Respiratory frequency

In the studies reviewed by Brock et al. (1995) and summarized in Section 3.1.1, no deaths occurred in male and female rats exposed at 29,958 or 45,781 ppm for 4 h or in male rats exposed at 31,730 or 42,800 ppm for 6 h. Shallow but rapid respiration and anesthesia were noted at concentrations above 29,000 ppm. A 25 min exposure at 10,000 ppm had no effect on respiratory frequency of male Wistar rats (Janssen 1989). 

Tidal volume and respiratory frequency are used with the anatomic dimensions to model airflow patterns in the respiratory tract. 

Bartlett et alP exposed 194 young rats (3-4 weeks old) continuously to ozone at 0.2 ppm for 28-32 days and observed that there was no effect on respiratory frequency, weight gain, tail-length increase, and external appearance in the ozone-exposed group and that, although both ozone-exposed and control groups looked healthy, 12 ozone-exposed and 11 control animals had pneumonitis at the end of the exposure period. The results with the latter animals were discarded in the later data analysis. 

Mechanism of Action A central nervous system stimulant that directly stimulates the respiratorycenterinthemedullaorindirectlybyeffectsonthecarotid. TfterflpeMtIc Effect Increases pulmonary ventilation by increasing resting minute ventilation, tidal volume, respiratory frequency, and inspiratory neuromuscular drive, and enhances the ventilatory response to carbon dioxide. 

These brain-stem regions are interrelated by diverse neuronal projections and are connected to adrenergic structures [Dampney et al. 1977 Marovitch et al. 1982], such as the locus coeruleus, which are postulated to play a role in panic attacks [Gorman et al. 1989]. Further, experimental evidence suggests that CCK interacts with these brain stem mechanisms in modulating respiratory and cardiovascular functions. Microiontophoretic application of CCK-8S to neurons of the nucleus tractus solitarius in cats decreased both neuronal firing and respiratory frequency, effects that were reversed by administration of CCK-4 [Denavit-Saubie et al. 1985]. 

Decrease in lung volume and increase in respiratory frequency maximum effects measured several days postexposure with return to control values (Burleigh-Flayer and Alarie 1988). 

Concentration-related decrease in lung volume and 2-fold increase in respiratory frequency 18 days postexposure (Burleigh-Flayer and Alarie 1987)... 

Male Fischer 344/N rats were exposed via the nose only for 6 h to concentrations of vinylidene fluoride ranging from 27 to 16 000 ppm [71-42 000 mg/m. Tidal volume (mean, 1.51 mL/brcath) and respiratory frequency (mean, 132 breaths/min) were not influenced by exposure concentration. Steady-state blood levels of vinylidene fluoride increased linearly with increasing exposure concentration up to 16 000 ppm. Vinylidene fluoride tissue/air partition coefficients were determined experimentally to be 0.07, 0.18, 0.8,10, and 0.29 for water, blood, liver, fat and muscle, respectively. Previously published detenninations (Filser Bolt, 1979) for the maximum velocity of metabolism in mg/li/kg) and Michaelis Menten constant (K in mg/L) are 0.07 and 0.13, respectively. Time to reach steady-state blood levels of vinylidene fluoride was less than 15 min for all concentrations. After cessation of exposure, blood levels of vinylidene fluoride decreased to 10% of steady-state levels within 1 h. Simulation of the metabolism of vinylidene fluoride mdicated that although blood levels of vinylidene fluoride increased linearly with increasing exposure concentration, the amount of vinylidene fluoride metabolized per 6-h exposure period approached a maximum at about 2000 ppm [5240 mg/m vinylidene fluoride (Medinsky et al., 1988). 

MDI delivery efficiency depends on the patient s inspiratory flow rate, breathing pattern and hand-mouth coordination. Increases in tidal volume and decreases in respiratory frequency enhance the peripheral deposition in the lung. Most patients need to be trained to use the MDI correctly, as up to 70% of patients fail to do so [26, 30]. 

Three animals are used for the test compound and the standard. Dose-response curves of the effect on respiratory frequency and volume are compared. While p, opioid agonists decrease respiratory function, k opioid agonist either increase or have no effect on respiratory function. The magnitude of respiratory depression produced by p, opioid agonists is related to their efficacy at opioid receptors with low efficacy agonists such as nalbuphine having much less effect on respiration as compared to morphine. 

Opioids are potent respiratory depressants, causing a dose-dependent decrease in respiratory frequency, tidal volume and minute ventilation and increased arterial partial pressure of carbon dioxide (PaC02) (Carvey 1998). Opioids depress chemosensors in the brainstem, decreasing the ventilatory response to carbon dioxide. Opioids also depress rhythmicity in the dorsal respiratory group in the nucleus tractus solitarius, attenuating the respiratory cycle. Opioids, however, do not diminish hypoxic ventilatory drive. Significant elevations in Paco2 can result in increased ICP after opioid administration. 

Other evidence corroborates these data, and confirms that vomeropherin stimulation of the VNO can affect autonomic functions [249e]. This study also tested various chemicals to show that they depolarized the VNO and only the VNO. It also found that such stimulation of the VNO eould alter such autonomic variables as cardiac frequency, respiratory frequency, and electrodermal activity, and supports the idea that vomeropherins can alter the ratio of alpha to beta brain waves in the cortex. 

Sulfur dioxide is rapidly absorbed in the nasopharynx of humans. Humans exposed to 5 ppm of the gas showed increased respiratory frequency and decreased tidal volume. Similar to observations made with animals, human exposure to S02 alters the mode of respiration, as demonstrated by increased frequency, decreased tidal volume, and lowered respiratory and expiration flow rates. Synergism and elevated airway resistance with S02 and aerosols of water and saline have been demonstrated. 

Respiratory Effects. Volunteers were exposed to 98, 113, or 195 ppm 2-butoxyethanol for 4-8 hours (Carpenter et al. 1956). The recorded responses of those exposed to 195 ppm included immediate irritation of the nose and throat. The subjects exposed to 113 ppm also experienced nasal irritation and a slight increase in nasal mucus discharge. In another study, no effects on pulmonary ventilation or respiratory frequency were found in seven male volunteers exposed to 2-butoxyethanol for 2 hours at the Swedish occupational exposure limit (20 ppm) during light physical exercise on a bicycle ergometer (Johanson et al. 1986a). 

Changes in log (rate of gliding motion) versus 1/7 of thiobacterium (Beggiatoa alba) Abrupt changes in log (respiratory frequency) versus temp for carp (Cyprinus carpio) Abrupt change in life expectancy. Drosophila subobscura... 

As in the case of s.c. toxicokinetics, the kinetics of C(+)P(-)- and C(—)P(—)-soman were described mathematically as a discontinuous process, with an equation for the exposure period and an equation for the post-exposure period. In view of the limited number of data points during exposure, the absorption phase was described with a mono-exponential function. In order to describe the exposure phase of C(+)P(-)-soman, lag times of 2 and 4 min were selected for the 8-min exposures to 0.8 and 0.4 LCtjo, respectively. These lag times correspond with the earliest time points at which this stereoisomer could be detected. Toxicokinetic parameters derived from the various calculated concentration-time curves are given in Table 2.6. There were no measurable effects of the exposures on the respiratory minute volume (RMV) and respiratory frequency (RF). 

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