On morphometric measurement of oxygen diffusing capacity in middle ear gas exchange.

An accurate mathematical model of transmucosal gas exchange is prerequisite to understanding middle ear (ME) physiology. Current models require experimentally measured gas species time constants for all extant conditions as input parameters. However, studies on pulmonary gas exchange have shown that a morphometric model that incorporates more fundamental physiochemical and anatomic parameters accurately simulates transport from which the species time constants can be derived for all extant conditions. Here, we implemented a variant of that model for ME gas exchange that requires the measurement of diffusional length (tau) for the ME mucosa. That measure contributes to the mucosal diffusing capacity and reflects the resistance to gas flow between air space and capillary. Two methods for measuring tau have been proposed: linear distance between the air-mucosal boundary and capillary and the harmonic mean of all contributing pathway lengths. Oxygen diffusing capacity was calculated for different ME mucosal geometries by using the two tau measures, and the results were compared with those predicted by a detailed, two-dimensional finite element analysis. Predictive accuracy was improved by incorporating the harmonic tau measure, which captures important information regarding variations in capillary shape and distribution. However, compared with the oxygen diffusing capacity derived from the finite element analysis, both measures yielded nonlinear, positively biased estimates. The morphometric techniques underestimate diffusion length by failing to account for the curvilinear gas flow pathways predicted by the finite element model.     

Gas exchange across avian eggshells oscillates in phase with heartbeat

Rahn et al. (J. Appl. Physiol. 69: 1546-1548, 1990) showed that the gas pressure in a plethysmograph containing an intact egg oscillates in phase with electrocardiogram (ECG) and that this pressure variation could be used as a noninvasive way to determine the heart rate of an avian embryo. One possible mechanism to account for the pressure oscillation is the mechanical movement of the embryonic heart, which leads to volume shifts of gas within the plethysmograph. Another possibility is that the oscillation of gas pressure with heartbeat is pulsatile gas exchange resulting from pulsatile blood flow. If gas exchange were transiently stopped, a pressure signal dependent on gas exchange should disappear, while a pressure signal dependent on cardiovascular motion should persist. Using a number of late-age hen eggs (at days 15-20 of incubation), we tested these hypotheses by suddenly changing the gas composition surrounding an egg and measuring the effect of the pressure oscillation. We found that 1) after 5% CO2-95% N2 was flushed into the plethysmograph (presumably halting gas exchange), pressure oscillations went almost to zero and the ECG signal remained; after air was flushed back to the plethysmograph, the pressure signal returned to control level; 2) after 20% CO2-20% O2-60% N2 was flushed into the plethysmograph (presumably increasing net gas exchange), the pressure signal increased 2.5-fold compared with that in air; and 3) after 1% CO2-99% N2 was flushed into the plethysmograph (presumably reversing gas exchange), the oscillation pressure decreased to one-fourth of that in air and the phase of pressure relative to ECG reversed compared with the phase in air.(ABSTRACT TRUNCATED AT 250 WORDS)     

Examining axial diffusion of nitric oxide in the lungs using heliox and breath hold.

Exhaled nitric oxide (NO) is highly dependent on exhalation flow; thus exchange dynamics of NO have been described by multicompartment models and a series of flow-independent parameters that describe airway and alveolar exchange. Because the flow-independent NO airway parameters characterize features of the airway tissue (e.g., wall concentration), they should also be independent of the physical properties of the insufflating gas. We measured the total mass of NO exhaled (A(I,II)) from the airways after five different breath-hold times (5-30 s) in healthy adults (21-38 yr, n = 9) using air and heliox as the insufflating gas, and then modeled A(I,II) as a function of breath-hold time to determine airway NO exchange parameters. Increasing breath-hold time results in an increase in A(I,II) for both air and heliox, but A(I,II) is reduced by a mean (SD) of 31% (SD 6) (P < 0.04) in the presence of heliox, independent of breath-hold time. However, mean (SD) values (air, heliox) for the airway wall diffusing capacity [3.70 (SD 4.18), 3.56 pl.s(-1).ppb(-1) (SD 3.20)], the airway wall concentration [1,439 (SD 487), 1,503 ppb (SD 644>)], and the maximum airway wall flux [4,156 (SD 2,502), 4,412 pl/s (SD 2,906)] using a single-path trumpet-shaped airway model that considers axial diffusion were independent of the insufflating gas (P > 0.55). We conclude that a single-path trumpet model that considers axial diffusion captures the essential features of airway wall NO exchange and confirm earlier reports that the airway wall concentration in healthy adults exceeds 1 ppm and thus approaches physiological concentrations capable of modulating smooth muscle tone.     

Contribution of gas exchange to slope of phase III of the single-breath nitrogen test

To study the influence of gas exchanges on the slope of phase III, single-breath nitrogen tests (SB-N2) and reversed tests (SB-R) were performed with 10 normal volunteers at expiratory flows of 100 ml.s-1, 500 ml.s-1,11.s-1, and 21.s-1. During the prolonged expiration required for the SB-N2 test, more O2 is consumed that CO2 eliminated. This factor could contribute to the rising slope of phase III. However, if one obtains a reversed slope of phase III (by having O2 as the residual gas and room air as the inspired gas), factors increasing N2 concentration with time of expiration should decrease the steepness of this reversed slope. Our data show that, at an expiratory flow of 100 ml.s-1, the slope of phase III was steeper in SB-N2 than in SB-R by 0.92 +/- 0.31% N2 1-1 (mean +/- SD, p less than 0.01). As the expiratory flow was increased to 500 ml.s-1, this difference decreased to 0.33 +/- 0.19% N2 1-1, and both slopes became similar in magnitude but opposite in direction at an expiratory flow of 1 1.s-1. These data suggest that active gas exchange has a significant influence on the slope of phase III of the SB-N2 test.     

Measuring airway exchange of endogenous acetone using a single-exhalation breathing maneuver.

Exhaled acetone is measured to estimate exposure or monitor diabetes and congestive heart failure. Interpreting this measurement depends critically on where acetone exchanges in the lung. Health professionals assume exhaled acetone originates from alveolar gas exchange, but experimental data and theoretical predictions suggest that acetone comes predominantly from airway gas exchange. We measured endogenous acetone in the exhaled breath to evaluate acetone exchange in the lung. The acetone concentration in the exhalate of healthy human subjects was measured dynamically with a quadrupole mass spectrometer and was plotted against exhaled volume. Each subject performed a series of breathing maneuvers in which the steady exhaled flow rate was the only variable. Acetone phase III had a positive slope (0.054+/-0.016 liter-1) that was statistically independent of flow rate. Exhaled acetone concentration was normalized by acetone concentration in the alveolar air, as estimated by isothermal rebreathing. Acetone concentration in the rebreathed breath ranged from 0.8 to 2.0 parts per million. Normalized end-exhaled acetone concentration was dependent on flow and was 0.79+/-0.04 and 0.85+/-0.04 for the slow and fast exhalation rates, respectively. A mathematical model of airway and alveolar gas exchange was used to evaluate acetone transport in the lung. By doubling the connective tissue (epithelium+mucosal tissue) thickness, this model predicted accurately (R2=0.94+/-0.05) the experimentally measured expirograms and demonstrated that most acetone exchange occurred in the airways of the lung. Therefore, assays using exhaled acetone measurements need to be reevaluated because they may underestimate blood levels.     

Effect of sampling on variability and plateau in oxygen uptake

To evaluate the effect of the gas exchange sampling interval on variability and plateau in O2 uptake (VO2), 10 subjects underwent steady-state treadmill exercise at 50% maximal VO2 and 6 subjects underwent maximal testing using a ramp protocol. During steady-state exercise, gas exchange data were acquired by using 10 different sampling intervals. The variability in VO2 was greater as the sampling interval shortened (SD = 4.5 ml.kg-1.min-1 for breath-by-breath vs. 0.8 ml.kg-1.min-1 for 60-s samples). The breath-by-breath data suggested a Gaussian distribution, and most of the variability was attributable to tidal volume (51%). During ramp testing, the slope of the change in VO2 (for each sample) was regressed with time. Considerable variability in the slopes was observed throughout exercise, and in each subject the slopes varied about zero, demonstrating both positive and negative values throughout submaximal effort. These observations were made despite the use of large sampling intervals. Shortening the sample resulted in even greater variability. We conclude that 1) the sampling interval can have a major impact on gas exchange data during exercise and 2) considerable variability exists in the slope of the change in VO2 with a consistent change in external work regardless of the sample used, suggesting that a plateau (defined as the slope of a VO2 sample at peak exercise that does not differ significantly from a slope of zero) in VO2 is not a reliable physiological marker for maximal effort.     

A simple technique to characterize proximal and peripheral nitric oxide exchange using constant flow exhalations and an axial diffusion model.

The most common technique employed to describe pulmonary gas exchange of nitric oxide (NO) combines multiple constant flow exhalations with a two-compartment model (2CM) that neglects 1) the trumpet shape (increasing surface area per unit volume) of the airway tree and 2) gas phase axial diffusion of NO. However, recent evidence suggests that these features of the lungs are important determinants of NO exchange. The goal of this study is to present an algorithm that characterizes NO exchange using multiple constant flow exhalations and a model that considers the trumpet shape of the airway tree and axial diffusion (model TMAD). Solution of the diffusion equation for the TMAD for exhalation flows >100 ml/s can be reduced to the same linear relationship between the NO elimination rate and the flow; however, the interpretation of the slope and the intercept depend on the model. We tested the TMAD in healthy subjects (n = 8) using commonly used and easily performed exhalation flows (100, 150, 200, and 250 ml/s). Compared with the 2CM, estimates (mean +/- SD) from the TMAD for the maximum airway flux are statistically higher (J'aw(NO) = 770 +/- 470 compared with 440 +/- 270 pl/s), whereas estimates for the steady-state alveolar concentration are statistically lower (CA(NO) = 0.66 +/- 0.98 compared with 1.2 +/- 0.80 parts/billion). Furthermore, CA(NO) from the TMAD is not different from zero. We conclude that proximal (airways) NO production is larger than previously predicted with the 2CM and that peripheral (respiratory bronchioles and alveoli) NO is near zero in healthy subjects.     

Pulmonary gas exchange in humans during normobaric hypoxic exercise

Previous studies (J. Appl. Physiol. 58: 978-988 and 989-995, 1985) have shown both worsening ventilation-perfusion (VA/Q) relationships and the development of diffusion limitation during heavy exercise at sea level and during hypobaric hypoxia in a chamber [fractional inspired O2 concentration (FIO2) = 0.21, minimum barometric pressure (PB) = 429 Torr, inspired O2 partial pressure (PIO2) = 80 Torr]. We used the multiple inert gas elimination technique to compare gas exchange during exercise under normobaric hypoxia (FIO2 = 0.11, PB = 760 Torr, PIO2 = 80 Torr) with earlier hypobaric measurements. Mixed expired and arterial respiratory and inert gas tensions, cardiac output, heart rate (HR), minute ventilation, respiratory rate (RR), and blood temperature were recorded at rest and during steady-state exercise in 10 normal subjects in the following order: rest, air; rest, 11% O2; light exercise (75 W), 11% O2; intermediate exercise (150 W), 11% O2; heavy exercise (greater than 200 W), 11% O2; heavy exercise, 100% O2 and then air; and rest 20 minutes postexercise, air. VA/Q inequality increased significantly during hypoxic exercise [mean log standard deviation of perfusion (logSDQ) = 0.42 +/- 0.03 (rest) and 0.67 +/- 0.09 (at 2.3 l/min O2 consumption), P less than 0.01]. VA/Q inequality was improved by relief of hypoxia (logSDQ = 0.51 +/- 0.04 and 0.48 +/- 0.02 for 100% O2 and air breathing, respectively). Diffusion limitation for O2 was evident at all exercise levels while breathing 11% O2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Implementing a mathematical model to compare oxygen uptake kinetics between cyclists and noncyclists during steady state

The purpose was to compare a mathematical model of oxygen uptake and bioenergetic systems to an experimental protocol. Twelve (N = 12) noncyclists (NC), age (21.8 ± 1.4 years), and 8 (N = 8) cyclists (C), age (30.5 ± 5.7 years), were subjects. All subjects signed an informed consent. Oxygen consumption (VO2, ml·kg?1·min?1) was measured with steady-state VO2 requirements and responses determined using the mathematical model from the following equation: VO2 (WR) = VO2 (rest) + VO2 (unloading pedaling) + α.WR; ΔVO2(t, WR) = ΔVO2 (WR) = [1-e[-(t-td)/tO2]. Exercise means (SD) included the following: VO2NC(WR) = 48.4 (16.6) ml?1·min?1 for NCs and VO2C(WR) = 56.4 (24.95) ml?1·min?1 for Cs ; ΔVO2C(t, WR) = 6:38 ml?1·min?1 for NCs and ΔVO2C(t, WR) = 7.44 ml?1·min?1 for Cs. The correlation between the mathematical model and actual measure was statistically significant (p < 0.01) with a coefficient of r = 0.947. The experimental protocol was significantly associated with the mathematical model. This allows for a quantitative analysis and safe prediction of steady-state oxygen uptake conditions on populations before exposure to exercising conditions. Through more precise analysis of conditions, greater specificity of training may lead to more predictable adaptation outcomes.     

Inhibitory effect of experimental colitis on fluid absorption in rat jejunum: role of the enteric nervous system, VIP, and nitric oxide

Impairment of small intestinal absorption has been described in patients with ulcerative colitis and in animal models of experimental colitis. The pathophysiology of this dysfunction has not been elucidated. The aim of this study was to investigate the effect of chemical colitis on jejunal fluid absorption and determine the role of the enteric nervous system and some putative neurotransmitters. In a rat model of iodoacetamide-induced colitis, jejunal net fluid absorption was evaluated by the in vivo single-pass perfusion technique. The effects of 1) tetrodotoxin (TTX), 2) benzylalkonium chloride (BAC), 3) capsaicin, 4) vasoactive intestinal polypeptide (VIP) antagonism, 5) nitric oxide (NO) synthase (NOS) inhibition, and 6) 5-hydroxytryptamine type 3 and 4 (5-HT(3) and 5-HT(4)) receptor antagonism on the changes in fluid movement were investigated. A significant decrease in jejunal net fluid absorption was found 2 and 4 days after colitis induction: 26 (SD 14) and 28 (SD 19) microl x min(-1) x g dry intestinal wt(-1), respectively [P < 0.0002 compared with sham rats at 61 (SD 6.5) microl x min(-1) x g dry intestinal wt(-1)]. No histological changes were evident in jejunal sections. TTX and BAC reversed this decrease in fluid absorption: 54 (SD 13) and 44 (SD 14) microl x min(-1) x g dry intestinal wt(-1) (P = 0.0005 and P = 0.019, respectively, compared with colitis). Ablation of capsaicin-sensitive primary afferent fibers had a partial effect: 45 (SD 5) microl x min(-1) x g dry intestinal wt(-1) (P = 0.001 and P = 0.003 compared with colitis and sham, respectively). Constitutive and neuronal NOS inhibition and VIP antagonism returned jejunal net fluid absorption to normal values: 66 (SD 19), 61 (SD 5), and 56 (SD 14) microl x min(-1) x g dry intestinal wt(-1), respectively. 5-HT(3) and 5-HT(4) receptor antagonism had no effect. Chemical colitis is associated with a significant decrease in jejunal net fluid absorption. This decrease is neurally mediated and involves VIP- and NO-related mechanisms.     

Effects of methyl-eugenol administration on behavioral models related to depression and anxiety, in rats

Croton zehntneri (Cz) is a popular plant in Brazilian folk medicine. Recently, the use of its essential oil showed depressive activity response in the central nervous system (CNS). Chemical studies show that the main compound of this oil is the methyl-eugenol (ME). This work seeks to evaluate the ME activity in behavioral models of depression and anxiety, in the rat. Male rats (60 days old) were divided into four groups (n = 10) and treated with doses of 1.0, 3.0 and 10.0 ml/100 g body wt., v.o., of ME (experimental) and saline (control). One hour after treatment, they were observed in the forced swimming test and 15 min later in the open-field test. A decrease was observed in the immobility time during the forced swimming test for all experimental groups, in comparison with control group (C = 168.8 +/- 27.3; 1.0 microl = 139.1 +/- 23.5; 3.0 microl = 137.2 +/- 18.7 and 10.0 microl = 139.8 +/- 23.6). The open-field results showed no differences in comparison to the control group. The same was observed for social interaction, plus-maze and holeboard tests, suggesting no alterations in anxiety behavior. These data suggest that ME administration induced antidepressive CNS alterations, expressed by the smallest immobility in the swimming model, and not of a level able to alter motor and exploratory activity in the open-field. The absence of effects observed in the open-field can be a result of the experimental contingency, taking low anxiety levels. These data are in contradiction to observations with Cz essential oil in these models.     

The apparent feedforward response of stomata to air vapour pressure deficit: information revealed by different experimental procedures with two rainforest trees

A decrease in steady-state leaf transpiration rate with increased vapour pressure difference between leaf and air, which is reversible and independent of leaf water status, is evidence for feedforward control of stomatal aperture (Cowan 1977). A recent survey of gas exchange data by Monteith (1995), covering 52 sets of measurements on 16 species, reported that evidence for feedforward control was rare and usually reliant on a single point. We conducted gas exchange experiments on an additional 13 species and observed an apparent feedforward response in only two. However, the response was not reversible and depended upon experimental procedure. In view of this we discuss the appropriate use of the term ‘feedforward’.     

Model of gas transport during high-frequency ventilation

We analyze gas exchange during high-frequency ventilation (HFV) by a stochastic model that divides the dead space into N compartments in series where each compartment has a volume equal to tidal volume (V). We then divide each of these compartments into alpha subcompartments in series, where each subcompartment receives a well-mixed concentration from one compartment and passes a well-mixed concentration to another in the direction of flow. The number of subcompartments is chosen on the basis that 1/alpha = (sigma t/-t)2, where -t is mean transit time across a compartment of volume, and sigma t is standard deviation of transit times. If (sigma t/-t)D applies to the transit times of the entire dead space, the magnitude of gas exchange is proportional to (sigma t/-t)D, frequency, and V raised to some power greater than unity in the range where V is close to VD. When V is very small in relation to VD, gas exchange is proportional to (sigma t/-t)2D, frequency, and V raised to a power equal to either one or two depending on whether the flow is turbulent or streamline, respectively. (sigma t/-t)D can be determined by the relation between the concentration of alveolar gas at the air outlet and volume expired as in a Fowler measurement of the volume of the dead space.     

Middle ear pressure change during controlled breathing with gas mixtures containing nitrous oxide.

The change in middle ear pressure while breathing gas mixtures containing N(2)O was studied in four monkeys. At each of three experimental sessions, monkeys were anesthetized, acclimated for 60 min, breathed with room air for 60 min, and then breathed with 5, 10, or 20% N(2)O for 60 min. Middle ear pressure, rectal temperature, and vital signs were recorded throughout. The time constant for blood-middle ear N(2)O exchange was calculated from these data. Middle ear pressure decreased during acclimation, was stable during air breathing, and increased during N(2)O breathing. The rate of pressure change was similar for both ears of each animal and was directly related to N(2)O percent. The calculated time constant ranged from 0.003 to 0.008 min(-1) across animals but was not different for a given ear across sessions. These results show that breathing gas mixtures containing N(2)O causes predictable and quantifiable increases in middle ear pressure.     

Ventilatory and gas exchange kinetics during exercise in chronic airways obstruction

The influence of chronic obstructive pulmonary disease (COPD) on exercise ventilatory and gas exchange kinetics was assessed in nine patients with stable airway obstruction (forced expired volume at 1 s = 1.1 +/- 0.33 liters) and compared with that in six normal men. Minute ventilation (VE), CO2 output (VCO2), and O2 uptake (VO2) were determined breath-by-breath at rest and after the onset of constant-load subanaerobic threshold exercise. The initial increase in VE, VCO2, and VO2 from rest (phase I), the subsequent slow exponential rise (phase II), and the steady-state (phase III) responses were analyzed. The COPD group had a significantly smaller phase I increase in VE (3.4 +/- 0.89 vs. 6.8 +/- 1.05 liters/min), VCO2 (0.10 +/- 0.03 vs. 0.22 +/- 0.03 liters/min), VO2 (0.10 +/- 0.03 vs. 0.24 +/- 0.04 liters/min), heart rate (HR) (6 +/- 0.9 vs. 16 +/- 1.4 beats/min), and O2 pulse (0.93 +/- 0.21 vs. 2.2 +/- 0.45 ml/beat) than the controls. Phase I increase in VE was significantly correlated with phase I increase in VO2 (r = 0.88) and HR (r = 0.78) in the COPD group. Most patients also had markedly slower phase II kinetics, i.e., longer time constants (tau) for VE (87 +/- 7 vs. 65 +/- 2 s), VCO2 (79 +/- 6 vs. 63 +/- 3 s), and VO2 (56 +/- 5 vs. 39 +/- 2 s) and longer half times for HR (68 +/- 9 vs. 32 +/- 2 s) and O2 pulse (42 +/- 3 vs. 31 +/- 2 s) compared with controls. However, tau VO2/tau VE and tau VCO2/tau VE were similar in both groups. The significant correlations of the phase I VE increase with HR and VO2 are consistent with the concept that the immediate exercise hyperpnea has a cardiodynamic basis. The slow ventilatory kinetics during phase II in the COPD group appeared to be more closely related to a slowed cardiovascular response rather than to any index of respiratory function. O2 breathing did not affect the phase I increase in VE but did slow phase II kinetics in most subjects. This confirms that the role attributed to the carotid bodies in ventilatory control during exercise in normal subjects also operates in patients with COPD.     

Plethysmographic estimation of thoracic gas volume in apneic mice.

Electrical stimulation of intercostal muscles was employed to measure thoracic gas volume (TGV) during airway occlusion in the absence of respiratory effort at different levels of lung inflation. In 15 tracheostomized and mechanically ventilated CBA/Ca mice, the value of TGV obtained from the spontaneous breathing effort available in the early phase of the experiments (TGVsp) was compared with those resulting from muscle stimulation (TGVst) at transrespiratory pressures of 0, 10, and 20 cmH2O. A very strong correlation (r2= 0.97) was found, although with a systematically (approximately 16%) higher estimation of TGVst relative to TGVsp, attributable to the different durations of the stimulated (approximately 50 ms) and spontaneous (approximately 200 ms) contractions. Measurements of TGVst before and after injections of 0.2, 0.4, and 0.6 ml of nitrogen into the lungs in six mice resulted in good agreement between the change in TGVst and the injected volume (r2= 0.98). In four mice, TGVsp and TGVst were compared at end expiration with air or a helium-oxygen mixture to confirm the validity of isothermal compression in the alveolar gas. The TGVst values measured at zero transrespiratory pressure in all CBA/Ca mice [0.29 +/- 0.05 (SD) ml] and in C57BL/6 (N = 6; 0.34 +/- 0.08 ml) and BALB/c (N = 6; 0.28 +/- 0.06 ml) mice were in agreement with functional residual capacity values from previous studies in which different techniques were used. This method is particularly useful when TGV is to be determined in the absence of breathing activity, when it must be known at any level of lung inflation or under non-steady-state conditions, such as during pharmaceutical interventions.     

Mechanisms of gas exchange response to lung volume reduction surgery in severe emphysema

Lung volume reduction surgery (LVRS) improves lung function, respiratory symptoms, and exercise tolerance in selected patients with chronic obstructive pulmonary disease, who have heterogeneous emphysema. However, the reported effects of LVRS on gas exchange are variable, even when lung function is improved. To clarify how LVRS affects gas exchange in chronic obstructive pulmonary disease, 23 patients were studied before LVRS, 14 of whom were again studied afterwards. We performed measurements of lung mechanics, pulmonary hemodynamics, and ventilation-perfusion (Va/Q) inequality using the multiple inert-gas elimination technique. LVRS improved arterial Po? (Pa(O?)) by a mean of 6 Torr (P = 0.04), with no significant effect on arterial Pco? (Pa(CO?)), but with great variability in both. Lung mechanical properties improved considerably more than did gas exchange. Post-LVRS Pa(O?) depended mostly on its pre-LVRS value, whereas improvement in Pa(O(2)) was explained mostly by improved Va/Q inequality, with lesser contributions from both increased ventilation and higher mixed venous Po(2). However, no index of lung mechanical properties correlated with Pa(O?). Conversely, post-LVRS Pa(CO?) bore no relationship to its pre-LVRS value, whereas changes in Pa(CO?) were tightly related (r2 = 0.96) to variables, reflecting decrease in static lung hyperinflation (intrinsic positive end-expiratory pressure and residual volume/total lung capacity) and increase in airflow potential (tidal volume and maximal inspiratory pressure), but not to Va/Q distribution changes. Individual gas exchange responses to LVRS vary greatly, but can be explained by changes in combinations of determining variables that are different for oxygen and carbon dioxide.     

A model for treating isopropyl alcohol and acetone mixtures in a trickle-bed air biofilter

A mathematical model that incorporates mass transfer process and biofilm reactions is presented to predict the performance of a trickle-bed air biofilter (TBAB) for treating isopropyl alcohol (IPA) and acetone (ACE) mixtures. The model consists of a set of mass balance equations for IPA, ACE and oxygen in the bulk gas phase and within the biofilm. The effluent gas phase IPA and ACE concentrations predicted by the present model were in good agreement with the measured data available in a previous study. The important parameters were evaluated by sensitivity analysis to determine their respective effects on model performance. Four parameters were identified that strongly influenced model performance: surface area of the biofilm per unit volume of packing material (A_S), empty-bed residence time (EBRT), maximum specific growth rate of microorganism (μ_m), and microbial yield coefficient (Y). Practical applications of the model to derive the performance equation of TBAB for treating different inlet IPA and ACE concentrations were also demonstrated.     

CO2 elimination as a function of frequency and tidal volume in rabbits during HFO

CO2 elimination (VCO2) was monitored during high-frequency oscillation (HFO) over a frequency (f) range of 2-30 Hz in anesthetized and paralyzed rabbits to determine whether effective gas exchange could be achieved in this species, to determine the f and tidal volume (VT) dependence of gas exchange in this species, and to compare these results with those from dog and human studies. We were able to produce VCO2 levels during HFO that exceeded normal steady-state levels of CO2 production with VT's less than the total dead space volume. VCO2 was related to f in a curvilinear fashion, whereas in some rabbits VCO2 became independent of f at higher frequencies. This curvilinear relationship between f and VCO2 is similar to data from humans but contrasts with the linear relationship found in dogs. Evidence is presented indicating frequency-dependent behavior of gas exchange is correlated with a frequency-dependent decrease in respiratory system resistance. We propose that the frequency-dependent mechanical properties of the rabbit lung may also account for the species differences in HFO gas exchange.