Whole-body plethysmography, does it measure tidal volume of small animals?

1998 ◽  
Vol 76 (10-11) ◽  
pp. 945-951 ◽  
Author(s):  
Goran Enhorning ◽  
Sandrijn van Schaik ◽  
Claes Lundgren ◽  
Ida Vargas
Keyword(s):  
Tidal Volume ◽  
Respiratory Rate ◽  
Airway Resistance ◽  
Pressure Oscillation ◽  
Whole Body ◽  
Polyethylene Tube ◽  
Temperature And Humidity ◽  
Metal Bellows ◽  
Pressure Changes ◽  
Whole Body Plethysmography

A whole-body plethysmograph was used for mice. The increase in pressure caused by each inhalation was equivalent to the increase that could be calculated to result from heating and humidification of the inhaled air. However, comprehending that a drop in temperature and humidity would cause an abrupt pressure decline during exhalation was difficult. Pressure changes in the plethysmograph were also studied with an artificial chest, modeling the respiratory mechanics, but without the "inhaled" air being heated or humidified. The "chest" consisted of a metal bellows oscillated by a stepper motor 25 to 175 times per minute. Hereby air (0.05 to 0.20 mL) moved in and out of the bellows. The air passed through a polyethylene tube, the length of which was proportional to "airway resistance" and varied from 5 to 35 cm. It was found that the pressure oscillation was affected not only by "tidal volume" of the mechanical chest but also by "respiratory rate" and by "airway resistance." We concur with previous investigators that the plethysmograph pressure reflects alveolar pressure and that fluctuations cannot be explained by changes in temperature and humidity. Accordingly, tidal volume can only be qualitatively and not quantitatively assessed.Key words: tidal volume, airway resistance, respiratory rate, chest model.

Ventilatory behavior after hypoxia in C57BL/6J and A/J mice

2001 ◽  
Vol 91 (5) ◽  
pp. 1962-1970 ◽  
Author(s):  
Fang Han ◽  
Shyam Subramanian ◽  
Thomas E. Dick ◽  
Ismail A. Dreshaj ◽  
Kingman P. Strohl
Keyword(s):  
Airway Resistance ◽  
Minute Ventilation ◽  
Genetic Effect ◽  
Strain Differences ◽  
Whole Body ◽  
Environmental Forcing ◽  
Ventilatory Responses ◽  
Term Potentiation ◽  
Genetic Mechanisms ◽  
Whole Body Plethysmography

Given the environmental forcing by extremes in hypoxia-reoxygenation, there might be no genetic effect on posthypoxic short-term potentiation of ventilation. Minute ventilation (V˙e), respiratory frequency (f), tidal volume (Vt), and the airway resistance during chemical loading were assessed in unanesthetized unrestrained C57BL/6J (B6) and A/J mice using whole body plethysmography. Static pressure-volume curves were also performed. In 12 males for each strain, after 5 min of 8% O2 exposure, B6 mice had a prominent decrease inV˙e on reoxygenation with either air (−11%) or 100% O2 (−20%), due to the decline of f. In contrast, A/J animals had no ventilatory undershoot or f decline. After 5 min of 3% CO2-10% O2 exposure, B6 exhibited significant decrease in V˙e (−28.4 vs. −38.7%, air vs. 100% O2) and f (−13.8 vs. −22.3%, air vs. 100% O2) during reoxygenation with both air and 100% O2; however, A/J mice showed significant increase inV˙e (+116%) and f (+62.2%) during air reoxygenation and significant increase in V˙e (+68.2%) during 100% O2 reoxygenation. There were no strain differences in dynamic airway resistance during gas challenges or in steady-state total respiratory compliance measured postmortem. Strain differences in ventilatory responses to reoxygenation indicate that genetic mechanisms strongly influence posthypoxic ventilatory behavior.

Maturation of baseline breathing and of hypercapnic and hypoxic ventilatory responses in newborn mice

2001 ◽  
Vol 281 (5) ◽  
pp. R1746-R1753 ◽  
Author(s):  
Sylvain Renolleau ◽  
Stéphane Dauger ◽  
Fanny Autret ◽  
Guy Vardon ◽  
Claude Gaultier ◽  
...  
Keyword(s):  
Cesarean Section ◽  
Tidal Volume ◽  
Mammalian Species ◽  
Whole Body ◽  
Body Plethysmography ◽  
Genetic Studies ◽  
Newborn Mice ◽  
Ventilatory Responses ◽  
Neuronal Mechanisms ◽  
Whole Body Plethysmography

Breathing during the first postnatal hours has not been examined in mice, the preferred mammalian species for genetic studies. We used whole body plethysmography to measure ventilation (V˙e), breath duration (TTOT), and tidal volume (Vt) in mice delivered vaginally (VD) or by cesarean section (CS). In experiment 1, 101 VD and 100 CS pups aged 1, 6, 12, 24, or 48 h were exposed to 8% CO2 or 10% O2for 90 s. In experiment 2, 31 VD pups aged 1, 12, or 24 h were exposed to 10% O2 for 5 min. Baseline breathing maturation was delayed in CS pups, but V˙eresponses to hypercapnia and hypoxia were not significantly different between VD and CS pups [at postnatal age of 1 h (H1): 48 ± 44 and 18 ± 32%, respectively, in VD and CS pups combined]. TheV˙e increase induced by hypoxia was greater at H12 (46 ± 27%) because of TTOT response maturation. At all ages, hypoxic decline was ascribable mainly to a Vtdecrease, and posthypoxic decline was ascribable to a TTOTincrease with apneas, suggesting different underlying neuronal mechanisms.

Amygdala mediates respiratory responses to sudden arousing stimuli and to restraint stress in rats

2014 ◽  
Vol 306 (12) ◽  
pp. R951-R959 ◽  
Author(s):  
Evgeny Bondarenko ◽  
Deborah M. Hodgson ◽  
Eugene Nalivaiko
Keyword(s):  
Respiratory Rate ◽  
Restraint Stress ◽  
Animal Studies ◽  
Whole Body ◽  
Acoustic Stimuli ◽  
Respiratory Parameters ◽  
Male Wistar Rats ◽  
The Mean ◽  
Whole Body Plethysmography ◽  
Respiratory Responses

Both human and animal studies have demonstrated that respiratory parameters change in response to presentation of alerting stimuli, as well as during stress, yet central neuronal pathways that mediate such responses remain unknown. The aim of our study was to investigate the involvement of the amygdala in mediating respiratory responses to stressors of various intensities and duration. Adult male Wistar rats ( n = 8) received microinjections of GABAA agonist muscimol or saline into the amygdala bilaterally and were subjected to a respiratory recording using whole body plethysmography. Presentation of acoustic stimuli (500-ms white noise, 40–90 dB) caused transient responses in respiratory rate that were proportional to the stimulus intensity, ranging from +13 ± 9 cpm to +276 ± 67 cpm for 40- and 90-dB stimuli, respectively. Inhibition of the amygdala significantly suppressed respiratory rate responses to the high-intensity stimuli (70–90 dB). Submitting rats to the restraint stress significantly elevated the mean respiratory rate (+72 ± 8 cpm) and the dominant respiratory rate (+51 ± 12 cpm), as well as the fraction of high-frequency respiratory rate (+10 ± 3%). Inhibition of the amygdala by muscimol significantly suppressed these responses. We conclude that the amygdala is one of the key structures that are essential for expression of respiratory responses to stressful or alerting stimuli in rats.

The respiratory responses of the fowl to hot climates

1982 ◽  
Vol 97 (1) ◽  
pp. 301-309
Author(s):  
H. Kassim ◽  
A. H. Sykes
Keyword(s):  
Heat Stress ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Linear Relation ◽  
Domestic Fowl ◽  
Whole Body ◽  
Second Phase ◽  
Direct Relation ◽  
Ambient Temperatures ◽  
Respiratory Responses

Respiratory rate (f) and tidal volume (VT) have been measured at normal and at warm ambient temperatures (Ta) in adult domestic fowl by means of a whole body plethysmograph. Resting values of f = 23 +/− 9 min-1 and of VT = 25.6 +/− 0.9 ml min-1 were found. At Ta 30, 35 or 40 degrees C f increased in direct relation to the severity of the heat stress reaching a maximum values of 273 +/− 12 min-1; VT fell uniformly in all three climates to a minimum of 9.0 +/− 0.5 ml. Total ventilation (V) showed a linear relation with f during first-phase panting. Second-phase panting occurred only at Ta 40 degrees C; V increased at first but subsequently fell as the decline in f became more pronounced.

scholarly journals Novel whole body plethysmography system for the continuous characterization of sleep and breathing in a mouse

2012 ◽  
Vol 112 (4) ◽  
pp. 671-680 ◽  
Author(s):  
A. B. Hernandez ◽  
J. P. Kirkness ◽  
P. L. Smith ◽  
H. Schneider ◽  
M. Polotsky ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Gold Standard ◽  
Inbred Mouse ◽  
Respiratory Movement ◽  
Whole Body ◽  
Mouse Strains ◽  
Obese Mouse ◽  
Body Plethysmography ◽  
Breathing Patterns ◽  
Whole Body Plethysmography

Sleep is associated with marked alterations in ventilatory control that lead to perturbations in respiratory timing, breathing pattern, ventilation, pharyngeal collapsibility, and sleep-related breathing disorders (SRBD). Mouse models offer powerful insight into the pathogenesis of SRBD; however, methods for obtaining the full complement of continuous, high-fidelity respiratory, electroencephalographic (EEG), and electromyographic (EMG) signals in unrestrained mice during sleep and wake have not been developed. We adapted whole body plethysmography to record EEG, EMG, and respiratory signals continuously in unrestrained, unanesthetized mice. Whole body plethysmography tidal volume and airflow signals and a novel noninvasive surrogate for respiratory effort (respiratory movement signal) were validated against simultaneously measured gold standard signals. Compared with the gold standard, we validated 1) tidal volume (correlation, R2 = 0.87, P < 0.001; and agreement within 1%, P < 0.001); 2) inspiratory airflow (correlation, R2 = 0.92, P < 0.001; agreement within 4%, P < 0.001); 3) expiratory airflow (correlation, R2 = 0.83, P < 0.001); and 4) respiratory movement signal (correlation, R2 = 0.79–0.84, P < 0.001). The expiratory airflow signal, however, demonstrated a decrease in amplitude compared with the gold standard. Integrating respiratory and EEG/EMG signals, we fully characterized sleep and breathing patterns in conscious, unrestrained mice and demonstrated inspiratory flow limitation in a New Zealand Obese mouse. Our approach will facilitate studies of SRBD mechanisms in inbred mouse strains and offer a powerful platform to investigate the effects of environmental and pharmacological exposures on breathing disturbances during sleep and wakefulness.

scholarly journals Whole-body plethysmography revisited

2021 ◽  
Author(s):  
Swen Hülsmann ◽  
Amara Khan ◽  
Liya Hagos ◽  
Martin Hindermann ◽  
Torsten Nägel ◽  
...  
Keyword(s):  
Airway Resistance ◽  
Pressure Profile ◽  
Lung Model ◽  
Whole Body ◽  
Chamber Pressure ◽  
Body Plethysmography ◽  
Relative Contribution ◽  
Pressure Peak ◽  
Temporal Pressure ◽  
Whole Body Plethysmography

AbstractWhole-body plethysmography (WBP) is an established method to determine physiological parameters and pathophysiological alteration of breathing in animals and animal models of a variety of diseases, reaching from pulmonary diseases to complex neurological syndromes. Although frequently used, there is ongoing debate about what exactly is measured by whole-body-plethysmography and how reliable the data derived from this method are? Here, we designed a simple device that can serve as an artificial lung model that enables a thorough evaluation of different predictions about and around whole-body plethysmography. Using our lung model, we confirmed that during WBP two components contribute to the pressure changes detected in the chamber: 1) the increase of the pressure due to heating and moistening of the air, termed as conditioning, during inspiration; 2) changes of chamber pressure that depend on airway resistance. Both components overlap and contribute to the temporal pressure-profile measured in the chamber or across the wall of the chamber. Our data showed that a precise measurement of the breathing volume appears to be hindered by at least two factors: 1) the unknown relative contribution of each of these components; 2) not only the air in the inspired volume is conditioned during inspiration, but also air within the residual volume and death space that is recruited during inspiration. Moreover, our data suggest that the expiratory negative pressure peak that is used to determine the so called “enhanced pause” (Penh) parameter is not a measure for airway resistance as such but rather a consequence of the animal’s response to the airway resistance, using active expiration to overcome the resistance by a higher thoracic pressure.

Restrained whole body plethysmography for measure of strain-specific and allergen-induced airway responsiveness in conscious mice

2006 ◽  
Vol 101 (5) ◽  
pp. 1495-1505 ◽  
Author(s):  
Jennifer L. S. Lofgren ◽  
Melissa R. Mazan ◽  
Edward P. Ingenito ◽  
Kara Lascola ◽  
Molly Seavey ◽  
...  
Keyword(s):  
Functional Residual Capacity ◽  
Airway Resistance ◽  
Allergen Challenge ◽  
Airway Disease ◽  
Airway Responsiveness ◽  
Whole Body ◽  
Forced Oscillation Technique ◽  
Body Plethysmography ◽  
Residual Capacity ◽  
Whole Body Plethysmography

The mouse is the most extensively studied animal species in respiratory research, yet the technologies available to assess airway function in conscious mice are not universally accepted. We hypothesized that whole body plethysmography employing noninvasive restraint (RWBP) could be used to quantify specific airway resistance (sRaw-RWBP) and airway responsiveness in conscious mice. Methacholine responses were compared using sRaw-RWBP vs. airway resistance by the forced oscillation technique (Raw-FOT) in groups of C57, A/J, and BALB/c mice. sRaw-RWBP was also compared with sRaw derived from double chamber plethysmography (sRaw-DCP) in BALB/c. Finally, airway responsiveness following allergen challenge in BALB/c was measured using RWBP. sRaw-RWBP in C57, A/J, and BALB/c mice was 0.51 ± 0.03, 0.68 ± 0.03, and 0.63 ± 0.05 cm/s, respectively. sRaw derived from Raw-FOT and functional residual capacity (Raw*functional residual capacity) was 0.095 cm/s, approximately one-fifth of sRaw-RWBP in C57 mice. The intra- and interanimal coefficients of variations were similar between sRaw-RWBP (6.8 and 20.1%) and Raw-FOT (3.4 and 20.1%, respectively). The order of airway responsiveness employing sRaw-RWBP was AJ > BALBc > C57 and for Raw-FOT was AJ > BALB/c = C57. There was no difference between the airway responsiveness assessed by RWBP vs. DCP; however, baseline sRaw-RWBP was significantly lower than sRaw-DCP. Allergen challenge caused a progressive decrease in the provocative concentration of methacholine that increased sRaw to 175% postsaline values based on sRaw-RWBP. In conclusion, the technique of RWBP was rapid, reproducible, and easy to perform. Airway responsiveness measured using RWBP, DCP, and FOT was equivalent. Allergen responses could be followed longitudinally, which may provide greater insight into the pathogenesis of chronic airway disease.

Cardiorespiratory changes during microwave-induced lethal heat stress and beta-adrenergic blockade

1994 ◽  
Vol 77 (1) ◽  
pp. 434-440 ◽  
Author(s):  
J. R. Jauchem ◽  
M. R. Frei
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Respiratory Rate ◽  
Survival Time ◽  
Whole Body ◽  
High Dose ◽  
Adrenergic Blockade ◽  
Lethal Temperatures ◽  
Pressure Changes

Ketamine-anesthetized Sprague-Dawley rats were exposed to 2,450-MHz microwaves at an average power density of 60 mW/cm2 (whole body specific absorption rate of approximately 14 W/kg) until lethal temperatures were attained. The effects of propranolol (2 or 10 mg/kg body wt), nadolol (10 mg/kg), and labetalol (10 mg/kg) on physiological responses (including changes in body temperature, heart rate, blood pressure, and respiratory rate) were examined. Lethal temperatures in the labetalol and both propranolol groups were significantly lower than in saline controls. Survival time was significantly less only in the high-dose propranolol group. In all groups, heart rate increased continuously during exposure; blood pressure increased until colonic temperature reached 41–41.5 degrees C and then decreased. These heart rate and blood pressure changes were similar to those that occur during environmental heat stress. Heart rate and blood pressure changes among groups were similar. Respiratory rate, however, was significantly elevated during most of the exposure period in the high-dose propranolol animals. This change in respiration, coupled with the significantly lower survival time in these animals, suggests a vital role of respiration in susceptibility to microwave-induced heating.

Modified control of breathing in genetically obese (ob/ob) mice

1996 ◽  
Vol 81 (2) ◽  
pp. 716-723 ◽  
Author(s):  
C. Tankersley ◽  
S. Kleeberger ◽  
B. Russ ◽  
A. Schwartz ◽  
P. Smith
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Whole Body ◽  
Breathing Frequency ◽  
Wild Type ◽  
Genetic Determinants ◽  
Human Obesity ◽  
Ventilatory Control ◽  
Age Dependent ◽  
Whole Body Plethysmography

Attenuated hypercapnic chemosensitivity and hypoventilation are characteristics periodically associated with human obesity. We tested the hypothesis that ventilatory control is altered by genetic determinants and age-dependent factors that influence the obese phenotype. To this end, the magnitude and pattern of breathing were examined before and associated with the development of obesity in C57BL/6J mice homozygous and heterozygous at the ob gene locus. Breathing frequency and tidal volume were measured using whole body plethysmography, and minute ventilation was assessed during acute hypoxic and hypercapnic challenges with intermittent room air exposures. In age- and weight-matched mice before pronounced obesity, significant (P < 0.05) reductions in hypercapnic ventilatory sensitivity occurred in mutant (ob/ob) mice relative to wild-type (+/+) homozygotes primarily because of an attenuated tidal volume. Longitudinal studies indicated that mutant ob mice developed rapid baseline breathing relative to the wild type, accompanying a twofold greater increase in body mass. Early differences between homozygotes in hypercapnic ventilatory sensitivity were maintained through 230 days. These data demonstrate that genetic determinants at or closely linked to the ob locus influence hypercapnic ventilation before the emergence of pronounced obesity, whereas changes in baseline breathing appear due to age-dependent increases in body weight.

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