scholarly journals Respiratory Frequency during Exercise: The Neglected Physiological Measure

2017 ◽  
Vol 8 ◽  
Author(s):  
Andrea Nicolò ◽  
Carlo Massaroni ◽  
Louis Passfield
Keyword(s):  
Respiratory Frequency ◽  
Physiological Measure

Ventilatory response to hypoxia in unanesthetized newborn kittens

1988 ◽  
Vol 64 (6) ◽  
pp. 2544-2551 ◽  
Author(s):  
H. Rigatto ◽  
C. Wiebe ◽  
C. Rigatto ◽  
D. S. Lee ◽  
D. Cates
Keyword(s):  
Tidal Volume ◽  
Chest Wall ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Quiet Sleep ◽  
Newborn Kitten ◽  
Peripheral Mechanism ◽  
Flow Through ◽  
Ventilatory Response To Hypoxia

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.

A Successful Adaptation of Systematic Desensitization in the Treatment of a Phobia of Babies

1985 ◽  
Vol 2 (1) ◽  
pp. 59-64
Author(s):  
Michael Free ◽  
Margaret Beekhuis
Keyword(s):  
Young Woman ◽  
Skin Conductance ◽  
Treatment Strategy ◽  
Physiological Measures ◽  
Systematic Desensitization ◽  
Physiological Measure ◽  
One Year

A case study is presented of a young woman with an unusual phobia, a fear of babies. Barabasz's (1977) technique of systematic desensitization using psycho-physiological measures was chosen as the main treatment strategy. Difficulties arose as the client was unable to visualise scenes involving babies. Nor could she look at photographs of babies long enough for the hierarchy to be ordered using a psycho-physiological measure (skin conductance). A set of photographs was eventually used for the hierarchy, but it was ordered in terms of the length of time the client could look at the various photographs. Systematic desensitization was carried out using the set of photographs instead of imaginary scenes, together with some in vivo exposure in the latter stages of treatment. At termination the client could approach babies without discomfort. Improvement was maintained at one year follow-up.

On the Regulation of the Respiration in Reptiles

1961 ◽  
Vol 38 (2) ◽  
pp. 301-314 ◽  
Author(s):  
BODIL NIELSEN
Keyword(s):  
Steady State ◽  
Body Temperature ◽  
Metabolic Rate ◽  
Temperature Interval ◽  
Normal Values ◽  
Pulmonary Ventilation ◽  
The Body ◽  
Respiratory Frequency ◽  
Temperature Changes ◽  
Instantaneous Increase

1. In two species of Lacerta (L. viridis and L. sicula) the effects on respiration of body temperature (changes in metabolic rate) and of CO2 added to the inspired air were studied. 2. Pulmonary ventilation increases when body temperature increases. The increase is brought about by an increase in respiratory frequency. No relationship is found between respiratory depth and temperature. 3. The rise in ventilation is provoked by the needs of metabolism and is not established for temperature regulating purposes (in the temperature interval 10°-35°C). 4. The ventilation per litre O2 consumed has a high numerical value (about 75, compared to about 20 in man). It varies with the body temperature and demonstrates that the inspired air is better utilized at the higher temperatures. 5. Pulmonary ventilation increases with increasing CO2 percentages in the inspired air between o and 3%. At further increases in the CO2 percentage (3-13.5%) it decreases again. 6. At each CO2 percentage the pulmonary ventilation reaches a steady state after some time (10-60 min.) and is then unchanged over prolonged periods (1 hr.). 7. The respiratory frequency in the steady state decreases with increasing CO2 percentages. The respiratory depth in the steady state increases with increasing CO2 percentages. This effect of CO2 breathing is not influenced by a change in body temperature from 20° to 30°C. 8. Respiration is periodically inhibited by CO2 percentages above 4%. This inhibition, causing a Cheyne-Stokes-like respiration, ceases after a certain time, proportional to the CO2 percentage (1 hr. at 8-13% CO2), and respiration becomes regular (steady state). Shift to room air breathing causes an instantaneous increase in frequency to well above the normal value followed by a gradual decrease to normal values. 9. The nature of the CO2 effect on respiratory frequency and respiratory depth is discussed, considering both chemoreceptor and humoral mechanisms.

Comparison of pre-emptive butorphanol or metamizole with ketamine +medetomidine and s-ketamine + medetomidine anaesthesia in improving intraoperative analgesia in mice

2018 ◽  
Vol 53 (5) ◽  
pp. 459-469
Author(s):  
C Bauer ◽  
U Schillinger ◽  
J Brandl ◽  
A Meyer-Lindenberg ◽  
A Ott ◽  
...  
Keyword(s):  
Body Temperature ◽  
Pulse Oximetry ◽  
Respiratory Frequency ◽  
Painful Stimulus ◽  
Male Mice ◽  
Controlled Ventilation ◽  
Withdrawal Reaction ◽  
Potential Improvement ◽  
Frequency Pulse

In accordance with the ‘refinement’ component of the 3Rs, the primary aim of this study was to investigate and compare ketamine + medetomidine (KM) and s-ketamine + medetomidine (SKM) anaesthetic protocols in C57BL/6J mice (both sexes). We sought to determine whether s-ketamine could provide adequate surgical tolerance at a 50% dose relative to that of ketamine racemate and whether antagonism of medetomidine could be initiated 15 min earlier. The second aim was to investigate the potential improvement in analgesia for both anaesthetic protocols by adding butorphanol or metamizole. Analgesia was tested via the pedal withdrawal reaction (PWR) to a painful stimulus. During anaesthesia, respiratory frequency, pulse oximetry, body temperature and PWR were monitored. Among the 16 mice in each group, the PWR was lost in all the KM + metamizole (35:56 ± 6:07 min), KM + butorphanol (43:45 ± 2:14 min) and SKM + butorphanol (24:03 ± 5:50 min) mice, 15 of the non-premedicated KM (37:00 ± 8:11 min) mice, and 9 of the pure SKM (20:00 ± 4:19 min) mice; the latter group increased to 11 mice (17:16 ± 5:10 min) with premedication of metamizole. In contrast to the racemic combination, s-ketamine at the dose used here did not lead to sufficient loss of the PWR. However, earlier partial antagonism of SKM resulted in a slightly shorter and qualitatively better recovery than later partial antagonism of SKM. The addition of metamizole or butorphanol to KM or SKM anaesthesia positively influences the analgesic quality. However, when butorphanol is added, controlled ventilation may be necessary, especially for male mice.

Respiratory syncytial virus infection in anesthetized weanling rather than adult rats prolongs the apneic responses to right atrial injection of capsaicin

2007 ◽  
Vol 102 (6) ◽  
pp. 2201-2206 ◽  
Author(s):  
Wenhong Peng ◽  
Jianguo Zhuang ◽  
Kevin S. Harrod ◽  
Fadi Xu
Keyword(s):  
Respiratory Syncytial Virus ◽  
Blood Gases ◽  
Respiratory Frequency ◽  
Right Atrial ◽  
Arterial Blood Gases ◽  
Adult Rats ◽  
Intranasal Inoculation ◽  
Arterial Blood ◽  
Rsv Infection ◽  
Syncytial Virus

Apnea is a common complication in infants infected by respiratory syncytial virus (RSV). A recent study has shown that intranasal inoculation of RSV in conscious weanling rats strengthens the apneic responses to right atrial injection of capsaicin (CAP), leading to 66% mortality. The objectives of the present study were to determine 1) whether RSV infection changes baseline minute ventilation (V̇e) and arterial blood gases in anesthetized rats; 2) what the effects of RSV infection are on the respiratory responses to CAP; and 3) whether the RSV-strengthened apneic responses are age dependent. Our experiments were conducted in anesthetized and spontaneously breathing rats divided into four groups of weanling and adult rats that received either intranasal inoculation of RSV or virus-free medium. Two days after RSV infection (0.7 ml/kg), animal blood gases, baseline V̇e, and V̇e responses to right atrial injection of three doses of CAP (4, 16, and 64 μg/kg) were measured and compared among the four groups. Our results showed that RSV infection increased respiratory frequency (∼25%, P < 0.05) in weanling but not adult rats, with little effect on arterial blood gases. RSV infection amplified the apneic responses to CAP in weanling but not adult rats, characterized by increases in the initial (40%) and the longest apneic duration (650%), the number of apneic episodes (139%), and the total duration of apneas (60%). These amplifications led to 50% mortality ( P < 0.05). We conclude that RSV infection increases respiratory frequency and strengthens the apneic responses to CAP only in anesthetized weanling but not adult rats.

scholarly journals Mechanisms Underlying Regulation of Respiratory Pattern by Nicotine in PreBötzinger Complex

2001 ◽  
Vol 85 (6) ◽  
pp. 2461-2467 ◽  
Author(s):  
Xuesi M. Shao ◽  
Jack L. Feldman
Keyword(s):  
Respiratory Frequency ◽  
Neonatal Rat ◽  
Respiratory Pattern ◽  
Dependent Manner ◽  
Baseline Noise ◽  
Arterial Blood ◽  
Inspiratory Neurons ◽  
Excitatory Neurotransmission ◽  
Prebotzinger Complex ◽  
Prebötzinger Complex

Cholinergic neurotransmission plays a role in regulation of respiratory pattern. Nicotine from cigarette smoke affects respiration and is a risk factor for sudden infant death syndrome (SIDS) and sleep-disordered breathing. The cellular and synaptic mechanisms underlying this regulation are not understood. Using a medullary slice preparation from neonatal rat that contains the preBötzinger Complex (preBötC), the hypothesized site for respiratory rhythm generation, and generates respiratory-related rhythm in vitro, we examined the effects of nicotine on excitatory neurotransmission affecting inspiratory neurons in preBötC and on the respiratory-related motor activity from hypoglossal nerve (XIIn). Microinjection of nicotine into preBötC increased respiratory frequency and decreased the amplitude of inspiratory bursts, whereas when injected into XII nucleus induced a tonic activity and an increase in amplitude but not in frequency of inspiratory bursts from XIIn. Bath application of nicotine (0.2–0.5 μM, approximately the arterial blood nicotine concentration immediately after smoking a cigarette) increased respiratory frequency up to 280% of control in a concentration-dependent manner. Nicotine decreased the amplitude to 82% and increased the duration to 124% of XIIn inspiratory bursts. In voltage-clamped preBötC inspiratory neurons (including neurons with pacemaker properties), nicotine induced a tonic inward current of −19.4 ± 13.4 pA associated with an increase in baseline noise. Spontaneous excitatory postsynaptic currents (sEPSCs) present during the expiratory period increased in frequency to 176% and in amplitude to 117% of control values; the phasic inspiratory drive inward currents decreased in amplitude to 66% and in duration to 89% of control values. The effects of nicotine were blocked by mecamylamine (Meca). The inspiratory drive current and sEPSCs were completely eliminated by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) in the presence or absence of nicotine. In the presence of tetrodotoxin (TTX), low concentrations of nicotine did not induce any tonic current or any increase in baseline noise, nor affect the input resistance in inspiratory neurons. In this study, we demonstrated that nicotine increased respiratory frequency and regulated respiratory pattern by modulating the excitatory neurotransmission in preBötC. Activation of nicotinic acetylcholine receptors (nAChRs) enhanced the tonic excitatory synaptic input to inspiratory neurons including pacemaker neurons and at the same time, inhibited the phasic excitatory coupling between these neurons. These mechanisms may account for the cholinergic regulation of respiratory frequency and pattern.

scholarly journals Impact of cervical spinal cord contusion on the breathing pattern across the sleep-wake cycle in the rat

2019 ◽  
Vol 126 (1) ◽  
pp. 111-123 ◽  
Author(s):  
Kun-Ze Lee
Keyword(s):  
Spinal Cord ◽  
Tidal Volume ◽  
Spinal Injury ◽  
Cervical Spinal Cord ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Breathing Patterns ◽  
Cord Injury ◽  
Spinal Contusion ◽  
Cervical Spinal Injury

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.

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