Biomedical subjects

E S Schelegle

Publications and source records attributed to E S Schelegle.

At least 37 records · Page 2Linked to original sources

PubMed1999

Evaluation of severe disease induced by aerosol inoculation of calves with bovine respiratory syncytial virus.

OBJECTIVE: To develop a model of bovine respiratory syncytial virus (BRSV) infection that induces severe disease similar to that seen in some cattle with naturally acquired BRSV infection. ANIMALS: 25 male Holstein calves, 8 to 16 weeks old. PROCEDURE: 17 calves were given a low-passage field isolate of BRSV by aerosolization; 8 control calves were given supernatant from noninfected cell culture. Disease was characterized by evaluating clinical signs, virus isolation and pulmonary function tests, and results of blood gas analysis, gross and histologic postmortem examination, and microbiologic testing. RESULTS: Cumulative incidence of cough, harsh lung sounds, adventitious sounds, and dyspnea and increases in rectal temperature and respiratory rate were significantly greater in infected calves. Three infected calves developed extreme respiratory distress and were euthanatized 7 days after inoculation. Virus was isolated from nasal swab specimens from all infected calves but not from mock infected calves. On day 7 after inoculation, mean PaO2 and PaCO2 were significantly lower, and pulmonary resistance was significantly higher, in infected calves. During necropsy, infected calves had varying degrees of necrotizing and proliferative bronchiolitis and alveolitis with syncytial formation. The 3 calves euthanatized on day 7 had emphysematous bullae in the caudal lung lobes; 1 had unilateral pneumothorax. CONCLUSION AND CLINICAL RELEVANCE: Severe disease similar to that seen in some cattle with naturally acquired BRSV infection can be induced in calves with a single aerosol exposure of a low-passage clinical isolate of BRSV. Our model will be useful for studying the pathogenesis of BRSV infection and for evaluating vaccines and therapeutics.

Aerosols↗

PubMed1999

Effect of diet-ingested pirfenidone on pulmonary function, cardiovasculature and blood gas measurements in rats.

Pirfenidone is an antifibrotic drug that we have shown attenuates the increase in collagen buildup in hamsters exposed to bleomycin, in turn reducing pulmonary function and blood gas decrements seen in this model of interstitial pulmonary fibrosis. The systemic effects of pirfenidone ingestion, however, are unknown. We examined the effect of diet-ingested pirfenidone on pulmonary function, systemic and pulmonary cardiovasculature and blood gas measurements, breathing pattern and lung hydroxyproline content in rats fed either a control diet or a diet containing 0.5% pirfenidone. Residual volume was higher and expiratory reserve volume lower in the pirfenidone group, with no change in functional residual capacity. Tidal volume was also lower in the pirfenidone group, with no change in the overall level of ventilation. There was a trend toward a reduced hydroxyproline content and an increased lung compliance in the pirfenidone group. There were no differences in systemic or pulmonary pressures, cardiac output, stroke volume, heart rate, pH or blood gases between the two groups. These data indicate that pirfenidone has few systemic side-effects but may have a mild effect on the basal level of lung collagen content with resulting clinical changes in some pulmonary function measurements and changes in breathing pattern.

Animals↗

PubMed1998

A bovine model of vaccine enhanced respiratory syncytial virus pathophysiology.

A critical issue has been the observation that vaccination of children with a formalin-inactivated respiratory syncytial virus (RSV) vaccine is associated with disease enhancement. We have taken advantage of bovine RSV and our experience with this disease in calves to develop a natural model that parallels human disease. Using formalin-inactivated bovine RSV vaccine calves were either sham-vaccinated/infected, vaccinated/infected, or vaccinated/sham-infected and their clinical signs, pulmonary function, and histological lung lesions quantitatively scored. Interestingly there was significantly greater disease in vaccinated/infected calves and histological lesions in calves were similar to those of affected children. Finally, we note that vaccination did not induce neutralizing antibodies, but IgG antibodies were detected by ELISA. Our model of RSV enhanced disease is important because it provides quantifiable evidence of disease severity that can be applied to evaluate the mechanisms of immunopathology and the safety of candidate RSV vaccines.

Analysis of Variance↗

PubMed1998

Control of ventilation during lung volume changes and permissive hypercapnia in dogs.

We investigated the effect changes in end-expiratory lung volume (EEVL) had on the response to progressive hypercapnia (CO2-response curve) in eight open-chest, anesthetized dogs, in order to clarify the role that vagal lung mechanoreceptors have in altered respiratory drive during permissive hypercapnia. The dogs were ventilated using a positive-pressure ventilator driven by phrenic neural activity. Systemic arterial CO2 tension (PaCO2) was elevated by increasing the fraction of CO2 delivered to the ventilator. EEVL was altered from approximated functional residual capacity ("FRC") to 1.5 and 0.5 "FRC" by changing positive end-expiratory pressure. Although the tidal volume (VT)-PaCO2 and inspiratory time (TI)-PaCO2 relationships were not affected, decreasing EEVL from 1.5 "FRC" to "FRC" and then to 0.5 "FRC" caused a significant (p < 0.01) upward shift in the CO2-response curves for minute ventilation (V I) and frequency (f ), and a significant (p < 0.01) downward shift in the CO2- response curve for expiratory time (TE). We conclude that these shifts were explained by a decrease in the inhibitory activity of slowly adapting pulmonary stretch receptors (PSRs) as EEVL was lowered. In addition, increases in EEVL from 0.5 "FRC" to 1.5 "FRC" caused a significant (p < 0.05) increase in the apneic threshold, which we attribute to an inhibitory effect on central drive caused by increased PSR activity.

Adaptation, Physiological↗

PubMed1997

Contribution of vagal afferents to breathing pattern in rats with lung fibrosis.

In anesthestized male Wistar rats with bleomycin-induced lung fibrosis we examined the influence of lung vagal non-myelinated and myelinated afferents in setting breathing pattern. Fourteen days after intratracheal instillation of bleomycin, lung compliance, total lung capacity (TLC) and inspiratory capacity were reduced while functional residual capacity and residual volume were increased. Baseline tidal volume (VT) was decreased and frequency (fR) increased in the bleomycin treated rats compared with controls. Selective vagal C-fiber blockade did not affect fR or VT in any group. Vagotomy resulted in an increase in VT and decrease in fR in both groups with the percent increase in VT/TLC and decrease in fR being significantly greater in the bleomycin rats compared with controls. Vagotomy also attenuated the significantly elevated PCO2 in the bleomycin treated rats suggesting that bleomycin-induced alterations in breathing pattern contribute to blood gas abnormalities. We conclude that vagal myelinated afferents contribute to the rapid shallow breathing in bleomycin treated rats.

Animals↗

PubMed1997

Pirfenidone attenuates bleomycin-induced changes in pulmonary functions in hamsters.

The antifibrotic potential of pirfenidone (5-methyl-1-phenyl-2-[1H]-pyridone) was examined in a single intratracheal bleomycin dose hamster model of pulmonary fibrosis. Bleomycin-induced fibrosis and the effectiveness of pirfenidone treatment were assessed by measuring pulmonary functions (Cqst, TLC, VC, IC, FRC, RV) and the level of hydroxyproline in whole lung homogenates. Thirty-five male golden Syrian hamsters were randomized into four experimental groups: saline instilled and fed a control diet of rat chow (SCD, n = 8); saline instilled and fed the control diet containing 0.5% (w/w) pirfenidone (SPD, n = 8); bleomycin instilled and fed the control diet (BCD, n = 7); and bleomycin instilled and fed the control diet containing 0.5% pirfenidone (BPD, n = 10). Twenty-one days following bleomycin instillation Cqst/TLC, TLC, VC, and IC were significantly reduced and total lung hydroxyproline levels were significantly increased in the BCD and BPD groups as compared with the SCD and SPD groups, respectively. Pirfenidone ingestion significantly attenuated these bleomycin-induced pertubations in pulmonary functions and lung hydroxyproline levels (BCD versus BPD). The data obtained in this study provide evidence of the benefical effects of pirfenidone in the hamster model of bleomycin-induced pulmonary fibrosis both at the functional and biochemical level.

Animals↗

PubMed1996

Neonatal capsaicin treatment increases the severity of ozone-induced lung injury.

To test the hypothesis that lung sensory C fibers protect the small distal airways and alveoli from oxidant injury, we compared the effects of inhalation of ozone (1 ppm) or filtered air for 8 h on lung injury and lung inflammation in four groups of rats: (1) normal rats exposed to filtered air; (2) normal rats exposed to ozone; (3) rats treated as neonates with capsaicin (50 mg/kg, intraperitoneally) and subsequently exposed to filtered air; and (4) rats treated as neonates with capsaicin and subsequently exposed to ozone. All rats were allowed to recover in filtered air for 0, 4, 16, and 40 h before necropsy. Rats exposed to filtered air (Groups 1 and 3) showed normal airway and parenchyma structure. Normal untreated rats exposed to ozone showed a random distribution of mild, interstitial inflammatory changes and epithelial necrosis of bronchi and bronchiolar epithelium. However, rats treated with capsaicin and subsequently exposed to ozone demonstrated severe acute interstitial inflammation and epithelial coagulate necrosis in all airways, especially in small, peripheral airways and parenchyma; all of these changes were statistically significant. These findings support our hypothesis that lung sensory C fibers protect the distal airways from oxidant injury during acute ozone inhalation.

Air↗

PubMed1995

Influence of background vagal C-fiber activity on eupneic breathing pattern in anesthetized dogs.

In 19 dogs anesthetized with xylazine and alpha-chloralose, we examined the influence of background vagal C-fiber activity on the breathing pattern using a modified perineural capsaicin treatment. In seven dogs, we tested the efficacy of this treatment by recording compound action potentials before and after capsaicin application. In the remaining 12 dogs, we examined the effect of vagal perineural capsaicin on the Hering-Breuer expiratory facilitatory inflation reflex, pulmonary chemoreflex, and breathing pattern (tidal volume and expiratory and inspiratory times). Neither the peak height nor integral of the A wave of the compound action potential was significantly affected. However, the peak height and integral of the C wave of the compound action potential were significantly affected. However, the peak height and integral of the C wave of the compound action potential were significantly reduced. The myelinated fiber-initiated Hering-Breuer reflex remained intact after perineural capsaicin, but the C-fiber-initiated pulmonary chemoreflex was abolished. Perineural capsaicin increased tidal volume (0.399 +/- 0.031 to 0.498 +/- 0.058 liter; P < 0.05), expiratory time (3.62 +/- 0.31 to 4.82 +/- 0.68 s; P < 0.05), inspiratory time (1.49 +/- 0.12 to 1.72 +/- 0.17 s; P < 0.10) and total time per breath (5.11 +/- 1.08 to 6.54 +/- 0.82 s; P < 0.05). We conclude that background vagal C-fiber activity exerts an inhibitory effect on tidal volume and an excitatory effect on breathing frequency.

Action Potentials↗

PubMed1994

Pulmonary mechanics of dogs during transtracheal jet ventilation.

STUDY OBJECTIVE: To quantify the delivered tidal volume and other selected measurements of pulmonary mechanics in an animal model during transtracheal jet ventilation (TTJV), with comparison to positive-pressure mechanical ventilation (PPMV) and spontaneous breathing. DESIGN: Prospective, nonblinded laboratory animal study. INTERVENTIONS: Seven mongrel dogs weighing 24.5 +/- 3.7 kg were anesthetized, paralyzed, and placed within a specially designed volume plethysmograph with the head and neck externalized. Ventilation was performed using TTJV under variable inspiratory time:expiratory time ratios (TI:TE) (1:1, 1:2, 1:3, 1:4, 1.5:2.5, 2:1, 2:2, 3:1, and 4:1) and variable driving air pressures (40, 45, and 50 psi). The dogs then were ventilated with PPMV. Tidal volume, tracheal pressure, transpulmonary pressure, air flow, arterial pressure, central venous pressure, and arterial blood gases were measured during spontaneous ventilation, TTJV, and PPMV. Quasistatic compliance of the lungs was measured after all methods of ventilation. Statistical significance was accepted at P < .05. RESULTS: There was no significant difference between delivered tidal volume during TTJV (446 +/- 69 mL at a TI:TE of 1:3 and 45 psi) and spontaneous breathing (506 +/- 72 mL). TTJV delivered a tidal volume significantly higher than the standard 15 mL/kg volume used for mechanical ventilation in dogs. Tracheal pressure and transpulmonary pressure were not significantly different between TTJV and PPMV. Variations in TI:TE had no significant effect on most of the measured variables, specifically tidal volume or transpulmonary pressure. Minute ventilation increased significantly and PCO2 decreased significantly as frequency increased during TI:TE settings of 1:1, 1:2, and 2:1. Increases in the driving air pressure during TTJV significantly increased the tidal volume as it was raised from 40 psi to 50 psi. There was no change in quasistatic lung compliance during any method of ventilation. CONCLUSION: TTJV delivers an effective tidal volume comparable to both spontaneous breathing and PPMV in a dog model. In the absence of upper-airway obstruction, there was no significant difference in the pulmonary pressures, resistance, and compliance during TTJV, as compared to mechanical ventilation. Variation in TI:TE during TTJV had no major effect on pulmonary mechanics, except to increase minute ventilation and decrease PCO2 as the frequency was increased significantly. Increasing the driving air pressure to the TTJV apparatus significantly augmented delivered tidal volume due to increased air flow.

Animals↗

PubMed1994

Effects of graded upper-airway obstruction on pulmonary mechanics during transtracheal jet ventilation in dogs.

STUDY OBJECTIVE: To quantify the effects of graded upper-airway obstruction on the delivered tidal volume and selected parameters of pulmonary mechanics during transtracheal jet ventilation (TTJV) in a dog model. DESIGN: Laboratory study in which seven dogs were anesthetized, paralyzed, and placed within a volume plethysmograph with the head and neck externalized. INTERVENTIONS: Ventilation was performed using TTJV at 45 psi and a frequency of 15 beats per minute. The upper trachea was occluded progressively using a Foley catheter balloon to induce tracheal pressure levels of approximately 150%, 200%, 250%, and 300% of the tracheal pressure obtained during TTJV-c. Tidal volume, tracheal pressure, transpulmonary pressure, airflow, arterial blood pressure, central venous pressure, and arterial blood gases were measured during all conditions of ventilation. Quasistatic compliance curves of the lungs were measured at the conclusion of spontaneous breathing, TTJV-c, and TTJV (at all levels of obstruction). Minute ventilation and pulmonary flow resistance were calculated for each condition of ventilation. RESULTS: Application of graded upper-airway obstruction during TTJV yielded mean tracheal pressures of 130% (level 1), 190% (level 2), 220% (level 3), and 230% (level 4) of that obtained during TTJV-c (10.9 +/- 2.0 cm H2O). Tidal volume significantly increased with each level of obstruction except between levels 3 and 4 (spontaneous breathing, 506 +/- 72 mL; TTJV-c, 446 +/- 69 mL; level 1, 663 +/- 139 mL; level 2, 780 +/- 140 mL; level 3, 931 +/- 181 mL; and level 4, 944 +/- 135 mL). During TTJV at obstruction level 1, transpulmonary pressure was not significantly higher than either spontaneous breathing or TTJV-c, but did significantly increase during higher levels of obstruction. The mean arterial PCO2 significantly decreased at all levels of obstruction due to significantly increased minute ventilation, with a concomitant increase in arterial pH. There was no significant difference seen in the quasistatic compliance of the lungs among spontaneous breathing, TTJV-c, or TTJV at any level of upper airway obstruction. CONCLUSION: Partial upper-airway obstruction increases the delivered tidal volume, minute ventilation, and transpulmonary pressure of the lungs during TTJV, with consequent decreases in the arterial PCO2 as the amount of obstruction increases. No significant changes were seen in the quasistatic compliance of the lungs, pulmonary flow resistance, or alveolar:arterial gradient, lending support to the position that TTJV is a safe technique under conditions of partial upper-airway obstruction. However, due to significant increases in tidal volume and functional residual capacity and decreases in mean arterial blood pressure, concerns still exist during near-total or total upper-airway obstruction.

Airway Obstruction↗

PubMed1993

Contribution of vagal afferents to respiratory reflexes evoked by acute inhalation of ozone in dogs.

Acute inhalation of ozone induces vagally mediated rapid shallow breathing and bronchoconstriction. In spontaneously breathing anesthetized dogs, we attempted to determine whether afferent vagal C-fibers in the lower airways contributed to these responses. Dogs inhaled 3 ppm ozone for 40-70 min into the lower trachea while cervical vagal temperature was maintained successively at 37, 7, and 0 degrees C. At 37 degrees C, addition of ozone to the inspired air decreased tidal volume and dynamic lung compliance and increased breathing frequency, total lung resistance, and tracheal smooth muscle tension. Ozone still evoked significant effects when conduction in myelinated vagal axons was blocked selectively by cooling the nerves to 7 degrees C. Ozone-induced effects were largely abolished when nonmyelinated vagal axons were blocked by cooling to 0 degree C, breathing during ozone inhalation at 0 degree C being generally similar to that during air breathing at 0 degree C, except that minute volume and inspiratory flow were higher. We conclude that afferent vagal C-fibers in the lower airways make a major contribution to the acute respiratory effects of ozone and that nonvagal afferents contribute to the effects that survive vagal blockade.

Administration, Inhalation↗

PubMed1993

Acute inhalation of ozone stimulates bronchial C-fibers and rapidly adapting receptors in dogs.

To identify the afferents responsible for initiating the vagally mediated respiratory changes evoked by acute exposure to ozone, we recorded vagal impulses in anesthetized, open-chest, artificially ventilated dogs and examined the pulmonary afferent response to ozone (2-3 ppm in air) delivered to the lower trachea for 20-60 min. Bronchial C-fibers (BrCs) were the lung afferents most susceptible to ozone, the activity of 10 of 11 BrCs increasing from 0.2 +/- 0.2 to 4.6 +/- 1.3 impulses/s within 1-7 min of ozone exposure. Ten of 15 rapidly adapting receptors (RARs) were stimulated by ozone, their activity increasing from 1.5 +/- 0.4 to 4.7 +/- 0.7 impulses/s. Stimulation of RARs (but not of BrCs) appeared secondary to the ozone-induced reduction of lung compliance because it was abolished by hyperinflation of the lungs. Ozone had little effect on pulmonary C-fibers or slowly adapting pulmonary stretch receptors. Our results suggest that both BrCs and RARs contribute to the tachypnea and bronchoconstriction evoked by acute exposure to ozone when vagal conduction is intact and that BrCs alone are responsible for the vagally mediated tachypnea that survives vagal cooling to 7 degrees C.

Action Potentials↗

PubMed1992

Corticosteroid administration modifies ozone-induced increases in sheep airway blood flow.

Recently, we have shown that exposure of intubated conscious sheep to 3 to 4 ppm ozone (O3) for 3 h increases bronchial blood flow (Qbr). The purpose of the present study was to assess the potential role of corticosteroids in modulating this increase. Six nasally intubated sheep were exposed to filtered room air, 3.5 ppm O3 on two separate occasions, and 3.5 ppm O3 plus methyl-prednisone, for 3 h. Qbr was measured using a chronically implanted 20 MHz pulsed Doppler flow probe. Qbr, mean aortic pressure, cardiac output, pulmonary artery pressure, arterial blood gases, and core temperature were monitored. After 3 h of 3.5 ppm O3, Qbr increased from 3.2 +/- 0.5 (mean +/- SEM) to 8.5 +/- 1.6 KHz, whereas bronchial vascular resistance (BVR) decreased from the baseline value of 43.6 +/- 8.0 to 15.0 +/- 3 mm Hg/KHz. With corticosteroids, baseline Qbr was 3.2 +/- 0.6 and BVR was 44.2 +/- 9.7; after 3 h of 3.5 ppm O3, Qbr was 3.3 +/- 0.5 KHz and BVR was 39.0 +/- 8.0 mm Hg/KHz. The two 3.5-ppm O3 exposures without corticosteroids were impressively reproducible. Except for Qbr and BVR, no other measured cardiovascular parameters were affected by O3. The results indicate that corticosteroids are capable of interfering with mediator, neurohumoral, or inflammatory cell mechanisms responsible for vasodilation of the airway microcirculation after O3 exposure, but do not specifically address the specific processes whereby this attenuation occurs.

Analysis of Variance↗

PubMed1991

Role of vagal afferents in the control of abdominal expiratory muscle activity in the dog.

We examined the contribution of afferent vagal A- and C-fibers on abdominal expiratory muscle activity (EMA). In seven spontaneously breathing supine dogs anesthetized with alpha-chloralose we recorded the electromyogram of the external oblique muscle at various vagal temperatures before and after the induction of a pneumothorax. When myelinated fibers were blocked selectively by cooling the vagus nerves to 7 degrees C, EMA decreased to 40% of control (EMA at 39 degrees C). With further cooling to 0 degrees C, removing afferent vagal C-fiber activity, EMA returned to 72% of control. On rewarming the vagus nerves to 39 degrees C, we then induced a pneumothorax (27 ml/kg) that eliminated the EMA in all the dogs studied. Cooling the vagus nerves to 7 degrees C, during the pneumothorax, produced a slight though not significant increase in EMA. However, further cooling of the vagus nerves to 0 degrees C caused the EMA to return vigorously to 116% of control. In three dogs, intravenous infusion of a constant incrementally increasing dose of capsaicin, a C-fiber stimulant, decreased EMA in proportion to the dose delivered. These results suggest that EMA is modulated by a balance between excitatory vagal A-fiber activity, most likely from slowly adapting pulmonary stretch receptors, and inhibitory C-fiber activity, most likely from lung C-fibers.

Abdomen↗

PubMed1991

Time course of ozone-induced neutrophilia in normal humans.

Five normal human subjects were exposed for 1 h to filtered air (FA) once and to 0.3 ppm O3 on 3 separate days. Bronchoalveolar lavage (BAL) fluid was obtained less than 1 h after FA and either less than 1, 6, or 24 h after O3 exposure. FEV1 was measured before the exposures and the BAL. The first aliquot [proximal airway (PA) sample] was analyzed separately from the pooled Aliquots 2 through 4 [distal airway and alveolar surface (DAAS) sample]. The data from the PA and DAAS samples were then combined to calculate the values that would have been obtained by pooling all BAL washes. FEV1 was significantly (p less than 0.05) decreased 1 h after O3 exposure, but it returned to preexposure values at 6 and 24 h after O3. The percent of neutrophils in the PA sample was significantly elevated at less than 1 h (3.7%) at 6 h (16.5%), and at 24 h (9.2%) after O3. The percent of neutrophils in the DAAS sample and calculated pooled values were significantly elevated at 6 h (4.1 and 7.6%) and at 24 h (5.1 and 5.8%) after O3. These data demonstrate that O3-induced symptoms, FEV1 decrements, and airway neutrophilia follow different time courses and indicate that the pooling of BAL washes may obscure the detection of an O3-induced bronchiolitis. The degree of neutrophilia in the BAL did not correlate with the sensitivity of the individual subjects when measured by acute changes in FEV1, suggesting a dichotomy of pathways that result in O3-induced airway neutrophilia and pulmonary function decrements.

Bronchoalveolar Lavage Fluid↗

PubMed1990

Acute ozone exposure increases bronchial blood flow in conscious sheep.

This study was initiated to determine the effects of ozone (O3) on sheep airway blood flow. Twenty-three nasally intubated sheep were exposed to filtered air (n = 5), 1 ppm O3 (n = 4), 2 ppm O3 (n = 5), 3 ppm O3 (n = 5), and 4 ppm O3 (n = 4) for 3 h. Bronchial artery flow (Qbr) was measured using a chronically implanted 20 MHz pulsed Doppler flow probe. Qbr, mean aortic pressure, cardiac output, pulmonary artery pressure, arterial blood gases, and core temperature were monitored during the period of the exposures. Exposure to 3 and 4 ppm O3 resulted in a significant increase in Qbr (103 and 204% change, respectively) without affecting any of the other cardiopulmonary parameters measured. These results indicate that O3 induces a dose dependent increase in Qbr which is the result of a vasodilation of the bronchial vasculature which is not dependent upon changes in blood gases or upstream driving pressure.

Administration, Intranasal↗

PubMed1989

O.35 ppm O3 exposure induces hyperresponsiveness on 24-h reexposure to 0.20 ppm O3.

Pulmonary function hyperresponsiveness, defined as enhanced response on reexposure to O3, compared with initial O3 exposure, has been previously noted in consecutive day exposures to high ambient O3 concentrations (i.e., 0.32-0.42 ppm). Effects of consecutive-day exposure to lower O3 concentrations (0.20-0.25 ppm) have yielded equivocal results. To examine the occurrence of hyperresponsiveness at two levels of O3 exposure, 15 aerobically trained males completed seven 1-h exposures of continuous exercise at work rates eliciting a mean minute ventilation of 60 1/min. Three sets of consecutive-day exposures, involving day 1/day 2 exposures to 0.20/0.20 ppm O3, 0.35/0.20 ppm O3, and 0.35/0.35 ppm O3, were randomly delivered via an obligatory mouthpiece inhalation system. A filtered-air exposure was randomly placed 24 h before one of the three sets. Treatment effects were assessed by standard pulmonary function tests, exercise ventilatory pattern (i.e., respiratory frequency, f; and tidal volume, VT) changes and subjective symptom (SS) response. Initial O3 exposures to 0.35 and 0.20 ppm had a statistically significant effect, compared with filtered air, on all measurements. On reexposure to 0.35 ppm O3 24 h after an initial 0.35 ppm O3 exposure, significant hyperresponsiveness was demonstrated for forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), f, VT, and total SS score. Exposure to 0.20 ppm O3 24 h after 0.35 ppm O3 exposure, however, resulted in significantly enhanced responses (compared with initial 0.20 ppm O3 exposure) only for FEV1, f, and VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Acute ozone exposure increases plasma prostaglandin F2 alpha in ozone-sensitive human subjects.

Twenty O3-sensitive and 2O O3-nonsensitive subjects participated in a study to investigate the effects of disparate O3 sensitivity on plasma prostaglandin F2 alpha) responses consequent to exposure to ambient O3 concentrations. Subjects were selected from a pool of 75 normal healthy college-aged males who had been previously exposed to 0.35 ppm O3 for 1 h at an exercising VE of 60 L/min. The selection criterion used was the observed decrement in FEV1 after the O3 exposure: O3-sensitive, FEV1 decrement greater than 24%; O3-nonsensitive, FEV1 decrement less than 11%. Each subject was exposed to filtered air and to 0.20 and 0.35 ppm O3 for 80 min while exercising at a VE of 50 L/min. These experimental protocols were divided into two 40-min sessions separated by a period of 4 to 10 min. PGF2 alpha, FVC, FEV1, and FEF25-75 were evaluated before, during, and after each protocol. SGaw and Vtg were measured before and after each protocol. Plasma PGF2 alpha was significantly increased in the O3-sensitive group during and after the 0.35-ppm O3 exposure.

Adult↗