Increase In Respiratory Frequency Research Articles

Respiration patterns of resting wasps (Vespula sp.)

We investigated the respiration patterns of wasps (Vespula sp.) in their viable temperature range (2.9–42.4°C) by measuring CO2 production and locomotor and endothermic activity.Wasps showed cycles of an interburst–burst type at low ambient temperatures (Ta<5°C) or typical discontinuous gas exchange patterns with closed, flutter and open phases. At high Ta of >31°C, CO2 emission became cyclic. With rising Ta they enhanced CO2-emission primarily by an exponential increase in respiration frequency, from 2.6mHz at 4.7°C to 74mHz at 39.7°C. In the same range of Ta CO2 release per cycle decreased from 38.9 to 26.4μlg−1cycle−1. A comparison of wasps with other insects showed that they are among the insects with a low respiratory frequency at a given resting metabolic rate (RMR), and a relatively flat increase of respiratory frequency with RMR.CO2 emission was always accompanied by abdominal respiration movements in all open phases and in 71.4% of the flutter phases, often accompanied by body movements. Results suggest that resting wasps gain their highly efficient gas exchange to a considerable extent via the length and type of respiration movements.

A Physiological Increase of Insulin in the Olfactory Bulb Decreases Detection of a Learned Aversive Odor and Abolishes Food Odor-Induced Sniffing Behavior in Rats

Insulin is involved in multiple regulatory mechanisms, including body weight and food intake, and plays a critical role in metabolic disorders such as obesity and diabetes. An increasing body of evidence indicates that insulin is also involved in the modulation of olfactory function. The olfactory bulb (OB) contains the highest level of insulin and insulin receptors (IRs) in the brain. However, a role for insulin in odor detection and sniffing behavior remains to be elucidated. Using a behavioral paradigm based on conditioned olfactory aversion (COA) to isoamyl-acetate odor, we demonstrated that an intracerebroventricular (ICV) injection of 14 mU insulin acutely decreased olfactory detection of fasted rats to the level observed in satiated animals. In addition, whereas fasted animals demonstrated an increase in respiratory frequency upon food odor detection, this effect was absent in fasted animals receiving a 14 mU insulin ICV injection as well as in satiated animals. In parallel, we showed that the OB and plasma insulin levels were increased in satiated rats compared to fasted rats, and that a 14 mU insulin ICV injection elevated the OB insulin level of fasted rats to that of satiated rats. We further quantified insulin receptors (IRs) distribution and showed that IRs are preferentially expressed in the caudal and lateral parts of the main OB, with the highest labeling found in the mitral cells, the main OB projection neurons. Together, these data suggest that insulin acts on the OB network to modulate olfactory processing and demonstrate that olfactory function is under the control of signals involved in energy homeostasis regulation and feeding behaviors.

The anti-malarial drug Mefloquine disrupts central autonomic and respiratory control in the working heart brainstem preparation of the rat

BackgroundMefloquine is an anti-malarial drug that can have neurological side effects. This study examines how mefloquine (MF) influences central nervous control of autonomic and respiratory systems using the arterially perfused working heart brainstem preparation (WHBP) of the rat. Recordings of nerve activity were made from the thoracic sympathetic chain and phrenic nerve, while heart rate (HR) and perfusion pressure were also monitored in the arterially perfused, decerebrate, rat WHBP. MF was added to the perfusate at 1 μM to examine its effects on baseline parameters as well as baroreceptor and chemoreceptor reflexes.ResultsMF caused a significant, atropine resistant, bradycardia and increased phrenic nerve discharge frequency. Chemoreceptor mediated sympathoexcitation (elicited by addition of 0.1 ml of 0.03% sodium cyanide to the aortic cannula) was significantly attenuated by the application of MF to the perfusate. Furthermore MF significantly decreased rate of return to resting HR following chemoreceptor induced bradycardia. An increase in respiratory frequency and attenuated respiratory-related sympathetic nerve discharge during chemoreceptor stimulation was also elicited with MF compared to control. However, MF did not significantly alter baroreceptor reflex sensitivity.ConclusionsThese studies indicate that in the WHBP, MF causes profound alterations in autonomic and respiratory control. The possibility that these effects may be mediated through actions on connexin 36 containing gap junctions in central neurones controlling sympathetic nervous outflow is discussed.

Focal microdialysis of CO2 in the perifornical-hypothalamic area increases ventilation during wakefulness but not NREM sleep

We investigated whether the perifornical-lateral hypothalamic area (PF-LHA), where the orexin neurons reside, is a central chemoreceptor site by microdialysis of artificial cerebrospinal fluid (aCSF) equilibrated with 25% CO2 into PF-LHA in conscious rats. This treatment is known to produce a focal tissue acidification like that associated with a 6–7mm Hg increase in arterial PCO2. Such focal acidification in the PF-LHA significantly increased ventilation up to 15% compared with microdialysis of normal aCSF equilibrated with 5% CO2 only in wakefulness but not in sleep in both the dark (P=0.004) and light (P<0.001) phases of the diurnal cycle. This response was predominantly due to a significant increase in respiratory frequency (11%, P<0.001). There were no significant effects on ventilation in the group with probes misplaced outside the PF-LHA. These results suggest that PF-LHA functions as a central chemoreceptor site in the central nervous system in a vigilant state dependent manner with predominant effects in wakefulness.

Effects of 28 days silicon dioxide aerosol exposure on respiratory parameters, blood biochemical variables and lung histopathology in rats

Inhalation toxicity of silicon dioxide aerosol (150, 300mg/m3) daily over a period of 28 days was carried out in rats. The changes in respiratory variables during the period of exposure were monitored using a computer programme that recognizes the modifications of the breathing pattern. Exposure to the aerosol caused a time dependent decrease in tidal volume, with an increase in respiratory frequency compared to the control. Biochemical variables and histopathological observation were noted at 28th day following the start of exposure. Biochemical markers of silica induced lung injury like plasma alkaline phosphatase, lactate dehydrogenase and angiotensine converting enzyme activities increased in a concentration dependent manner compared to control. Increase in the plasma enzymatic activities indicates endothelial lung damage, increased lung membrane permeability. Histopathological observation of the lungs confirmed concentration dependent granulomatous inflammation, fibrosis and proteinacious degeneration. Aggregates of mononuclear cells with entrapped silica particles circumscribed by fibroblast were observed in 300mg/m3 silica aerosol exposed group at higher magnification. Decrease in tidal volume and increase in respiratory frequency might be due to the thickening of the alveolar wall leading to a decreased alveolar volume and lowered elasticity of the lung tissue. The trends in histological and biochemical data are in conformity with the respiratory data in the present study. This study reports for the first time, the changes in respiratory variables during silica aerosol exposure over a period of 28 days.

Effects of acute passive stretching on ventilatory pattern during prolonged cycle exercise

Passive stretching, by inducing mechanical and chemical stimuli that activate receptors on the terminal end of group III and IV nerve fibres located within joints and muscle, may increase ventilation \((\dot VE)\)) during exercise. The aim of the study was to assess the effects of an acute bout of passive stretching on the ventilatory pattern. Maximum oxygen uptake was determined in nine participants who then performed a sustained cycle exercise of high intensity (constant workload of 85% of the minimum power to elicit maximum oxygen uptake, \(\dot W_{85} \)) with and without previous stretching. During the tests metabolic and respiratory parameters were recorded breath-by-breath. Time to exhaustion in the \(\dot W_{85} \) test was significantly shorter (−29%) with stretching. During the first 12 min of exercise the following parameters were significantly higher with stretching than without: oxygen uptake (+4%), ventilation (+9%), respiratory muscle power (+16%) and respiratory muscle oxygen uptake (+13%; P < 0.05). The increase in ventilation was accompanied mainly by an increase in respiratory frequency rather than in tidal volume. However, after stretching the metabolic rate also increased. Thus, the higher ventilation might have been a consequence of both higher muscle afferent activation and higher metabolic rate. Stretching alters the respiratory and metabolic response to exercise, but its effects on ventilation need further investigation.

Respiratory and cardiovascular indicators of autonomic nervous system dysregulation in familial dysautonomia

Familial dysautonomia (FD) is a profound sensory and autonomic nervous system disorder associated with an increased risk for sudden death. While bradycardia resulting from loss of sympathetic tone has been hypothesized to play a role in this mortality, extended in-home monitoring has failed to find evidence of low heart rates in children with FD. In order to better characterize the specific cardio-respiratory pathophysiology and autonomic dysregulation in patients with FD, 25 affected children and matched controls were studied with in-home technology, during day and night. Respiratory and heart rate timing and variability metrics were derived from inductance plethysmography and electrocardiogram signals. Selective shortening of inspiratory time produced an overall increase in respiratory frequency in children with FD, with higher daytime respiratory variability (vs. controls), suggesting alterations in central rhythm generating circuits that may contribute to the heightened risk for sudden death. Overall heart rate was increased and variability reduced in FD cases, with elevated heart rates during 20% of study time. Time and frequency domain measures of autonomic tone indicated lower parasympathetic drive in FD patients (vs. controls). These results suggest withdrawal of vagal, rather than sympathetic tone, as a cause for the sustained increase and dramatic lability in respiration and heart rates that characterize this disorder.

Disparate purinergic modulation of respiration in rats and mice

Disparate purinergic modulation of respiration in rats and mice

Acute Changes in Pulmonary Function Following Microinstillation Inhalation Exposure to Soman in Nonatropenized Guinea Pigs

Barometric whole-body plethysmography (WBP) was used to examine pulmonary functions at 4 and 24 hours postexposure to soman (GD) in guinea pigs without therapeutics to improve survival. Endotracheal aerosolization by microinstillation was used to administer GD (280, 561, and 841 mg/m(3)) or saline to anesthetized guinea pigs. Significant increases in respiratory frequency (RF), tidal volume (TV), and minute volume (MV) were observed with 841 mg/m(3) GD at 4 hours and that were reduced at 24 hours postexposure. A dose-dependent increase in peak inspiration flow and peak expiration flow was present at 4-hour post-GD exposure that was reduced at 24 hours. Time of inspiration and expiration were decreased in all doses of GD exposure at 4 and 24 hours, with significant inhibition at 841 mg/m(3). End-expiratory pause (EEP) increased at 280 and 561 mg/m(3), but decreased in animals exposed 841 mg/m(3) at 24 hours postexposure. Pseudo-lung resistance (Penh) and pause followed similar patterns and increased at 4 hours, but decreased at 24 hours postexposure to 841 mg/m(3) of GD compared to control. These studies indicate GD exposure induces dose-dependent changes in pulmonary function that are significant at 841 mg/m(3) at 4 hours and remains 24 hours postexposure. Furthermore, at 4 hours, GD induces bronchoconstriction possibly due to copious airway secretion and ongoing lung injury in addition to cholinergic effects, while at 24 hours GD induces bronchodilation a possible consequence of initial compensatory mechanisms.

Respiratory responses to somatostatin microinjections into the Bötzinger complex and the pre-Bötzinger complex of the rabbit

The respiratory responses to bilateral microinjections (30–50nl) of 5mM somatostatin (SOM) or 10mM cyclosomatostatin (c-SOM, a SOM antagonist) into the Bötzinger complex (BötC), the pre-Bötzinger complex (preBötC) and the rostral inspiratory portion of the ventral respiratory group (iVRG) were investigated in urethane–chloralose anesthetized, vagotomized, paralysed and artificially ventilated rabbits. SOM microinjections into the BötC decreased respiratory frequency and the rate of rise of phrenic nerve activity without obvious changes in its peak amplitude. SOM microinjected into the preBötC caused increases in respiratory frequency and decreases in peak phrenic activity associated with increases in its rate of rise. No changes in respiration were induced by SOM microinjections into the iVRG. Microinjections of c-SOM into the preBötC caused decreases in respiratory frequency as well as in peak amplitude and rate of rise of phrenic nerve activity. The results show that endogenously released SOM within the preBötC contributes to shape the pattern of baseline respiratory activity and that SOM receptors within the BötC and the preBötC have a role in the modulation of respiration in the rabbit.

Prelimbic but not infralimbic cortex is involved in the pressor response to chemoreflex activation in awake rats

The ventral portion of the medial prefrontal cortex comprises the prelimbic cortex (PL) and the infralimbic cortex (IL). Several studies have indicated that both the PL and the IL play an important role in cardiovascular control. Chemoreflex activation by systemic administration of potassium cyanide (KCN) evokes pressor and bradycardiac responses in conscious rats, in addition to an increase in respiratory frequency. We report here a comparison between the effects of pharmacological inhibition of PL and IL neurotransmission on blood pressure and heart rate responses evoked by chemoreflex activation using KCN (i.v.) in conscious rats. Bilateral microinjection of 200 nl of the unspecific synaptic blocker CoCl(2) (1 mm) into the PL evoked a significant attenuation of the pressor response, without affecting the chemoreflex-induced heart rate decrease. However, IL local synapse inhibition evoked no changes in cardiovascular responses induced by chemoreflex activation. Thus, our results suggest that the pressor but not the bradycardiac response to chemoreflex activation is, at least in part, mediated by local neurotransmission present in the PL cortex, without influence of the IL cortex.

Inhalation of isoflurane alters the pulmonary C‐fiber‐mediated respiratory responses in anesthetized rats

This study is aimed to explore the effect of inhaling isoflurane, a commonly used volatile anesthetic, on pulmonary C-fiber (PCF)-mediated respiratory responses. We recorded ventilatory (Study Series I) and nodose ganglion neuronal responses (Study Series II) to right atrial bolus injection of phenylbiguanide (PBG, 20μg/kg), a selective PCF's stimulant, before and during 5% isoflurane exposure for 8 s in anesthetized spontaneously breathing and paralyzed rats, respectively. Isoflurane initially caused a remarkable increase in respiratory frequency (f) during the first 3–5 s exposure, and this response gradually disappeared during the following exposure without significant change in tidal volume. PBG evoked an apnea which was markedly reduced by isoflurane. Correspondingly, isoflurane also increased baseline firing rate of all C-type neurons (n = 17) extracellularly recorded in the nodose ganglia by 136% and attenuated the PBG-induced C-type neuronal excitation by 52%. In sharp contrast, the firing rate of pump-neurons (n = 5) and rapid adapting type neurons (n = 2) was not be affected by PBG injection, but decreased by isoflurane. Our result suggests that isoflurane can stimulate PCFs to produce tachypnea and depress PBG-induced PCF's activity probably through different mechanisms.

Phasic Motor Activity of Respiratory and Non-Respiratory Muscles in REM Sleep

In this study, we quantified the profiles of phasic activity in respiratory muscles (diaphragm, genioglossus and external intercostal) and non-respiratory muscles (neck and extensor digitorum) across REM sleep. We hypothesized that if there is a unique pontine structure that controls all REM sleep phasic events, the profiles of the phasic twitches of different muscle groups should be identical. Furthermore, we described how respiratory parameters (e.g., frequency, amplitude, and effort) vary across REM sleep to determine if phasic processes affect breathing. Electrodes were implanted in Wistar rats to record brain activity and muscle activity of neck, extensor digitorum, diaphragm, external intercostal, and genioglossal muscles. Ten rats were studied to obtain 313 REM periods over 73 recording days. Data were analyzed offline and REM sleep activity profiles were built for each muscle. In 6 animals, respiratory frequency, effort, amplitude, and inspiratory peak were also analyzed during 192 REM sleep periods. Respiratory muscle phasic activity increased in the second part of the REM period. For example, genioglossal activity increased in the second part of the REM period by 63.8% compared to the average level during NREM sleep. This profile was consistent between animals and REM periods (η(2)=0.58). This increased activity seen in respiratory muscles appeared as irregular bursts and trains of activity that could affect rythmo-genesis. Indeed, the increased integrated activity seen in the second part of the REM period in the diaphragm was associated with an increase in the number (28.3%) and amplitude (30%) of breaths. Non-respiratory muscle phasic activity in REM sleep did not have a profile like the phasic activity of respiratory muscles. Time in REM sleep did not have an effect on nuchal activity (P=0.59). We conclude that the concept of a common pontine center controlling all REM phasic events is not supported by our data. There is a drive in REM sleep that affects specifically respiratory muscles. The characteristic increase in respiratory frequency during REM sleep is induced by this drive.

Commentaries on Viewpoint: Initiating inspiration outside the medulla does produce eupneic breathing

Commentaries on Viewpoint: Initiating inspiration outside the medulla does produce eupneic breathing

Phase synchronization of hemodynamic variables and respiration during mental challenge

We studied the synchronization of heart rate, blood pressure and respiration in the sympathetic and parasympathetic branches of the autonomic nervous system during a cancellation test of attention and during mental arithmetic tasks. The synchronization was quantified by the index γ, which has been adopted from the analysis of weakly coupled chaotic oscillators. We analyzed in twenty healthy women the continuous signals partitioned in low (LF, 0.04–0.15Hz) and high (HF, 0.15–0.40Hz) frequencies to investigate whether or not respiration is a main determinant of cardiovascular synchronization. We used surrogate data analysis to distinguish between causal relationships from those that occur by chance. The LF-components of R–R interval and blood pressure showed no synchronization with respiration, whereas synchronization between blood pressure and R–R interval exceeded that occurring by chance (p<.001). Although heart rate, blood pressure and respiratory frequency increased from rest to mental challenge, no effect of mental challenge on the synchronization of the LF-components was seen. The HF-components showed significant synchronization for all variables (p<.001). During mental challenge, synchronization between respiration and R–R interval, respiration and systolic blood pressure (SBP), as well as R–R interval and SBP decreased (p<.01), whereas under resting conditions, respiration was one of the dominant mechanisms determining heart rate variability and systolic blood pressure fluctuations. We conclude that the observed decrease of synchronization during mental challenge is not only driven by the increase in respiratory frequency but that ‘top down’ intervention by the control system at higher levels may play an additional role.

Anesthetic Activation of Central Respiratory Chemoreceptor Neurons Involves Inhibition of a THIK-1-Like Background K+ Current

At surgical depths of anesthesia, inhalational anesthetics cause a loss of motor response to painful stimuli (i.e., immobilization) that is characterized by profound inhibition of spinal motor circuits. Yet, although clearly depressed, the respiratory motor system continues to provide adequate ventilation under these same conditions. Here, we show that isoflurane causes robust activation of CO(2)/pH-sensitive, Phox2b-expressing neurons located in the retrotrapezoid nucleus (RTN) of the rodent brainstem, in vitro and in vivo. In brainstem slices from Phox2b-eGFP mice, the firing of pH-sensitive RTN neurons was strongly increased by isoflurane, independent of prevailing pH conditions. At least two ionic mechanisms contributed to anesthetic activation of RTN neurons: activation of an Na(+)-dependent cationic current and inhibition of a background K(+) current. Single-cell reverse transcription-PCR analysis of dissociated green fluorescent protein-labeled RTN neurons revealed expression of THIK-1 (TWIK-related halothane-inhibited K(+) channel, K(2P)13.1), a channel that shares key properties with the native RTN current (i.e., suppression by inhalational anesthetics, weak rectification, inhibition by extracellular Na(+), and pH-insensitivity). Isoflurane also increased firing rate of RTN chemosensitive neurons in urethane-anesthetized rats, again independent of CO(2) levels. In these animals, isoflurane transiently enhanced activity of the respiratory system, an effect that was most prominent at low levels of respiratory drive and mediated primarily by an increase in respiratory frequency. These data indicate that inhalational anesthetics cause activation of RTN neurons, which serve an important integrative role in respiratory control; the increased drive provided by enhanced RTN neuronal activity may contribute, in part, to maintaining respiratory motor activity under immobilizing anesthetic conditions.

Role of neurokinin receptors and ionic mechanisms within the respiratory network of the lamprey

We have suggested that in the lamprey, a medullary region called the paratrigeminal respiratory group (pTRG), is essential for respiratory rhythm generation and could correspond to the pre-Bötzinger complex (pre-BötC), the hypothesized kernel of the inspiratory rhythm-generating network in mammals. The present study was performed on in vitro brainstem preparations of adult lampreys to investigate whether some functional characteristics of the respiratory network are retained throughout evolution and to get further insights into the recent debated hypotheses on respiratory rhythmogenesis in mammals, such as for instance the “group-pacemaker” hypothesis. Thus, we tried to ascertain the presence and role of neurokinins (NKs) and burst-generating ion currents, such as the persistent Na+ current (INaP) and the Ca2+-activated non-specific cation current (ICAN), described in the pre-Bötzinger complex. Respiratory activity was monitored as vagal motor output. Substance P (SP) as well as NK1, NK2 and NK3 receptor agonists (400–800 nM) applied to the bath induced marked increases in respiratory frequency. Microinjections (0.5–1 nl) of SP as well as the other NK receptor agonists (1 μM) into the pTRG increased the frequency and amplitude of vagal bursts. Riluzole (RIL) and flufenamic acid (FFA) were used to block INaP and ICAN, respectively. Bath application of either RIL or FFA (20–50 μM) depressed, but did not suppress respiratory activity. Coapplication of RIL and FFA at 50 μM abolished the respiratory rhythm that, however, was restarted by SP microinjected into the pTRG. The results show that NKs may have a modulatory role in the lamprey respiratory network through an action on the pTRG and that INaP and ICAN may contribute to vagal burst generation. We suggest that the “group-pacemaker” hypothesis is tenable for the lamprey respiratory rhythm generation since respiratory activity is abolished by blocking both INaP and ICAN, but is restored by enhancing network excitability.

Sedation at Sea of Entangled North Atlantic Right Whales (Eubalaena glacialis) to Enhance Disentanglement

BackgroundThe objective of this study was to enhance removal of fishing gear from right whales (Eubalaena glacialis) at sea that evade disentanglement boat approaches. Titrated intra muscular injections to achieve sedation were undertaken on two free swimming right whales.Methodology/Principal FindingsFollowing initial trials with beached whales, a sedation protocol was developed for right whales. Mass was estimated from sighting and necropsy data from comparable right whales. Midazolam (0.01 to 0.025 mg/kg) was first given alone or with meperidine (0.17 to 0.25 mg/kg) either once or four times over two hours to whale #1102 by cantilevered pole syringe. In the last attempt on whale #1102 there appeared to be a mild effect in 20–30 minutes, with duration of less than 2 hours that included exhalation before the blowhole fully cleared the water. Boat avoidance, used as a measure of sedation depth, was not reduced. A second severely entangled animal in 2009, whale #3311, received midazolam (0.03 mg/kg) followed by butorphanol (0.03 mg/kg) an hour later, delivered ballistically. Two months later it was then given midazolam (0.07 mg/kg) and butorphanol (0.07 mg/kg) simultaneously. The next day both drugs at 0.1 mg/kg were given as a mixture in two darts 10 minutes apart. The first attempt on whale #3311 showed increased swimming speed and boat avoidance was observed after a further 20 minutes. The second attempt on whale #3311 showed respiration increasing mildly in frequency and decreasing in strength. The third attempt on whale #3311 gave a statistically significant increase in respiratory frequency an hour after injection, with increased swimming speed and marked reduction of boat evasion that enabled decisive cuts to entangling gear.Conclusions/SignificanceWe conclude that butorphanol and midazolam delivered ballistically in appropriate dosages and combinations may have merit in future refractory free swimming entangled right whale cases until other entanglement solutions are developed.

Acute Microinstillation Inhalation Exposure to Sarin Induces Changes in Respiratory Dynamics and Functions in Guinea Pigs

This study investigates the toxic effects of sarin on respiratory dynamics following microinstillation inhalation exposure in guinea pigs. Animals are exposed to sarin for 4 minutes, and respiratory functions are monitored at 4 hours and 24 hours by whole-body barometric plethysmography. Data show significant changes in respiratory dynamics and function following sarin exposure. An increase in respiratory frequency is observed at 4 hours post exposure compared with saline controls. Tidal volume and minute volume are also increased in sarin-exposed animals 4 hours after exposure. Peak inspiratory flow increases, whereas peak expiratory flow increases at 4 hours and is erratic following sarin exposure. Animals exposed to sarin show a significant decrease in expiratory time and inspiratory time. End-inspiratory pause is unchanged whereas end-expiratory pause is slightly decreased 24 hours after sarin exposure. These results indicate that inhalation exposure to sarin alters respiratory dynamics and function at 4 hours, with return to normal levels at 24 hours post exposure.

Acute microinstillation inhalation exposure to soman induces changes in respiratory dynamics and functions in guinea pigs

We investigated the toxic effects of the chemical warfare nerve agent (CWNA) soman (GD) on the respiratory dynamics of guinea pigs following microinstillation inhalation exposure. Male Hartley guinea pigs were exposed to 841 mg/m3 of GD or saline for 4 min. At 24 and 48 h post GD exposure, respiratory dynamics and functions were monitored for 75 min after 1 h of stabilization in a barometric whole-body plethysmograph. GD-exposed animals showed a significant increase in respiratory frequency (RF) at 24 h postexposure compared to saline controls. The 24-h tidal volume (TV) increased in GD-exposed animals during the last 45 min of the 75-min monitoring period in the barometric whole-body plethysmograph. Minute ventilation also increased significantly at 24 h post GD exposure. The peak inspiratory flow (PIF) increased, whereas peak expiratory flow (PEF) decreased at 24 h and was erratic following GD exposure. Animals exposed to GD showed a significant decrease in expiratory (Te) and inspiratory time (Ti). Although end inspiratory pause (EIP) and end expiratory pause (EEP) were both decreased 24 h post GD exposure, EEP was more evident. Pause (P) decreased equally during the 75-min recording in GD-exposed animals, whereas the pseudo lung resistance (Penh) decreased initially during the monitoring period but was near control levels at the end of the 75-min period. The 48-h respiratory dynamics and function parameter were lower than 24 post GD exposures. These results indicate that inhalation exposure to soman in guinea pigs alters respiratory dynamics and function at 24 and 48 h postexposure.