Sinus ◽  
Initial Increase ◽  
Respiratory Response ◽  
Dopaminergic Mechanisms ◽  
Central Response ◽  
The Central Nervous System ◽  
Adult Cat ◽  
End Tidal ◽  
Awake Cats ◽  
Sustained Hypoxia

In a previous work, we showed that the adult cat demonstrates a ventilatory decline during sustained hypoxia (the “roll off” phenomenon) and that the mechanism responsible for this secondary decrease in ventilation lies within the central nervous system (J. Appl. Physiol. 63: 1658–1664, 1987). In this study, we sought to determine whether central dopaminergic mechanisms could have a role in the roll off. We studied the effects of haloperidol, a peripheral and centrally acting dopamine receptor antagonist, on the ventilatory response to sustained isocapnic hypoxia (end-tidal PO2 40–50 Torr, 20–25 min) in awake cats. In vehicle control cats (n = 5), sustained hypoxia elicited a biphasic respiratory response, during which an initial ventilatory stimulation is followed by a 24 +/- 6% (P less than 0.01) reduction. In contrast, in haloperidol- (0.1 mg/kg) treated cats (n = 5) the ventilatory roll off was virtually abolished (-1 +/- 1%; P = NS). We also measured ventilatory, carotid sinus nerve (CSN) and phrenic nerve (PhN) responses to sustained isocapnic hypoxia in anesthetized animals (n = 6) to explore the influence of haloperidol on peripheral and central response during the roll off. Control responses to hypoxia showed an initial increase in ventilation, PhN, and CSN activity, followed by a subsequent decline in ventilation and PhN activity of 17 +/- 3 and 17 +/- 5%, respectively (P less than 0.05). In contrast, CSN activity remained unchanged during the roll off. Administration of haloperidol (1 mg/kg) reduced the initial increment in ventilation, while the initial increase in CSN activity was augmented.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Evaluation of Protection Level, Respiratory Safety, and Practical Aspects of Commercially Available Snorkel Masks as Personal Protection Devices Against Aerosolized Contaminants and SARS-CoV2

2020 ◽  
Vol 17 (12) ◽  
pp. 4347 ◽  
Author(s):  
Peter Germonpre ◽  
Dirk Van Rompaey ◽  
Costantino Balestra
Keyword(s):  
Initial Increase ◽  
Personal Protection ◽  
Physiological Limits ◽  
Fit Testing ◽  
3D Printed ◽  
Protection Devices ◽  
Carbon Dioxide Co2 ◽  
End Tidal ◽  
Full Face ◽  
End Tidal Co2

Introduction: The “Severe Acute Respiratory Syndrome Coronavirus 2″ (SARS-CoV2) pandemic has led to a worldwide shortage of personal protection devices (PPD) for medical and paramedical personnel. Adaptation of commercially available snorkel masks to serve as full face masks has been proposed. Even not formally approved as PPD, they are publicized on social media as suitable for this use. Concerns about actual protection levels and risk of carbon dioxide (CO2) accumulation while wearing them for extended periods made us perform a systematic testing of various brands, in order to verify whether they are as safe and effective as claimed. Methods: A ‘fit’ test was performed, analogous to gas mask testing. Respiratory safety was evaluated by measuring end-tidal CO2 and oxygen saturation while wearing the masks in rest and during physical exercise. Masks were tested with 3D adaptors to mount regular bacterial-viral ventilator filters when available, or with snorkel openings covered with N95/FFP2 cloth. Results: Modified masks performed reasonably well on the fit test, comparable to regular N95/FFP2 masks. Not all ventilator filters are equally protective. For all masks, a small initial increase in end-tidal CO2 was noted, remaining within physiological limits. 3D printed adaptors are safer, have more flexibility and reliability than makeshift adaptations. Conclusions: These masks can offer benefit as a substitute for complete protective gear as they are easier to don and remove and offer full-face protection. They may be more comfortable to wear for extended periods. Proper selection of mask size, fit testing, quality of 3D printed parts, and choice of filter are important.

Inspiratory rhythm in airway smooth muscle tone

1985 ◽  
Vol 58 (3) ◽  
pp. 911-920 ◽  
Author(s):  
R. A. Mitchell ◽  
D. A. Herbert ◽  
D. G. Baker
Keyword(s):  
Smooth Muscle ◽  
Vagus Nerve ◽  
Airway Smooth Muscle ◽  
Phrenic Nerve ◽  
Nerve Activity ◽  
Lung Inflation ◽  
Phrenic Nerve Activity ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Stimulation Of

In anesthetized paralyzed open-chested cats ventilated with low tidal volumes at high frequency, we recorded phrenic nerve activity, transpulmonary pressure (TPP), and either the tension in an upper tracheal segment or the impulse activity in a pulmonary branch of the vagus nerve. The TPP and upper tracheal segment tension fluctuated with respiration, with peak pressure and tension paralleling phrenic nerve activity. Increased end-tidal CO2 or stimulation of the carotid chemoreceptors with sodium cyanide increased both TPP and tracheal segment tension during the increased activity of the phrenic nerve. Lowering end-tidal CO2 or hyperinflating the lungs to achieve neural apnea (lack of phrenic activity) caused a decrease in TPP and tracheal segment tension and abolished the inspiratory fluctuations. During neural apnea produced by lowering end-tidal CO2, lung inflation caused no further decrease in tracheal segment tension and TPP. Likewise, stimulation of the cervical sympathetics, which caused a reduction in TPP and tracheal segment tension during normal breathing, caused no further reduction in these parameters when the stimulation occurred during neural apnea. During neural apnea the tracheal segment tension and TPP were the same as those following the transection of the vagi or the administration of atropine (0.5 mg/kg). Numerous fibers in the pulmonary branch of the vagus nerve fired in synchrony with the phrenic nerve. Only these fibers had activity which paralleled changes in TPP and tracheal tension. We propose that the major excitatory input to airway smooth muscle arises from cholinergic nerves that fire during inspiration, which have preganglionic cell bodies in the ventral respiratory group in the region of the nucleus ambiguus and are driven by the same pattern generators that drive the phrenic and inspiratory intercostal motoneurons.

Carbon dioxide effects on the ventilatory response to sustained hypoxia

1988 ◽  
Vol 64 (4) ◽  
pp. 1451-1456 ◽  
Author(s):  
P. A. Easton ◽  
N. R. Anthonisen
Keyword(s):  
Carbon Dioxide ◽  
Young Adults ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Initial Response ◽  
Initial Increase ◽  
Additional Increase ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Sustained Hypoxia

We examined the interrelation between CO2 and the ventilatory response to moderate (80% arterial saturation) sustained hypoxia in normal young adults. On a background of continuous CO2-stimulated hyperventilation, hypoxia was introduced and sustained for 25 min. Initially, with the introduction of hypoxia onto hypercapnia, there was a brisk additional increase in inspiratory minute ventilation (VI) to 284% of resting VI, but the response was not sustained and hypoxic VI declined by 36% to a level intermediate between the initial increase and the preexisting hypercapnic hyperventilation. Through the continuous hypercapnia, the changes in hypoxic ventilation resulted from significant alterations in tidal volume (VT) and mean inspiratory flow (VT/TI) without changes in respiratory timing. In another experiment, sustained hypoxia was introduced on the usual background of room air, either with isocapnia or without maintenance of end-tidal CO2 (ETCO2) (poikilocapnic hypoxia). Regardless of the degree of maintenance of ETCO2, during 25 min of sustained hypoxia, VI showed an initial brisk increase and then declined by 35-40% of resting VI to a level intermediate between the initial response and resting room air VI. For both isocapnia and poikilocapnic conditions, the attenuation of VI was an expression of a diminished VT. Thus the decline in ventilation with sustained hypoxia occurred regardless of the background ETCO2, suggesting that the mechanism underlying the hypoxic decline is independent of CO2.

Characteristics of airway tone during exercise in patients with asthma

1983 ◽  
Vol 54 (4) ◽  
pp. 934-942 ◽  
Author(s):  
D. R. Stirling ◽  
D. J. Cotton ◽  
B. L. Graham ◽  
W. C. Hodgson ◽  
D. W. Cockcroft ◽  
...  
Keyword(s):  
Treadmill Exercise ◽  
Specific Conductance ◽  
Base Line ◽  
Pulmonary Resistance ◽  
Asthmatic Patients ◽  
Residual Capacity ◽  
Preceding Period ◽  
End Tidal ◽  
Airway Tone ◽  
End Tidal Co2

In 10 nonasthmatic subjects and 11 patients with asthma, we measured pulmonary resistance (RL), functional residual capacity (FRC), and specific conductance (sGaw) before, during, and after submaximal treadmill exercise. Nonasthmatic subjects did not change RL, FRC, or sGaw from base-line resting values during or after exercise. In patients with asthma, RL decreased significantly during exercise, both when exercise was begun from the control resting state and from conditions of elevated RL after a preceding period of exercise. When asthmatic patients inhaled a standardized dose of aerosolized histamine, the increase in RL during exercise was significantly less than the increase in RL when they breathed histamine at rest. When patients hyperventilated at rest with tidal volumes, breathing frequencies, and end-tidal CO2 tensions similar to those during exercise conditions, bronchodilatation also occurred, and the increase in RL following inhaled histamine during isocapnic hyperventilation was also less than at rest. Since bronchodilatation and inhibition of histamine-induced bronchoconstriction occur during both exercise and isocapnic hyperventilation, we suggest that the mechanism of bronchodilatation during exercise may not necessarily be related to metabolic factors associated with exercise.

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