Extrathoracic and intrathoracic removal of O3 in tidal-breathing humans

We measured the efficiency of O3 removal from inspired air by the extrathoracic and intrathoracic airways in 18 healthy, nonsmoking, young male volunteers. Removal efficiencies were measured as a function of O3 concentration (0.1, 0.2, and 0.4 ppm), mode of breathing (nose only, mouth only, and oronasal), and respiration frequency (12 and 24 breaths/min). Subjects were placed in a controlled environmental chamber into which O3 was introduced. A small polyethylene tube was then inserted into the nose of each subject, with the tip positioned in the posterior pharynx. Samples of air were collected from the posterior pharynx through the tube and into a rapidly responding O3 analyzer yielding inspiratory and expiratory O3 concentrations in the posterior pharynx. The O3 removal efficiency of the extrathoracic airways was computed with the use of the inspiratory concentration and the chamber concentration, and intrathoracic removal efficiency was computed with the use of the inspiratory and expiratory concentrations. The mean extrathoracic removal efficiency for all measurements was 39.6 +/- 0.7% (SE), and the mean intrathoracic removal efficiency was 91.0 +/- 0.5%. Significantly less O3 was removed both extrathoracically and intrathoracically when subjects breathed at 24 breaths/min compared with 12 breaths/min (P less than 0.001). O3 concentration had no effect on extrathoracic removal efficiency, but there was a significantly greater intrathoracic removal efficiency at 0.4 ppm than at 0.1 ppm (P less than 0.05). Mode of breathing significantly affected extrathoracic removal efficiency, with less O3 removed during nasal breathing than during either mouth breathing or oronasal breathing (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Ozone uptake in the intact human respiratory tract: relationship between inhaled dose and actual dose.

Inhaled concentration (C), minute volume (MV), and exposure duration (T) are factors that may affect the uptake of ozone (O(3)) within the respiratory tract. Ten healthy adult nonsmokers participated in four sessions, inhaling 0.2 or 0.4 ppm O(3) through an oral mask while exercising continuously to elicit a MV of 20 l/min for 60 min or 40 l/min for 30 min. In each session, fractional absorption (FA) was determined on a breath-by-breath basis as the ratio of O(3) uptake to the inhaled O(3) dose. The mean +/- SD value of FA for all breaths was 0.86 +/- 0.06. Although C, MV, and T all had statistically significant effects on FA (P < 0.0001, P = 0.004, and P = 0.026, respectively), the magnitudes of these effects were small compared with intersubject variability. For an average subject, a 0. 05 change in FA would require that C change by 1.3 ppm, MV change by 46 l/min, or T change by 1.7 h. It is concluded that inhaled dose is a reasonable surrogate for the actual dose delivered to a particular subject during O(3) exposures of <2 h, but it is not a reasonable surrogate when comparisons are made between individuals.     

Canine model of nasal congestion and allergic rhinitis.

The ragweed- and histamine-induced decreases in nasal patency in cohorts of ragweed-sensitized and nonsensitized dogs were assessed. The volume of nasal airways (V(NA)) was assessed by acoustic rhinometry and resistance to airflow (R(NA)) by anterior rhinomanometry. Histamine delivered to the nasal passages of five dogs caused a rapid and prolonged increase in R(NA) (0.75 +/- 0.26 to 3.56 +/- 0.50 cmH(2)O. l(-1). min), an effect that was reversed by intranasal delivery of aerosolized phenylephrine. Ragweed challenge in five ragweed-sensitized dogs increased R(NA) from 0.16 +/- 0.02 to 0.53 +/- 0.07 cmH(2)O. l(-1). min and decreased V(NA) from 12.5 +/- 1.9 to 3.9 +/- 0.3 cm(3), whereas administration of saline aerosol neither increased R(NA) nor decreased V(NA). Prior administration of d-pseudoephedrine (30 mg po) attenuated the ragweed-induced increase in R(NA) and decrease in V(NA). Ragweed challenge changed neither R(NA) nor V(NA) in four nonsensitized dogs. Mediator-induced nasal congestion and allergen-induced allergic rhinitis in ragweed-sensitized dogs, which exhibit symptoms similar to human disease, can be used in the evaluation of safety and efficacy of antiallergic activity of potential drugs.     

Role of the nose in resistive load detection

Previous resistive load detection (RLD) studies have ignored the nose, the usual route of breathing. Weber's law predicts the delta R50 (the added load detectable on 50% of presentations) to be a fixed percent of the background resistance (R0) and thus the delta R50/R0 ratio (the Weber fraction) is constant. We have noted the nose to be sensitive to added load, we wondered if the nose might play a role in RLD. To determine whether this was true and to characterize the effects of changes in R0 in the range of normal nasal resistance (RN), we determined R0 and delta R50 using standard techniques under the following conditions: nose vs. decongested nose, nose vs. nose with added external R0 (3.0 and 8.0 cmH2O X l-1 X s), nose vs. anesthetized nose, nose vs. mouth, and mouth vs. mouth with added load (3 cmH2O X l-1 X s). We found that decongestant decreased RN [4.3 +/- 0.6 (SE) to 3.1 +/- 0.5 cmH2O X l-1 X s, P less than 0.05] and delta R50 (1.7 +/- 0.5 to 1.1 +/- 0.3 cmH2O X l-1 X s, P less than 0.05). When an external load of 3 cmH2O X l-1 X s was added to the nose, delta R50 did not change significantly (1.4 +/- 0.2 to 1.1 +/- 0.2 cmH2O X l-1 X s), but the Weber fraction decreased (0.28 +/- 0.05 to 0.15 +/- 0.03, P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Production and absorption of nitric oxide gas in the nose

Some nitric oxide gas (NO) produced in thesinuses and nasal cavity is absorbed before leaving the nose. Tomeasure production and absorption, we introduced NO at differentconcentrations into one nostril while sampling the NO leaving theopposite nostril with the soft palate closed. The quantity of NO gasproduced in six normal subjects (amount leaving plus the amountabsorbed) averaged 352 nl/min and was the same at gas flows rangingfrom 8 to 347 ml/min and at 10 l/min. An absorption coefficientA was calculated by dividing theamount of NO absorbed by the concentration leaving the nose.A ranged from 17 ml/min at a nasal gasflow of 8 ml/min to an A of 24 ml/minat a nasal gas flow of 347 ml/min. The calculated rates of productionand absorption did not change when gas flow rate was increased,suggesting diffusion equilibrium. The amount of uptake of NO in thenasal mucosa can be explained by its solubility coupled with tissue andblood reactivity.

     

Structural basis of muscle O(2) diffusing capacity: evidence from muscle function in situ.

Although evidence for muscle O(2) diffusion limitation of maximal O(2) uptake has been found in the intact organism and isolated muscle, its relationship to diffusion distance has not been examined. Thus we studied six sets of three purpose-bred littermate dogs (aged 10-12 mo), with 1 dog per litter allocated to each of three groups: control (C), exercise trained for 8 wk (T), or left leg immobilized for 3 wk (I). The left gastrocnemius muscle from each animal was surgically isolated, pump-perfused, and electrically stimulated to peak O(2) uptake at three randomly applied levels of arterial oxygenation [normoxia, arterial PO(2) (Pa(O(2))) 77 +/- 2 (SE) Torr; moderate hypoxia, Pa(O(2)): 33 +/- 1 Torr; and severe hypoxia, Pa(O(2)): 22 +/- 1 Torr]. O(2) delivery (ml. min(-1). 100 g(-1)) was kept constant among groups for each level of oxygenation, with O(2) delivery decreasing with decreasing Pa(O(2)). O(2) extraction (%) was lower in I than T or C for each condition, but calculated muscle O(2) diffusing capacity (Dmus(O(2))) per 100 grams of muscle was not different among groups. After the experiment, the muscle was perfusion fixed in situ, and a sample from the midbelly was processed for microscopy. Immobilized muscle showed a 45% reduction of muscle fiber cross-sectional area (P < 0.05), and a resulting 59% increase in capillary density (P < 0.05) but minimal reduction in capillary-to-fiber ratio (not significant). In contrast, capillarity was not significantly different in T vs. C muscle. The results show that a dramatically increased capillary density (and reduced diffusion distance) after short-term immobilization does not improve Dmus(O(2)) in heavily working skeletal muscle.     

Experimental and numerical determination of odorant solubility in nasal and olfactory mucosa

Odorant deposition in the nasal and olfactory mucosas is dependent on a number of factors including local air/odorant flow distribution patterns, odorant mucosal solubility and odorant diffusive transport in the mucosa. Although many of these factors are difficult to measure, mucosal solubility in the bullfrog mucus has been experimentally determined for a few odorants. In the present study an experimental procedure was combined with computational fluid dynamic (CFD) techniques to further describe some of the factors that govern odorant mucosal deposition. The fraction of odorant absorbed by the nasal mucosa (eta) was experimentally determined for a number of odorants by measuring the concentration drop between odorant 'blown' into one nostril and that exiting the contralateral nostril while the subject performed a velopharyngeal closure. Odorant concentrations were measured with a photoionization detector. Odorants were delivered to the nostrils at flow rates of 3.33 and 10 l/min. The velopharyngeal closure nasal air/odorant flows were then simulated using CFD techniques in a 3-D anatomically accurate human nose modeland the mucosal odorant uptake was numerically calculated. The comparison between the numerical simulations and the experimental results lead to an estimation of the human mucosal odorant solubility and the mucosal effective diffusive transport resistance. The results of the study suggest that the increase in diffusive resistance of the mucosal layer over that of a thin layer of water seemed to be general and non-odorant-specific; however, the mucosa solubility was odorant specific and usually followed the trend that odorants with lower water solubility were more soluble in the mucosa than would be predicted from water solubility alone. The ability of this approach to model odorant movement in the nasal cavity was evaluated by comparison of the model output with known values of odorant mucosa solubility.     

Ventilation-perfusion relationships following experimental pulmonary contusion.

Ventilation-perfusion changes after right-sided pulmonary contusion (PC) in swine were investigated by means of the multiple inert gas elimination technique (MIGET). Anesthetized swine (injury, n = 8; control, n = 6) sustained a right-chest PC by a captive-bolt apparatus. This was followed by a 12-ml/kg hemorrhage, resuscitation, and reinfusion of shed blood. MIGET and thoracic computed tomography (CT) were performed before and 6 h after injury. Three-dimensional CT scan reconstruction enabled determination of the combined fractional volume of poorly aerated and non-aerated lung tissue (VOL), and the mean gray-scale density (MGSD). Six hours after PC in injured animals, Pa(O(2)) decreased from 234.9 +/- 5.1 to 113.9 +/- 13.0 mmHg. Shunt (Q(S)) increased (2.7 +/- 0.4 to 12.3 +/- 2.2%) at the expense of blood flow to normal ventilation/perfusion compartments (97.1 +/- 0.4 to 87.4 +/- 2.2%). Dead space ventilation (V(D)/V(T)) increased (58.7 +/- 1.7% to 67.2 +/- 1.2%). MGSD increased (-696.7 +/- 6.1 to -565.0 +/- 24.3 Hounsfield units), as did VOL (4.3 +/- 0.5 to 33.5 +/- 3.2%). Multivariate linear regression of MGSD, VOL, V(D)/V(T), and Q(S) vs. Pa(O(2)) retained VOL and Q(S) (r(2) = .835) as independent covariates of Pa(O(2)). An increase in Q(S) characterizes lung failure 6 h after pulmonary contusion; Q(S) and VOL correlate independently with Pa(O(2)).     

Effect of inspired air temperature on genioglossus activity during nose breathing in awake humans

Experimental data suggest the presence of sensory receptors specific to the nasopharynx that may reflexly influence respiratory activity. To investigate the effects of inspired air temperature on upper airway dilator muscle activity during nose breathing, we compared phasic genioglossus electromyograms (EMGgg) in eight normal awake adults breathing cold dry or warm humidified air through the nose. EMGgg was measured with peroral bipolar electrodes during successive trials of cold air (less than or equal to 15 degrees C) and warm air (greater than or equal to 34 degrees C) nasal breathing and quantified for each condition as percent activity at baseline (room temperature). In four of the subjects, the protocol was repeated after topical nasal anesthesia. For all eight subjects, mean EMGgg was greater during cold air breathing than during baseline (P less than 0.005) or warm air breathing (P less than 0.01); mean EMGgg during warm air breathing was not significantly changed from baseline. Nasal anesthesia significantly decreased the mean EMGgg response to cold air breathing. Nasal airway inspiratory resistance, measured by posterior rhinomanometry in six subjects under similar conditions, was no different for cold or warm air nose breathing [cold 1.4 +/- 0.7 vs. warm 1.4 +/- 1.1 (SD) cmH2O.l-1.s at 0.4 l/s flow]. These data suggest the presence of superficially located nasal cold receptors that may reflexly influence upper airway dilating muscle activity independently of pressure changes in awake normal humans.     

Kinetic characteristics of n-butyl alcohol and iso-butyl alcohol in a composite bead air biofilter

Kinetic characteristics of n-butyl alcohol and iso-butyl alcohol in a composite bead biofilter were investigated. The microbial growth rate of n-butyl alcohol was greater than that of iso-butyl alcohol in the average inlet concentration range of 50-300 ppm. The microbial growth rate was inhibited at higher inlet concentration, and the inhibitive effect in the concentration range of 50-150 ppm was more pronounced than that in the concentration range of 150-300 ppm. The degree of inhibitive effect for n-butyl alcohol was more sensitive than that for iso-butyl alcohol in the concentration range of 50-150 ppm. The zero-order kinetic with the diffusion rate limitation could be regarded as the most adequate biochemical reaction model. The biodegradation rate of n-butyl alcohol was greater than that of iso-butyl alcohol in the average inlet concentration range of 50-300 ppm. The biochemical reaction rate was also inhibited at higher inlet concentration, and the inhibitive effect for iso-butyl alcohol was more pronounced than that for n-butyl alcohol. The factor of the chemical structure of compound was more predominant in the microbial growth and biochemical reaction processes. The maximum elimination capacity of n-butyl alcohol and iso-butyl alcohol were 55.7 and 34.8 g C h(-1)m(-3) bed volume, respectively. The compound with no side group in the main chain would be easier biodegraded by the microbial.     

Longitudinal distribution of chlorine absorption in human airways: a comparison to ozone absorption.

The bolus inhalation method was used to measure the fraction of inhaled chlorine (Cl(2)) and ozone (O(3)) absorbed during a single breath as a function of longitudinal position in the respiratory system of 10 healthy nonsmokers during oral and nasal breathing at respired flows of 150, 250, and 1,000 ml/s. At all experimental conditions, <5% of inspired Cl(2) penetrated beyond the upper airways and none reached the respiratory air spaces. On the other hand, larger penetrations of O(3) beyond the upper airways occurred as flow increased and during nasal than during oral breathing. In the extreme case of oral breathing at 1,000 ml/s, 35% of inhaled O(3) penetrated beyond the upper airways and approximately 10% reached the respiratory air spaces. Mass transfer theory indicated that the diffusion resistance of the tissue phase was negligible for Cl(2) but important for O(3). The gas phase resistances were the same for Cl(2) and O(3) and were directly correlated with the volume of the nose and mouth during nasal and oral breathing, respectively.     

Comparison between the uptake of nitrous oxide and nitric oxide in the human nose

The absorption of nitrous oxide(N₂O) during unidirectional flowwas compared with the rate of uptake of nitric oxide (NO). At flowrates of 10, 20, and 60 ml/min from one nostril to the other, with thesoft palate closed, the N₂Oreached a steady-state rate of absorption in 5-15 min. The meansuperficial capillary blood flow (n = 5) calculated from solubility and the steady-state rate ofN₂O absorption ranged from 13.3 to15.9 ml/min. The relation between absorption ofN₂O in the nose and capillaryblood flow fits a ventilation-perfusion model used by others todescribe uptake of inert, soluble gases in the rat nose. By contrast,the rate of uptake of NO gas, which is chemically reactive, is25-31 times as great as predicted by just its blood-to-airpartition coefficient. Exogenous NO (16.9 parts/million) did not induce nasal vasodilation as measured with laser Doppler andN₂O absorption methods. Thedifference between the measured rate of uptake of NO and the rate ofuptake attributable to its partition coefficient in blood at the rateof blood flow calculated from N₂Ouptake is probably due to chemical reaction of NO in mucous secretions, nasal tissues, and capillary blood.

     

Biofiltration of ethyl acetate and amyl acetate using a composite bead biofilter

Biodegradation kinetic behaviors of ethyl acetate and amyl acetate in a composite bead biofilter were investigated. The composite bead was the spherical PVA/peat/KNO(3)/GAC composite bead which was prepared in our previous works. Both microbial growth rate and biochemical reaction rate were inhibited at higher inlet concentration. For the microbial growth process, the microbial growth rate of ethyl acetate was greater than that of amyl acetate in the inlet concentration range of 100-400ppm. The degree of inhibitive effect was almost the same for ethyl acetate and amyl acetate in this concentration range. The half-saturation constant K(s) values of ethyl acetate and amyl acetate were 16.26 and 12.65ppm, respectively. The maximum reaction rate V(m) values of ethyl acetate and amyl acetate were 4.08 and 3.53gCh(-1)kg(-1) packed material, respectively. Zero-order kinetic with the diffusion limitation could be regarded as the most adequate biochemical reaction model. For the biochemical reaction process, the biochemical reaction rate of ethyl acetate was greater than that of amyl acetate in the inlet concentration range of 100-400ppm. The inhibitive effect for ethyl acetate was more pronounced than that for AA in this concentration range. The maximum elimination capacity of ethyl acetate and amyl acetate were 82.3 and 37.93gCh(-1)m(-3) bed volume, respectively. Ethyl acetate degraded by microbial was easier than amyl acetate did.     

Inhibition of nitric oxide synthase enhances superoxide activity in canine kidney

To evaluate the role of a potential interaction between superoxide anion (O(2)(-)) and nitric oxide (NO) in regulating kidney function, we examined the renal responses to intra-arterial infusion of a superoxide dismutase mimetic, tempol (0.5 mg.kg(-1).min(-1)), in anesthetized dogs treated with or without NO synthase inhibitor, N(omega)-nitro-l-arginine (NLA; 50 microg.kg(-1).min(-1)). In one group of dogs (n = 10), tempol infusion alone for 30 min before NLA infusion did not cause any significant changes in renal blood flow (RBF; 5.2 +/- 0.4 to 5.0 +/- 0.4 ml.min(-1).g(-1)), glomerular filtration rate (GFR; 0.79 +/- 0.04 to 0.77 +/- 0.04 ml.min(-1).g(-1)), urine flow (V; 13.6 +/- 2.1 to 13.9 +/- 2.5 microl.min(-1).g(-1)), or sodium excretion (U(Na)V; 2.4 +/- 0.3 to 2.2 +/- 0.3 micromol.min(-1).g(-1)). Interestingly, when tempol was infused in another group of dogs (n = 12) pretreated with NLA, it caused increases in V (4.4 +/- 0.4 to 9.7 +/- 1.4 microl.min(-1).g(-1)) and in U(Na)V (0.7 +/- 0.1 to 1.3 +/- 0.2 micromol.min(-1).g(-1)) without affecting RBF or GFR. Although NO inhibition caused usual qualitative responses in both groups of dogs, the antidiuretic (47 +/- 5 vs. 26 +/- 4%) and antinatriuretic (67 +/- 4 vs. 45 +/- 11%) responses to NLA were seen much less in dogs pretreated with tempol. NLA infusion alone increased urinary excretion of 8-isoprostane (13.9 +/- 2.7 to 22.8 +/- 3.6 pg.min(-1).g(-1); n = 7), which returned to the control levels (11.6 +/- 3.4 pg.min(-1).g(-1)) during coadministration of tempol. These data suggest that NO synthase inhibition causes enhancement of endogenous O(2)(-) levels and support the hypothesis that NO plays a protective role against the actions of O(2)(-) in the kidney.     

The maximally attainable VO2 during exercise in humans: the peak vs. maximum issue.

The quantification of maximum oxygen uptake (V(O2 max)), a parameter characterizing the effective integration of the neural, cardiopulmonary, and metabolic systems, requires oxygen uptake (VO2) to attain a plateau. We were interested in whether a VO2 plateau was consistently manifest during maximal incremental ramp cycle ergometry and also in ascertaining the relationship between this peak VO2 (V(O2 peak)) and that determined from one, or several, maximal constant-load tests. Ventilatory and pulmonary gas-exchange variables were measured breath by breath with a turbine and mass spectrometer. On average, V(O2 peak) [3.51 +/- 0.8 (SD) l/min] for the ramp test did not differ from that extrapolated from the linear phase of the response in 71 subjects. In 12 of these subjects, the V(O2 peak) was less than the extrapolated value by 0.1-0.4 l/min (i.e., a "plateau"), and in 19 subjects, V(O2 peak) was higher by 0.05-0.4 l/min. In the remaining 40 subjects, we could not discriminate a difference. The V(O2 peak) from the incremental test also did not differ from that of a single maximum constant-load test in 38 subjects or from the V(O2 max) in 6 subjects who undertook a range of progressively greater discontinuous constant-load tests. A plateau in the actual VO2 response is therefore not an obligatory consequence of incremental exercise. Because the peak value attained was not different from the plateau in the plot of VO2 vs. work rate (for the constant-load tests), the V(O2 peak) attained on a maximum-effort incremental test is likely to be a valid index of V(O2 max), despite no evidence of a plateau in the data themselves. However, without additional tests, one cannot be certain.     

Training at high exercise intensity promotes qualitative adaptations of mitochondrial function in human skeletal muscle

This study explored mitochondrial capacities to oxidize carbohydrate and fatty acids and functional optimization of mitochondrial respiratory chain complexes in athletes who regularly train at high exercise intensity (ATH, n = 7) compared with sedentary (SED, n = 7). Peak O(2) uptake (Vo(2max)) was measured, and muscle biopsies of vastus lateralis were collected. Maximal O(2) uptake of saponin-skinned myofibers was evaluated with several metabolic substrates [glutamate-malate (V(GM)), pyruvate (V(Pyr)), palmitoyl carnitine (V(PC))], and the activity of the mitochondrial respiratory complexes II and IV were assessed using succinate (V(s)) and N,N,N',N'-tetramethyl-p-phenylenediamine dihydrochloride (V(TMPD)), respectively. Vo(2max) was higher in ATH than in SED (57.8 +/- 2.2 vs. 31.4 +/- 1.3 ml.min(-1).kg(-1), P < 0.001). V(GM) was higher in ATH than in SED (8.6 +/- 0.5 vs. 3.3 +/- 0.3 micromol O(2).min(-1).g dry wt(-1), P < 0.001). V(Pyr) was higher in ATH than in SED (8.7 +/- 1.0 vs. 5.5 +/- 0.2 micromol O(2).min(-1).g dry wt(-1), P < 0.05), whereas V(PC) was not significantly different (5.3 +/- 0.9 vs. 4.4 +/- 0.5 micromol O(2).min(-1).g dry wt(-1)). V(S) was higher in ATH than in SED (11.0 +/- 0.6 vs. 6.0 +/- 0.3 micromol O(2).min(-1).g dry wt(-1), P < 0.001), as well as V(TMPD) (20.1 +/- 1.0 vs. 16.2 +/- 3.4 micromol O(2).min(-1).g dry wt(-1), P < 0.05). The ratios V(S)/V(GM) (1.3 +/- 0.1 vs. 2.0 +/- 0.1, P < 0.001) and V(TMPD)/V(GM) (2.4 +/- 1.0 vs. 5.2 +/- 1.8, P < 0.01) were lower in ATH than in SED. In conclusion, comparison of ATH vs. SED subjects suggests that regular endurance training at high intensity promotes the enhancement of maximal mitochondrial capacities to oxidize carbohydrate rather than fatty acid and induce specific adaptations of the mitochondrial respiratory chain at the level of complex I.     

Effect of carbohydrate ingestion on glucose kinetics during exercise in the heat.

Six endurance-trained men [peak oxygen uptake (V(O(2))) = 4.58 +/- 0.50 (SE) l/min] completed 60 min of exercise at a workload requiring 68 +/- 2% peak V(O(2)) in an environmental chamber maintained at 35 degrees C (<50% relative humidity) on two occasions, separated by at least 1 wk. Subjects ingested either a 6% glucose solution containing 1 microCi [3-(3)H]glucose/g glucose (CHO trial) or a sweet placebo (Con trial) during the trials. Rates of hepatic glucose production [HGP = glucose rate of appearance (R(a)) in Con trial] and glucose disappearance (R(d)), were measured using a primed, continuous infusion of [6,6-(2)H]glucose, corrected for gut-derived glucose (gut R(a)) in the CHO trial. No differences in heart rate, V(O(2)), respiratory exchange ratio, or rectal temperature were observed between trials. Plasma glucose concentrations were similar at rest but increased (P < 0.05) to a greater extent in the CHO trial compared with the Con trial. This was due to the absorption of ingested glucose in the CHO trial, because gut R(a) after 30 and 50 min (16 +/- 5 micromol. kg(-1). min(-1)) was higher (P < 0.05) compared with rest, whereas HGP during exercise was not different between trials. Glucose R(d) was higher (P < 0.05) in the CHO trial after 30 and 50 min (48.0 +/- 6.3 vs 34.6 +/- 3.8 micromol. kg(-1). min(-1), CHO vs. Con, respectively). These results indicate that ingestion of carbohydrate, at a rate of approximately 1.0 g/min, increases glucose R(d) but does not blunt the rise in HGP during exercise in the heat.     

Adenylate gradients and Ar:O2 effects on legume nodules. II. Changes in the subcellular adenylate pools

Central infected zone tissue of soybean (Glycine max L. Merr.) nodules was fractionated into separate subcellular compartments using density gradient centrifugation in nonaqueous solvents to better understand how exposure to Ar:O(2) (80:20%, v/v) atmosphere affects C and N metabolism, and to explore a potential role for adenylates in regulating O(2) diffusion. When nodules were switched from air to Ar:O(2), adenylate energy charge (AEC) in the plant cytosol rose from 0.63 +/- 0.02 to 0.73 +/- 0.02 within 7 min and to 0.80 +/- 0.01 by 60 min. In contrast, AEC of the mitochondrial compartment of this central zone tissue remained high (0.80 +/- 0.02 to 0.81 +/- 0.02) following Ar treatment while that of the bacteroid compartment was unchanged, at 0.73 +/- 0.02, after 7 min, but declined to 0.57 +/- 0.03 after 60 min. These results were consistent with a simulation model that predicted Ar:O(2) exposure would first reduce ATP demand for ammonia assimilation and rapidly increase cytosolic AEC, before the Ar:O(2)-induced decline mediated by a decrease in nodule O(2) permeability reduces bacteroid AEC. The possibility that adenylates play a key, integrating role in regulating nodule permeability to oxygen diffusion is discussed.     

Selective transport of adenosine into porcine coronary smooth muscle

Adenosine (ADO), an endogenous regulator of coronary vascular tone, enhances vasorelaxation in the presence of nucleoside transport inhibitors such as dipyridamole. We tested the hypothesis that coronary smooth muscle (CSM) contains a high-affinity transporter for ADO. ADO-mediated relaxation of isolated large and small porcine coronary artery rings was enhanced 12-fold and 3.4-fold, respectively, by the transport inhibitor, S-(4-nitrobenzyl)-6-thioinosine (NBTI). Enhanced relaxation was independent of endothelium and was selective for ADO over synthetic analogs. Uptake of [(3)H]ADO into freshly dissociated CSM cells or endothelium-denuded rings was linear and concentration dependent. Kinetic analysis yielded a maximum uptake (V(max)) of 67 +/- 7.0 pmol. mg protein(-1). min(-1) and a Michaelis constant (K(m)) of 10. 5 +/- 5.8 microM in isolated cells and a V(max) of 5.1 +/- 0.5 pmol. min(-1). mg wet wt(-1) and a K(m) of 17.6 +/- 2.6 microM in intact rings. NBTI inhibited transport into small arteries (IC(50) = 42 nM) and cells. Analyses of extracellular space and diffusion kinetics using [(3)H]sucrose indicate the V(max) and K(m) for ADO transport are sufficient to clear a significant amount of extracellular adenosine. These data indicate CSM possess a high-affinity nucleoside transporter and that the activity of this transporter is sufficient to modulate ADO sensitivity of large and small coronary arteries.     

Temporal integration in nasal lateralization of ethanol

Two experiments examined the trade-off between concentration and stimulus duration in nasal lateralization of n-ethyl alcohol. In nasal lateralization, a common measure of irritation threshold, subjects receive chemical vapor in one nostril and clean air in the other. Subjects try to determine which nostril received the chemical. Within experimental runs, subjects received fixed concentrations (1650-5000 ppm) of ethanol, and duration was varied to find the shortest, lateralizable stimulus. In Experiment 1, a small group of subjects was tested intensively to obtain stable individual data. In Experiment 2, a larger group was studied using more rapid methods. In both cases, subjects could lateralize increasingly weaker concentrations with longer stimulus presentations. Hence integration occurred. However, more than a twofold increase in duration was required to compensate for a twofold decrease in concentration to maintain threshold lateralization. These results suggest that an imperfect, mass-integrator model can describe short-term integration of nasal lateralization of ethanol.