Increase In Residual Volume Research Articles

Physiologic Responses of Sheep to Two Different Methods of Papain Exposure

Human emphysema is a progressive, destructive lung disease that produces morphologic and functional heterogeneity throughout its course. Consequently, the mature form of the disease is described by a broad range of anatomic, radiological, and physiologic patterns. This report describes the development and characterization of a sheep model of emphysema that represents many of the essential features of both homogeneous and heterogeneous emphysema. Emphysema was produced by two different techniques of papain exposure: (1) aerosol (75 IU/kg) given weekly for 4 treatments (HM) or (2) aerosol (75 IU/kg) weekly for 3 treatments following subsegmental intrabronchial instillations, 75 IU (in 10 saline) per lobe in 6 lobes (HT). Dexamethasone (0.06 mg/kg iv) was administered prior intrabronchial instillations only. On computed tomography, the HM group had homogeneous emphysema, the HT group gross nonuniformity of disease and bullae formation. Both groups demonstrated a significant (p < .05) increase in residual volume (HM, +38%; HT, +30%). There was a significant increase (p = .002) in total lung capacity per kilogram for the HM group. Emphysema had no effect on active or passive chest wall compliances. Diffusion capacity was significantly (p < .05) reduced in both groups. Both elastic (p = .066) and resistive (p = .025) components of impedance were increased in the HT, and airway resistance increased significantly in the HM groups. The HM model demonstrated gas trapping, a characteristic feature of emphysema, but failed to replicate the alterations in lung dynamics observed in the human form of this disease. The HT model demonstrated less static hyperinflation but significant frequency dependence and hence appeared to better represent the dynamic characteristics of human emphysema.

Data from frequency-volume charts versus maximum free flow rate, residual volume, and voiding cystometric estimated urethral obstruction grade and detrusor contractility grade in men with lower urinary tract symptoms suggestive of benign prostatic hyperplasia.

To examine associations of data from frequency-volume charts with maximum free flow rate, residual volume, and voiding cystometric estimated urethral obstruction grade and detrusor contractility in men with lower urinary tract symptoms suggestive of benign prostatic hyperplasia (BPH). The 160 men included in the study met the criteria of the International Scientific Committee on BPH, i.e., they voided more than 150 mL during uroflowmetry, their residual volume and prostate size were estimated, and they completed frequency-volume charts correctly. From the frequency-volume charts, voiding habits and fluid intake were evaluated. Pressure-flow studies were performed as well. Increasing residual volume was related to a decrease of maximum voided volume and to a decrease of maximum free flow rate. Cystometric capacity was little affected by residual volume. Low contractility did not result in high residual volume. A marked decrease in voided volumes with increasing obstruction grade was observed, due to a decrease of cystometric capacity and an increase of residual volume. Detrusor contractility was little associated with voided volumes. A higher voiding frequency was related to a higher fluid intake. However, increased standardized frequency (number of voidings per 1,000 mL) was associated with a substantial reduction of fluid intake. Infravesical obstruction is the most important factor influencing voided volumes, cystometric capacity, and residual urine volume. Frequency of voiding was not influenced significantly because patients with small voided volumes minimized their fluid intake.

Pulmonary responses during the cycle-run succession in elite and competitive triathletes.

The purpose of this study was to determine the effect of performance level on the pulmonary responses in triathletes during the cycle-run succession. Eight regionally and nationally ranked (Competitive) and six internationally ranked (Elite) male triathletes underwent 30 min of cycling followed by 20 min of running (C-R) and 30 min of control cycling (C). Before and 10 min after each trial, the triathletes underwent lung function testing. Ventilatory data were collected every minute using an automated breath-by-breath system. The results showed that (a) cycling induced a significant increase in residual volume and functional residual capacity in the Elite group (P <.05); (b) although cycling induced a significant decrease in DLCO in both groups, this decrease persisted at the end of the cycle-run exercise in the Competitive group only (P <.05); and (c) the rise in breathing frequency was significantly greater in the Competitive triathletes during the first 8 min of the subsequent run (P <.04). We conclude that the internationally ranked--or elite-performance--triathletes may have developed specific responses to the cycle-run succession.

In vivo effects of head-to-tail 3-alkylpiridinium polymers isolated from the marine sponge Raniera sarai

Water soluble polymeric 3-alkylpyridinium salts (poly APS; MW 18900 and 5520 Da) were isolated from the marine sponge Raniera sarai. In vitro it strongly inhibited acetyl cholinesterase (AChE) from different species (electric eel, horse serum, human erythrocytes). In our experiments the importance of anti AChE activity in the toxin lethality was evaluated. In vivo experiments were performed on male Wistar rats and ECG, blood pressure and breathing pattern were monitored. After i.v. application of lethal doses of the toxin ECG showed signs of hypo perfusion. Arterial blood pressure fell to mid-circulatory pressure, and breathing stopped after a few breaths At sublethal doses the toxin caused an increase of residual volume, prolongation of expiration, and bradycardia. Patho-anatomical examination revealed that the plugs in lung circulation may cause the death of experimental animals due to cardiorespiratory failure.

Upper abdominal surgery: does a lung function test exist to predict early severe postoperative respiratory complications?

We evaluated the capacity to predict severe respiratory complications (SRCs) following upper abdominal surgery (UAS) by using the results of a respiratory questionnaire and preoperative pulmonary function tests. Lung volumes, flows and transfer factor of the lung for carbon monoxide (TL,CO,sb) were assessed in 361 consecutive adult patients (248 males and 113 females). SRCs were diagnosed 24 h after UAS by clinical examination and chest radiography. Univariate and stepwise multiple logistic regression analyses were performed to estimate the odds ratio (OR) and 95% confidence interval (95% CI) of each single input variable, and to determine which indices best predicted outcome. These patients had a 1% mortality rate and 14% incidence of SRCs, with a male:female ratio of 0.86. The best predictors for SRCs by multiple analysis were: preoperative current hypersecretion of mucus (OR=133; p<0.0001); an increase in residual volume (RV) (OR=3.11; p=0.01); and, to a lesser extent, low percentage of predicted values both of forced expiratory volume in one second (FEV1 % pred) and TL,CO,sb. The algorithm thus obtained (logit theta) was extremely sensitive (84%), specific (99%), and accurate (95%) for preoperative prediction of SRCs. We have found that preoperative current hypersecretion of mucus and pulmonary hyperinflation, and to a lesser extent percentage predicted values both of forced expiratory volume in one second and transfer factor of the lung for carbon monoxide, have a significant predictive capacity for severe respiratory complications following upper abdominal surgery.

Hyperpnea-induced changes in parenchymal lung mechanics in normal subjects and in asthmatics.

The effects of hyperpnea on parenchymal lung mechanics are unknown, but they may contribute to the resultant airflow limitation commonly seen in asthma. To investigate these effects, we measured the following parameters in seven asthmatic and six normal subjects before and after 5 min of hyperpnea: specific conductance, upstream resistance, static compliance, the coefficient of retraction, lung volumes, lung hysteresis, and the ratio of maximal to partial flow rates (the M:P ratio, an indicator of the effect of deep inhalation on airflow, and a measure of relative airway and parenchymal hysteresis). In addition to a central effect on the airways, as shown by significant falls in specific conductance, hyperpnea in asthmatics, but not in normal subjects, resulted in significant increases in residual volume and pressure-volume hysteresis, suggestive of changes in parenchymal lung mechanics. The M:P ratio also increased in the asthmatics, consistent with greater increases in airway than in parenchymal hysteresis after hyperpnea. We conclude that hyperpnea has significant effects on the lung parenchyma that contribute to airflow limitation in asthmatics, and we hypothesize that these effects may be due to alterations in peripheral airway smooth muscle tone and surfactant function.

Ozone toxicity in the rat. III. Effect of changes in ambient temperature on pulmonary parameters.

Pulmonary toxicity of ozone (O3) was examined in adult male Fischer 344 rats exposed to 0.5 parts/million O3 for either 6 or 23 h/day over 5 days while maintained at an ambient temperature (Ta) of either 10, 22, or 34 degrees C. Toxicity was evaluated by using changes in lung volumes and the concentrations of constituents of bronchoalveolar lavage fluid that signal lung injury and/or inflammation. Results indicated that toxicity increased as Ta decreased. Exposures conducted at 10 degrees C were associated with the greatest decreases in body weight and total lung capacity and the greatest increases in lavageable protein, lysozyme, alkaline phosphatase activity, and percent neutrophils. O3 effects not modified by Ta included increases in residual volume and lavageable potassium, glucose, urea, and ascorbic acid with exposure at 34 degrees C. Most effects were attenuated during the 5 exposure days and/or returned to normal levels after 7 air recovery days, regardless of prior O3 exposure or Ta. It is possible that Ta-induced changes in metabolic rate may have altered ventilation and, therefore, the O3 doses among rats exposed at the three different Ta levels.

Obstructive and restrictive pulmonary dysfunction increases disability in Parkinson disease

Objective:: The purpose of this study was to determine in Parkinson disease the impact of pulmonary dysfunction on daily living activities (DLA). Patients:: Extrapyramidal motor impairment, pulmonary dysfunction, and DLA disabilities were studied in 58 Parkinson patients consecutively enrolled in a rehabilitation service at a universal hospital. Main Outcome Measures: Extrapyramidal motor impairments were assessed by the United Parkinson's Disease Rating Scale (IPDRS) and the DLA disabilities by the ipdrs, Hoehn-Yahr, and Schwab-England scales. The pulmonary dysfunctions were assessed by spirometry with flow-volume loops, body plethysmography with lung volumes computation, and maximal inspiratory and expiratory slatic mouth pressures. Results: Parkinson patients showed important modifications of pulmonary function with a decrease in forced vital capacity, forced expiratory volume in the first minute, and arterial P o 2, and an increase in residual volume and total airway resistance (RAW). In addition, they showed a high incidence of airway ventilatory obstructions and restrictive dysfunction. The impact of lung disease on daily living activities in Parkinson disease patients was higher in subjects with restrictive pulmonary dysfunctions (Schwab-England test and turning in bed and adjusting bedclothes, walking, falling, and freezing when walking items of UPDRS) and airway obstructions (handling utensils, dressing and hygiene items of UPDRS). Concusions: Airway obstructions or restrictive pulmonary dysfunctions present a high prevalence in Parkinson disease, contributing as a main factor for DLA dysfunctions. The evauation and rehabilitation of respiratory disturbances should be systematically included in the management of these patients.

Length density and total length of acetylcholinesterase positive nerves related to cystometry and in vitro studies of muscle strips in mini‐pig urinary bladder after chronic outflow obstruction and recovery from obstruction

Chronic partial bladder outlet obstruction was created in mini-pigs by implanting a 6-7 mm ring around the proximal urethra. After a median obstruction period of 63 days, the ring was removed and after a median recovery period of 60 days the animals were sacrificed. At each occasion stepwise cystometry, measurement of residual urine, muscle strips studies with electrical and carbachol stimulation, and stereological estimations of length density and total length of acetylcholinesterase positive nerves were performed. The results can be summarized as follows: (1) unchanged sensitivity of muscle strips to carbachol, but markedly decreased contractility and rate of contraction to carbachol, (2) no evidence of detrusor instability, but severely decompensated bladders in two pigs, (3) a significant increase in residual volume, (4) a pronounced decrease in length density and total length of acetylcholinesterase positive nerves, and (5) at field stimulation strips from some pigs showed increased sensitivity and contractility with high atropine and TTX resistance, while strips from the other pigs revealed decreased sensitivity and markedly decreased contractility to electrical stimulation. In general, most of the changes were markedly, though incompletely, reversed after recovery. Light and electron microscopy of muscle strips showed no histological or ultrastructural changes during the experiments or after storing 1 day at 4 degrees C.

ASSESSMENT OF VENTILATORY FUNCTION IN PATIENTS WITH NEUROMUSCULAR DISEASE

In early phases of neuromuscular disease, patients are either free of respiratory symptoms or have exertional dyspnea not explained by obvious obstructive or restrictive lung disease. Physical examination may be negative because generalized muscle weakness does not correlate with the degree of respiratory muscle involvement. When the diaphragm is involved, one may detect the absence of outward excursion during inspiration or even paradoxic inward inspiratory movement of the abdomen on one side. A substantial loss of respiratory muscle strength is typically accompanied by little or no change in spirometry or arterial blood gas composition. Other characteristics are moderate loss of maximal voluntary ventilation and an increase in residual volume, yet PImax and PEmax may be as low as 50% of the predicted value. In more advanced neuromuscular disease, patients may have severe symptoms if the onset is acute or subacute; however, patients with chronic advanced generalized muscle weakness do not exercise and, therefore, may not be breathless. Many patients with advanced neuromuscular disease present with daytime somnolence as a manifestation of a sleep-related breathing disorder. Physical examination may reveal generalized muscle weakness and difficulty with speech or swallowing. Signs specific to respiratory involvement include tachypnea, use of neck inspiratory muscles and abdominal expiratory muscles, and loss of chest-abdomen synchrony. Sometimes paradoxic bilateral inward movement of the abdomen with inspiration is overt. Patients may be unable to cough effectively, have scoliosis, and lack a gag reflex. At this advanced stage, PImax and PEmax are lower than 50% of the predicted value, and the vital capacity is reduced. Maximal voluntary ventilation increases, and residual volume increases further. Patients may not yet exhibit CO2 retention during the day and may even have a low PaCO3. A sleep study may reveal significant hypopneas with severe desaturation and hypercapnia, especially during REM sleep. It is important to be aware that overt ventilatory failure can occur abruptly and that measurement of arterial blood gas composition is not a reliable indicator of this danger. Therefore, it is critically important to heed clinical phenomena, such as increasing dyspnea and tachypnea, and symptoms of sleep disturbance, such as morning headache and daytime somnolence. Physicians should make serial measurements of VC and respiratory muscle strength in patients considered to be at risk for further deterioration.(ABSTRACT TRUNCATED AT 400 WORDS)

Changes in residual volume during induced bronchoconstriction in healthy and asthmatic subjects.

The increase of residual volume (RV) was investigated during acute bronchoconstriction induced in healthy subjects by methacholine (MCh) (Group 1, n = 13) and in asthmatics by MCh (Group 2, n = 21), or housemite dust (Group 3, n = 11) during early and late airway responses (EAR and LAR), or a series of deep breaths (Group 4, n = 7). In all subjects the difference between residual volume after partial (RVp) and maximal maneuver (RV), expressed as a percentage of control FVC, increased during bronchoconstriction and was correlated with the percent increase of maximal to partial flow ratio at 50% of control FVC (M/P50) (r = 0.854, p < 0.0001). At comparable reduction of partial expiratory flow at 50% of control FVC (VP50), the decreases of FEV1 and FVC were less in healthy than asthmatic subjects, whereas the change of FEV1/FVC was similar in all groups, reflecting similar change in slope of flow-volume curves. The increase of RVp was similar in all groups (range: 15 to 19%), but the increase of RV was 6 +/- 1% (SEM) in healthy subjects and significantly greater (range: 11.1 to 13.3%) in all groups of asthmatics (p < 0.02, analysis of variance [ANOVA]). The effect of deep inhalation (DI) on the airway caliber as assessed by the increase of M/P50 was higher in normal subjects than in all groups of asthmatics (p < 0.0001). A negative correlation was found between the increases of RV and M/P50 in all groups (r = -0.358, p < 0.01), suggesting that healthy subjects had a limited increase of RV because of a marked bronchodilator effect of DI.(ABSTRACT TRUNCATED AT 250 WORDS)

Lung structure and function in cigarette smokers.

Cigarette smoking produces an inflammatory response in the airways of everyone but only 15-20% of smokers develop airways obstruction. The present study concerns the relative importance of peripheral airways inflammation and the emphysematous destruction of the parenchymal support of the airways in the pathogenesis of this obstruction. A total of 407 patients with a diagnosis of lung tumour performed pulmonary function tests a day or two before a lung or lobar resection. The specimens were fixed in inflation and analysed at the gross and microscopic level to determine the extent and severity of the emphysematous process, the number of alveoli supporting the outer walls of the airways, and the average distance between alveolar walls. The severity of the inflammatory process in the respiratory and nonrespiratory bronchioles was also assessed using a previously established grading system. The lung function test showed that a decline in FEV1 was associated with an increase in residual volume and a decrease in the diffusing capacity for carbon monoxide and a reduction in the lung maximum elastic recoil pressure. The prevalence of grossly visible emphysema increased as FEV1 declined, but the extent and severity of these lesions and the number of alveoli supporting the outer walls of the peripheral airways was similar at all levels of FEV1. The system used to grade inflammatory response in the peripheral airways failed to identify a specific defect responsible for the physiological abnormalities. The reduction in FEV1 associated with chronic cigarette smoking can be partially explained by loss of lung elastic recoil pressure which reduces the force driving air out of the lung. This loss of elastic recoil pressure is attributed to microscopic enlargement of the air spaces rather than to grossly visible emphysema. The exact nature of the lesions responsible for the peripheral airways obstruction remains to be identified.

Aging, Respiratory Function, and Exercise

Aging leads to a progressive deterioration of lung function, including a decrease of vital capacity, an increase of residual volume, a tendency for the airways to collapse during expiration, enlargement of all components of the respiratory dead space, a poor mixing of inspired gas, poor matching of ventilation with perfusion, a decrease of pulmonary diffusing capacity, and a substantial increase in the work of breathing. Ventilatory demand is increased during most physical tasks, but arterial blood homeostasis is surprisingly well maintained when elderly persons undertake vigorous exercise because peak cardiac output declines in parallel with the loss of ventilatory function. However, dyspnea progressively restricts peak effort as one ages. The exercise specialist cannot restore aged or damaged pulmonary tissue but can attempt to reduce the rate of future functional loss by encouraging smoking cessation, avoiding air pollution, and controlling acute infections. Enhanced fitness, stronger skeletal muscles, and better coordination can reduce ventilatory demand. Resisted breathing exercises may also strengthen the chest muscles and allow a mechanically more efficient pattern of breathing.

Restrictive pattern of pulmonary functions in idiopathic and congenital scoliosis following spinal fusion

This paper presents the results of pulmonary function analysis in 141 subjects. Thirty-five of these were patients with adolescent idiopathic scoliosis, 36 had congenital scoliosis, and the remaining 70 were age-, sex-, height-, weight- and arm-span-matched normal subjects used as controls for adolescent idiopathic scoliosis. The patients with adolescent idiopathic scoliosis had their pulmonary function evaluated pre- and post-operatively. At pre-operative evaluation the mean age was 13.7 years and the mean cobb angle 48 degrees; at post-operative evaluation the figures were 17.1 years and 36 degrees respectively. In the congenital scoliosis group the mean age was 14.5 years and the mean Cobb angle 42 degrees, and pulmonary functions were evaluated at a minimum of 3 years after surgery. The results are as follows: Adolescent idiopathic scoliosis: (i) Marked disproportion was found in the pulmonary volumes following spinal surgery. After taking growth of the thoracic cage into account, the total lung capacity remained unchanged whilst the vital capacity was significantly reduced and there was a significant increase in residual volume. (ii) This disproportionate increase in residual volume was further confirmed by very highly significantly increased residual volume/vital capacity and residual volume/total lung capacity ratios at post-operative evaluation compared to pre-operative ratios (Mann-Whitney test, P = 0.001). (iii) The residual volume was 48% of vital capacity preoperatively compared to 35% in normal controls. The percentages increased to 70% post-operatively, whilst it was unchanged in the matched controls. Congenital scoliosis: (i) The mean residual volume was markedly increased (154% of predicted value). (ii) Vital capacity was significantly reduced in surgically treated patients (68% of predicted values). (iii) This pattern of reduced vital capacity was more marked in those patients who had multiple thoracic anomalies and were treated surgically (46% of predicted value). However, those patients with multiple thoracic anomalies who did not require surgery did not show such reduction of vital capacity. Comparison between idiopathic and congenital scoliosis: (i) In unoperated patients, the percentages of predicted values of total lung capacity, vital capacity and residual volume were significantly greater in congenital scoliosis than in adolescent idiopathic scoliosis. (ii) Post-operatively there was no significant difference in the percentages of predicted values of total lung capacity, vital capacity and residual volume between patients with congenital scoliosis and those with adolescent idiopathic scoliosis, despite the difference in pathogenesis. These findings have relevance to scoliotic patients treated with spinal fusion with regard to their capability to perform strenuous physical activities.

Changes in bladder and external urethral sphincter function after spinal cord injury in the rat.

Spinal cord injury (SCI) in humans results in inappropriate contractions of the external urethral sphincter muscle (EUS) during micturition (bladder-sphincter dyssynergia), leading to urinary retention. The major goal of this study was to determine whether SCI in rats has similar detrimental effects on micturition. After chronic SCI, urethan-anesthetized rats had a significantly (15-fold) increased bladder capacity and impaired voiding (31-fold increase in residual volume) compared with control rats. Bladder contractions in SCI rats were accompanied by abnormal tonic EUS electromyographic activity, whereas the EUS electromyograms of control rats exhibited a burst pattern (4-8 Hz) during voiding. Suppression of EUS activity with neuromuscular blockade did not improve the fraction of urine voided in SCI rats and reduced the fraction voided in control rats. Therefore, both tonic activity and complete quiescence of the rat's EUS appear to be detrimental to voiding, suggesting that the normal bursting EUS activity facilitates bladder emptying. In summary, rats and humans exhibit similar micturition dysfunctions after SCI (e.g., bladder-sphincter dyssynergia and impaired voiding).

Changes in residual volume relative to vital capacity and total lung capacity after arthrodesis of the spine in patients who have adolescent idiopathic scoliosis.

We evaluated pulmonary functions before correction and again after a mean follow-up of three years in thirty-five patients who had adolescent idiopathic scoliosis. The mean age (and standard deviation) at the time of correction was 13.7 +/- 1.8 years, and at the time of follow-up it was 17.1 +/- 2.5 years. The findings in the patients were compared with those in matched normal control subjects. With the exception of forced vital capacity, all of the determinations of absolute pulmonary volume increased postoperatively, but the increases were not all proportional. When the preoperative and follow-up determinations were expressed as percentages of the predicted pulmonary volumes (on the basis of age) to eliminate any effects of the difference in age, there was no change in total lung capacity, but vital capacity and forced vital capacity were significantly reduced. In addition, there was a significant increase in residual volume. Of the mean increase in total lung capacity after correction of the scoliosis, 82 per cent was due to an increase in residual volume and 18 per cent, to an increase in vital capacity. However, in control subjects age-matched at the time of follow-up, the increase in vital capacity contributed 69 per cent of the mean increase in total lung capacity, a very marked difference from the findings in the patients who had scoliosis. In addition, two pulmonary-volume ratios--residual volume to vital capacity and residual volume to total lung capacity--increased in a highly significant fashion (Mann-Whitney test, p < 0.001) after arthrodesis of the spine.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of the axon reflex in capsaicin-induced bronchoconstriction in guinea pigs

To study the axon reflex as a contributing factor to capsaicin-induced bronchoconstriction in vivo, 30 guinea pigs weighing 325 ± 7 g were randomly divided into four groups: Group 1, control( n = 6); Group 2, bupivacaine(n = 11); Group 3, tetrodotoxin (TTX, n = 10); and Group 4, tachykinin depletion ( n = 3). Each animal was anesthetized with pentobarbital sodium, cannulated with a tracheal cannula and venous catheter, paralyzed with gallamine triethiodide, and artificially ventilated. All animals were treated with atropine and phenoxybenzamine, and a ganglionic blocking agent (chlorisondamine) was given to about half of the animals. Capsaicin (16 μg/kg) was intravenously injected to induce bronchoconstriction. Immediately upon the capsaicin being induced each animal exhibited a decrease in vital capacity, maximal expiratory flow and respiratory compliance, as well as a more than six-fold increase in residual volume, indicating severe bronchoconstriction. Then, the airway spasm decreased gradually toward the baseline values. The animals in Group 4 indicated a complete abolishment of the capsaicin-induced bronchoconstriction, whereas Group 2 and Group 3 displayed a significantly attenuated constriction at 15 to 20 min after capsaicin injection. Administration of chlorisondamine did not alter the capsaicin-induced bronchospasm. Since it is known that bupivacaine and TTX block nerve conduction, the data suggest that the axon reflex plays a significant role in the late phase of bronchoconstriction, which is apparently mediated via tachykinins.

Cardiopulmonary Effects of a Brief Exposure to Cigarette Smoke in the Guinea Pig

To investigate whether the acute inflammatory response produced by acute cigarette smoke exposure is associated with alterations in pulmonary and cardiovascular function, using a respirator we exposed 8 guinea pigs to 350 ml of cigarette smoke diluted in 2,000 ml room air for 10 min. Lung volumes, pressure volume curves and flow volume curves were performed. Measurements of pulmonary artery pressure, systemic pressure, heart rate and cardiac output were taken at baseline, immediately after the smoke exposure, and 1.5 h after smoke exposure. Aliquots of peripheral blood for total white cell count and differential count were obtained. After animal sacrifice, the right lung was lavaged and white cell count and differential count performed. We found that acute exposure to cigarette smoke produced a peripheral blood neutrophilia which rose progressively from a baseline of 36.3 +/- 8% to a maximum of 72.2 +/- 7.7% at 1.5 h after exposure. There was pulmonary neutrophilia with 24.6 +/- 6.3% neutrophils in the lavage fluid of the smoke-exposed animals compared to 8.4 +/- 4.3% in the control animals. Immediately after smoke exposure, there was acute airflow obstruction with a decrease in the peak flow and forced expiratory flow between 25-75% vital capacity. This was associated with airtrapping, as shown by a transient increase in residual volume. There was a slight decrease in systemic blood pressure in the smoke-exposed animals associated with a nonsignificant decrease in the heart rate, and the cardiac output remained stable.(ABSTRACT TRUNCATED AT 250 WORDS)

Lung function and bronchial reactivity in aluminum potroom workers.

Lung function and bronchial reactivity were measured in 38 aluminum potroom workers with no airway symptoms and in 20 healthy referents (office workers). All of the participants were non-smokers. The magnitude of exposure to airborne dust (alumina) and fluorides was determined. The aluminum potroom workers had obstructive lung function impairment with a significant decrease in expiratory flow and an increase in residual volume. Diffusing capacity was found to be lower than in the referents. No bronchial hyperreactivity was found in the aluminum potroom workers. The exposure to inhaled alumina and particulate and gaseous fluorides in the plant was low, 15-20% of the Swedish exposure limits. The finding of only modest lung function alterations with no bronchial hyperreactivity in the aluminum potroom workers is not consistent with the results of other authors. This discrepancy can probably be explained by the fact that the exposure to inhaled contaminants in the investigated aluminum plant was low.

Effects of sulfur dioxide or ammonium sulfate exposure, alone or combined, for 4 or 8 months on normal and elastase-impaired rats

Normal and lung-impaired rats were compared after exposure to SO2 and/or (NH4)2SO4 for 4 or 8 months, or for 8 months plus 3 months recovery. Young adult male Sprague-Dawley rats were pretreated intratracheally with either physiologic saline (normal lungs) or porcine pancreatic elastase (impaired lungs). Rats from each pretreatment group were exposed to filtered air (control), to SO2 (1 ppm) or (NH4)2SO4 (0.5 mg/m3), or to combined SO2 + (NH4)2SO4 for 5 hr/day, 5 days/week. Morphologic, physiologic, and immunologic criteria were evaluated. At 4 months cellular immunologic responsiveness was not impaired, but physiologic changes were detected. Morphologic changes were apparent in all time periods. Elastase-induced changes included greater lung volumes, emphysema, and alveolar interstitial fibrosis. Pollutant effects included bronchiolar epithelial hyperplasia and changes in alveolar mean chord length (MCL). Relative to controls, bronchiolar epithelial hyperplasia and MCL increased in saline/pollutant groups, but decreased in elastase/pollutant rats at 4 months. The pretreatment/pollutant interaction was not observed at 8 months. Elastase effects persisted throughout the recovery period. Pollutant effects were more transitory, although alveolar septal fibrosis was greater in saline/(NH4)2SO4 rats at 8 months. Pulmonary function changes associated with elastase included increases in residual volume, functional residual capacity, and the residual volume/total lung capacity ratios. The alveolar plateau of single-breath washout (N2 slope) was significantly steeper in elastase-treated rats but less steep in animals exposed to SO2 or to (NH4)2SO4 than in those exposed to air only.