Biomedical subjects

N Zamel

Publications and source records attributed to N Zamel.

At least 37 records · Page 2Linked to original sources

PubMed1999

Aspiration flow optimized for nasal nitric oxide measurement.

The aim of the present study was to evaluate some of the factors which may influence the reliability of nasal NO measurements, and to optimize methods suitable for children and adults. Nasal nitric oxide (NO) output was determined by chemiluminescent analysis of aspirated samples in 16 adults and 6 children. With the velopharyngeal aperture closed, stable NO levels were obtained at flows ranging form 0.9 to 6.2 L/min. NO output averaged 401.0 +/- 145.4 nL/min./M2 in 6 children, 338.2 +/- 92.3 in 7 adult females and 268.6 +/- 70.2 in 9 adult males. Nasal NO output was independent of flow provided a stable plateau of NO value was reached. In this study, the optimal range of flows was 3.2-5.2 L/min. in adults and 2.2-3.2 L/min. in children. This enables selection of the most favorable flow to be chosen for individual subjects and situations.

Adult↗

PubMed1999

Does nasal nitric oxide come from the sinuses?

OBJECTIVE: The purpose of this study was to assess nitric oxide (NO) output by the nose and sinuses. METHOD: In one volunteer, the osteomeatal complex and sphenoethmoidal recess were occluded to isolate the nose from the sinuses. The antrum and frontal sinus were each punctured by two catheters and irrigated with air at constant flow. Nitric oxide output and its rate of accumulation in the absence of air flow were measured in each sinus and in the adjacent nasal cavity. RESULTS: Prior to ostial occlusion, NO output in the nose was 96 nL/min. It decreased by 12% after blockage of all of the ostia. In the isolated sinuses, it was 190 nL/min (antrum) and 68 nL/min (frontal). After 5 minutes stagnation; NO concentration [NO] rose in the occluded sinuses to 24,700 nL/L in the antrum and 22,300 nL/L in the frontal sinus. In the nose, it increased to 29,000 nL/L. When the period of stagnation was prolonged in the frontal sinus, the [NO] reached a plateau. NO output and accumulation were not altered in the nose or either sinus by opening their ostia. In the antrum and frontal sinus, lidocaine reduced NO output and the rate of NO accumulation, but not in the nose. CONCLUSIONS: In this volunteer, 88% of nasal NO was derived from the nose itself. Nitric oxide exchange between the frontal sinus, antrum, and nose was negligible. In the absence of air flow, [NO] rose to a plateau in the nose and frontal sinus. Lidocaine inhibited NO output in the sinuses but not the nose.

Humans↗

PubMed1998

A significant proportion of exhaled nitric oxide arises in large airways in normal subjects.

Nitric oxide (NO) of endogenous origin is present in exhaled breath. An increase in exhaled NO concentration (ENO) has been described in bronchial asthma and ENO falls after inhaled steroid therapy. The sources of ENO may include pulmonary blood, the gas exchange region, conducting airways and the nasal cavity. In four healthy volunteers, a catheter was placed in a main bronchus after topical anesthesia in order to sample airway NO (CNO). Exhaled nitric oxide of bronchopulmonary and oropharyngeal origin (ENO(b/o)) was measured while excluding nasal NO and was controlled for expiratory flow. During the same exhalation, ENO(b/o) was compared to CNO at multiple sites in the airway as the catheter was progressively withdrawn. Mean CNO concentration in a position corresponding to a main bronchus was 51.4 +/- 10.8% of ENO(b/o). As the catheter was withdrawn, mean CNO concentration progressively increased both in absolute values and as a proportion of ENO(b/o), until in the oropharynx, it was 96.1 +/- 5.2% ENO(b/o). We conclude that a significant proportion of ENO(b/o) arises in the large airways and trachea in normal subjects and contains a minor oropharyngeal component.

Adult↗

PubMed1998

Role of the external nasal dilator in the management of nasal obstruction.

The aim of this study is to evaluate the effect of an external nasal dilator in patients with nasal obstruction secondary to mucosal congestion (n = 33) or to septal deviation in the nasal valve area (n = 28). A group of subjects with healthy nasal cavities was tested also (n = 51). Acoustic rhinometric and rhinomanometric nasal measurements were performed with and without the dilator and before and after topical decongestion of the nasal mucosa. A visual analog scale was employed to evaluate the subjective sensation of nasal obstruction. Objective measurements showed that the external dilator increased the minimum cross-sectional area and decreased the nasal resistance significantly in all three groups (P < 0.01). The effect was more impressive in patients with septal deviation (P < 0.001). Subjective assessments reflected patency in all subjects except those in the mucosal swelling group (P = 0.06). From this study the authors conclude that the external nasal dilator offers an effective, nonsurgical therapeutic approach in the management of septal deviation that obstructs the nasal valve area. Although patients with nasal obstruction secondary to mucosal congestion showed objective improvement with the nasal dilator, these changes were not accompanied by a sensation of enhanced patency.

Adolescent↗

PubMed1998

Exhaled nitric oxide in human lung transplantation. A noninvasive marker of acute rejection.

Acute allograft rejection in animals and humans has been associated with increased nitric oxide production in the graft. Exhaled nitric oxide (ENO) measurement is a noninvasive method of assessing inflammation in airway diseases, e.g., asthma, which might be applicable to lung transplant recipients. Over 12 months, ENO of lower respiratory origin was measured in 108 lung transplant recipients with a mean time after transplant of 1,083 d. ENO (mean +/- SEM; ppb) in stable patients (19.5 +/- 1.1; p < 0.001) was not different from that of healthy controls (23.8 +/- 3.2). ENO was significantly higher in episodes of clinical acute rejection (51.1 +/- 6.3) compared with stable patients but not elevated in bronchiolitis obliterans syndrome (18.6 +/- 1.5) or pulmonary infection (25.9 +/- 4.0). A retrospective analysis of bronchoscopy findings and concurrent ENO (n = 99) showed that ENO did not vary according to histological findings (normal, acute rejection grade I, nonspecific inflammatory change) or with a positive BAL culture. ENO was not correlated with differential lymphocyte and neutrophil counts. ENO appears to be a valid marker of clinical acute rejection in human lung transplantation as distinct from infection or bronchiolitis obliterans. Furthermore, bronchoscopic findings in the absence of a clinical illness were not associated with a rise in ENO.

Adult↗

PubMed1998

Pseudophysiologic emphysema resulting from severe small-airways disease.

Loss of lung elastic recoil causing hyperinflation with increased TLC and decreased diffusing capacity and expiratory airflow are physiologic hallmarks of emphysema. We studied lung mechanics in 10 patients (seven men and three women) aged 69 +/- 9 yr (mean +/- SD) who had fixed, severe expiratory airflow limitation with a mean FEV1 = 0.73 +/- 0.1 L (mean +/- SD) (32 +/- 7% predicted) and lung computed tomographic picture grade score <= 20, indicating no or trivial emphysema. Three patients died, in whom whole-lung emphysema scores were 15 each and small airways were abnormal. Marked hyperinflation was present in all 10 patients studied, with TLC 7.3 +/- 1.1 L (140 +/- 12% predicted); FRC 5.6 +/- 0.8 L (177 +/- 30% predicted); and RV 5.2 +/- 0.8 L (242 +/- 28% predicted). Diffusing capacity of carbon monoxide (DLCO was reduced, at 12 +/- 6 ml/min/mm Hg (61 +/- 29% predicted). The pressure-volume curves of the lung were markedly abnormal. Pst(L) at TLC was 11.6 +/- 1.4 cm H2O. Transdiaphragmatic pressure (Pdi) in five patients was 66 +/- 13 cm H2O. These results indicate that severe small-airways disease with no or trivial emphysema may cause a spurious reduction in diffusing capacity as well as severe loss of lung elastic recoil resulting in marked hyperinflation, increased TLC, and decreased Pdi and expiratory airflow.

Aged↗

PubMed1998

Serial lung function and elastic recoil 2 years after lung volume reduction surgery for emphysema.

STUDY OBJECTIVE: To evaluate serial lung function studies, including elastic recoil, in patients with severe emphysema who undergo lung volume reduction surgery (LVRS). To determine mechanism(s) responsible for changes in airflow limitation. METHODS: We studied 12 (10 male) patients aged 68+/-9 years (mean+/-SD) 6 to 12 months prior to and at 6-month intervals for 2 years after thoracoscopic bilateral LVRS for emphysema. RESULTS: At 2 years post-LVRS, relief of dyspnea remained improved in 10 of 12 patients, and partial or full-time oxygen dependency was eliminated in 2 of 7 patients. There was significant reduction in total lung capacity (TLC) compared with pre-LVRS baseline, 7.8+/-0.6 L (mean+/-SEM) (133+/-5% predicted) vs 8.6+/-0.6 L (144+/-5% predicted) (p=0.003); functional residual capacity, 5.6+/-0.5 L (157+/-9% predicted) vs 6.7+/-0.5 L (185+/-10% predicted) (p=0.001); and residual volume, 4.9+/-0.5 L (210+/-16% predicted) vs 6.0+/-0.5 L (260+/-13% predicted) (p=0.000). Increases were noted in FEV1, 0.88+/-0.08 L (37+/-6% predicted) vs 0.72+/-0.05 L (29+/-3% predicted) (p=0.02); diffusing capacity, 8.5+/-1.0 mL/min/mm Hg (43+/-3% predicted) vs 4.2+/-0.7 mL/min/mm Hg (18+/-3% predicted) (p=0.001); static lung elastic recoil pressure at TLC (Pstat), 13.7+/-0.5 cm H2O vs 11.3+/-0.6 cm H2O (p=0.008); and maximum oxygen consumption, 8.7+/-0.8 mL/min/kg vs 6.9+/-1.5 mL/min/kg (p=0.03). Increase in FEV1 correlated with the increase in TLC Pstat/TLC (r=0.75, p=0.03), but not with any baseline parameter. CONCLUSION: Two years post-LVRS, there is variable clinical and physiologic improvement that does not correlate with any baseline parameter. Increased lung elastic recoil appears to be the primary mechanism for improved airflow limitation.

Aged↗

PubMed1998

The influence of 6 months of oral anabolic steroids on body mass and respiratory muscles in undernourished COPD patients.

STUDY OBJECTIVE: To evaluate the influence of oral anabolic steroids on body mass index (BMI), lean body mass, anthropometric measures, respiratory muscle strength, and functional exercise capacity among subjects with COPD. DESIGN: Prospective, randomized, controlled, double-blind study. SETTING: Pulmonary rehabilitation program. PARTICIPANTS: Twenty-three undernourished male COPD patients in whom BMI was below 20 kg/m2 and the maximal inspiratory pressure (PImax) was below 60% of the predicted value. INTERVENTION: The study group received 250 mg of testosterone i.m. at baseline and 12 mg of oral stanozolol a day for 27 weeks, during which time the control group received placebo. Both groups participated in inspiratory muscle exercises during weeks 9 to 27 and cycle ergometer exercises during weeks 18 to 27. MEASUREMENTS AND RESULTS: Seventeen of 23 subjects completed the study. Weight increased in nine of 10 subjects who received anabolic steroids (mean, +1.8+/-0.5 kg; p<0.05), whereas the control group lost weight (-0.4+/-0.2 kg). The study group's increase in BMI differed significantly from that of the control group from weeks 3 to 27 (p<0.05). Lean body mass increased in the study group at weeks 9 and 18 (p<0.05). Arm muscle circumference and thigh circumference also differed between groups (p<0.05). Changes in PImax (study group, 41%; control group, 20%) were not statistically significant. No changes in the 6-min walk distance or in maximal exercise capacity were identified in either group. CONCLUSION: The administration of oral anabolic steroids for 27 weeks to malnourished male subjects with COPD was free of clinical or biochemical side effects. It was associated with increases in BMI, lean body mass, and anthropometric measures of arm and thigh circumference, with no significant changes in endurance exercise capacity.

Administration, Oral↗

PubMed1998

Effect of exposure to low levels of ozone on the response to inhaled allergen in allergic asthmatic patients.

STUDY OBJECTIVES: In a previous study published by our group, six out of nine subjects with mild allergic asthma were shown to have an enhanced response to allergen challenge following a 1-h exposure in an 0.8-m3 exposure chamber (modified from a body plethysmograph) to an average of 120 parts per billion (ppb) ozone at rest. Other studies failed to confirm this effect. In the present study, using a similar design, we reexamined this effect using a larger group of asthmatics and a larger chamber allowing minimal fluctuations in ozone levels during exposures. DESIGN: Prospective, randomized single-blinded crossover study. SETTING: Pulmonary function laboratory equipped with an exposure chamber. SUBJECTS: Fifteen subjects had mild allergic asthma; 9 men and 6 women; the mean (SD) age was 32.5 (10) years; FEV1 was 3.4 (0.8) L; baseline methacholine provocation concentration causing a 20% fall in FEV1 was (PC20) 3.28 (4.1) mg/mL. INTERVENTIONS: Each participant was exposed, at rest, on 1 day to filtered air and on another day to ozone (mean level=120 ppb) in a larger exposure chamber than the one used in our first study with less variability in ozone level (110 to 130 vs 85 to 175 ppb) using a random, single-blinded design. After each exposure, the subject was challenged with allergen (nine with grass pollen extract and six with ragweed extract) and allergen PC15 was measured. RESULTS: Ozone preexposure did not affect allergen PC15 when compared with clean air preexposure (allergen PC15 dilution 1/114 vs 1/119, respectively). Ozone vs air preexposure resulted in an allergen PC15 that was lower in five subjects, higher in six, and unchanged (within one doubling dose) in four. CONCLUSIONS: At this low level with less variability and lower peaks than our previous study, ozone had no significant effect on airway allergen responsiveness.

Administration, Inhalation↗

PubMed1998

Exhaled nitric oxide and bronchial reactivity during and after inhaled beclomethasone in mild asthma.

The measurement of exhaled nitric oxide (ENO) is recognized as a marker of airway inflammation. ENO was measured in 10 nonsteroid-treated asthmatics at recruitment, during 3 weeks of inhaled beclomethasone (1000 microg/day) and for 3 weeks after withdrawal. Baseline ENO was increased in asthma compared with nonasthmatics (85.0+/-54.5 vs. 24.5+/-14.8 ppb, p < 0.0001). After inhaled steroid, there was no significant change in forced expiratory volume in 1 sec (FEV1) and forced vital capacity (FVC), but methacholine PC20 rose significantly (p = 0.0345). ENO (mean+/-SD; % baseline) fell after 1 week on steroid to 60.6+/-31.1 and rose to 95.3+/-46.1 at 1 week after withdrawal. ENO did not correlate with PC20 or FEV1. The changes in ENO and PC20 were inversely correlated (r2 = 0.325). ENO may be an index of airway inflammation and therapeutic response in bronchial asthma.

Administration, Inhalation↗

PubMed1997

Marked flow-dependence of exhaled nitric oxide using a new technique to exclude nasal nitric oxide.

Exhaled nitric oxide (NO) may aid in monitoring pulmonary disease. The single-breath NO profile (subjects with nose clip) was described as a NO peak followed by a plateau (NO(PLAT)). Published exhaled NO values vary greatly, possibly due to contamination with nasal NO and differing respiratory maneuvers. We developed a technique to measure pulmonary NO, without nasal NO, by having the subject maintain a positive expiratory pressure (ensuring vellum closure), and we examined the variation in NO(PLAT) over a range of expiratory flows (4.2 to 1,550 ml/s). NO(PLAT) values rose almost 35-fold (3.2 +/- 1.4 ppb to 110.5 +/- 54.8 ppb) with decreasing flow, described by NO(PLAT) = 208.6795 x (flow rate)(-0.5995). However, NO excretion showed an almost 11-fold rise as flow increased. In summary, we present a simple technique for measuring exhaled NO without contamination by nasal NO. There is a marked flow dependence of exhaled NO concentration and excretion. Exhaled pulmonary NO is best measured at very low flow rates to amplify the signal and must be related to the expiratory flow employed.

Administration, Inhalation↗

PubMed1997

Genetics of asthma: the University of Toronto Program. University of Toronto Genetics of Asthma Research Group.

In 1991, we initiated a study to identify susceptibility gene(s) predisposing individuals to the development of asthma. Our strategy was to focus on the collection of inbred populations because (1) they are likely to exhibit greater homogeneity than outbred populations, potentially important in multigenic diseases, (2) there may be fewer genes explaining the asthma diathesis in families with a "founder effect," (3) it is possible to follow the pattern of inheritance more closely, and (4) environmental factors are likely to be more uniform in geographically isolated poulations. We have identified, and in some cases collected data on inbred and/or isolated populations in Brazil, China, Easter Island, Israel, and Tristan da Cunha. We have completed a genome-wide scan on samples from Tristan da Cunha based on a coverage of approximately 20 cM between markers. In addition, we have collected hundreds of outbred individuals from Canada; these data have been helpful in narrowing a linked region based on the transmission/disequilibrium test.

Adult↗

PubMed1997

Defining the asthma phenotype for the purpose of genetic analysis.

In 1991, we began a project to search for the genetic basis of asthma using linkage analysis. We encountered discord between a history of asthma and physiological measures of variable airflow obstruction and sought to examine the frequency of such occurrences and the issues surrounding phenotyping of patients with asthma. We reviewed our experience in ascertaining the asthma phenotype in 50 nuclear families comprised of 219 subjects (110 male, 109 female). Three respiratory physicians reviewed data including a questionnaire, skin testing, objective measures of variable airflow obstruction [increase in FEV1 > or = 15% following salbutamol 400 micrograms of PC20 (methacholine) < or = 4 mg/ml], and serum for IgE. Thirty-eight percent of subjects had both objective and questionnaire data consistent with asthma (++) whereas 39% had negative objective and negative questionnaire findings (--) (i.e., no asthma). A positive history but negative objective findings occurred in 7% of subjects, 2% had a negative history and positive objective findings. Retesting was requested in 13% of subjects; review of historical data was requested in 1% (i.e., childhood asthma but no present asthma). Retesting was requested for either (a) positive history, negative objective if symptoms were seasonal or the subject was using medications known to affect the challenge study, (b) viral infection within 6 weeks of a positive methacholine study, or (c) technically inadequate study. Overall, after the initial assessment, all members of only 22 families could be catagorized as either ++ or --. The diagnostic group requested at least 1 retest in 19 families and a review of historical records in 2 families. We conclude that discordance between self-reported questionnaire data and laboratory measures of variable airflow limitation is common and will increase the numbers of asthmatic subjects in studies that seek to determine the genetic basis of asthma.

Adolescent↗

PubMed1997

The role of acoustic rhinometry in nasal provocation testing.

Geometric changes of the nasal airway in response to allergen challenge were measured by acoustic rhinometry (AR) and the sensitivity of the method was compared with that of rhinomanometry. Ten asymptomatic patients who suffered from ragweed allergic rhinitis were challenged out of season. The use of a custom-made noninvasive nasal adapter was an important feature of the measurement technique. A dose-dependent decrease in nasal cross-sectional area was found at and posterior to the entrance to the nasal valve. Both rhinometric and rhinomanometric methods were equivalent in sensing the changes in nasal patency due to allergen exposure (p = 0.73). Acoustic rhinometry, however, was simpler, more quickly performed and more comfortable for the subjects than was rhinomanometry by body plethysmography. AR is an alternative objective method for measurement of nasal mucosal responses, as in allergen challenge.

Acoustics↗

PubMed1996

Asthma on Tristan da Cunha: looking for the genetic link. The University of Toronto Genetics of Asthma Research Group.

Although asthma has a significant heritable component, the mode of inheritance remains controversial because of the complexity of the disease and the influence of environmental factors. Isolated, inbred populations serve to reduce variability, thus increasing the probability of gene localization. We studied the inbred population of the remote island of Tristan da Cunha to document asthma prevalence for the purpose of genetic linkage analysis. Medical histories and skin atopy were determined on 282 islanders, representing 97% of the population, and airway responsiveness was measured in 254; 226 by methacholine challenge (tidal breathing method) and 28 by bronchodilator response (400 micrograms salbutamol aerosol). Blood samples were collected from 275 islanders. Participants ranged in age from 3 to 94 yr. Asthma was defined as increased airway responsiveness (AR+: PC20 < 4 mg/ml or > or = 15% increase in FEV1 postbronchodilator) combined with a positive history (Hx+). Fifty-seven percent of the islanders had at least partial evidence of asthma (Hx+ and/or AR+) and 23% had a definitive diagnosis of asthma (AR+ with Hx+). Overall 47% of the population were atopic, atopy was proportionally higher in asthmatics (74%) than nonasthmatics (32%; p < 0.01). Analysis of the methacholine dose-response curves demonstrated that asthmatics were significantly (p < 0.01) more responsive than those with AR+ only, and nonasthmatics (AR-, Hx-) were more responsive than laboratory control subjects (p < 0.05), suggesting that these islanders may also carry an airway hyperresponsiveness gene. A frequency plot of the percent fall in FEV1 for all Hx- subjects compared with control data suggests a bimodal distribution consistent with a major gene mechanism for airway responsiveness. Genealogy mapping revealed that the islanders are direct descendants of the 15 original settlers, and historical records suggest at least two founders may have been asthmatic. The data confirm previous reports of a high asthma prevalence on Tristan and support the postulate that this prevalence is a result of gene enrichment occurring in isolated populations by virtue of extensive inbreeding and a probable founder effect.

Adolescent↗

PubMed1996

Mechanism of short-term improvement in lung function after emphysema resection.

We prospectively investigated the mechanism of airflow limitation before and after targeted emphysematous resection in 12 consecutively studied adult patients 68 +/- 4 yr of age (mean +/- SD) with very severe COPD undergoing bilateral thoracoscopic stapling techniques. Lung function, static lung elastic recoil, and airway conductance was measured 2 wk before and 5 to 6 mo after surgery. After surgery, there was a significant (p < 0.01) reduction in TLC (9.3 +/- 0.3 [mean +/- SEM] to 7.7 +/- 0.4 L), functional residual capacity, and residual volume. Airway conductance, FVC, and FEV1 (0.7 +/- 0.1 to 1.2 +/- 0.2 L) all improved significantly (p < 0.01). Lung elastic recoil increased markedly at TLC (from 10.3 +/- 0.5 to 14.6 +/- 1.0 cm H20; p < 0.001) as did maximal expiratory airflow in every patient. Analysis of maximal expiratory flow-static elastic recoil pressure curve indicated that conductance of the S segment (Gs) increased from 0.20 +/- 0.03 (mean +/- SEM) to 0.27 +/- 0.03 L/s/cm H20 (p < 0.01), and the critical transmural pressure (Ptm') decreased from 3.1 +/- 0.2 to 2.4 +/- 0.2 cm H20 (p < 0.02). Mean airway conductance increased from 0.14 to 0.22 L/s/cm H20 (p < 0.01). The improvement in maximal expiratory airflow can be primarily attributed to increased lung elastic recoil and its secondary effect on enlarging airway diameter causing increased airway conductance, increased Gs, and decreased Ptm'.

Aged↗

PubMed1996

Contribution of emphysema and small airways in COPD.

BACKGROUND: The contribution and role of emphysema and small airways disease in causing expiratory airflow limitation in COPD is controversial. METHODS: We obtained high-resolution thin-section 2-mm CT scans of the lung for emphysema grading and lung function in 116 consecutively seen COPD outpatients with fixed expiratory airflow limitation. In this group, inflated whole lung(s) were subsequently obtained in 24 patients (23 autopsy, 1 surgery) for morphologic studies and results compared with lung CT. Airway histologic condition was studied in 17 of the 24 patients. RESULTS: There was fair to weak negative correlation between CT emphysema score and either FEV1/FVC percent (r = -0.51, p = 0.001) or FEV1 percent predicted (r = -0.31, p = 0.001). In only 24 of the 81 patients (30%) with FEV1 less than 50% predicted, the CT emphysema score was 60 or more, indicating severe emphysema. In the 24 patients studied, there was a good correlation (r = 0.86, p = 0.001) between CT and pathologic grade of emphysema. While respiratory bronchioles (RBs) and membranous bronchioles (MBs) demonstrated marked morphologic abnormalities, there was a weak correlation with emphysema grade (for RB, r = 0.36, p = 0.16; for MB, r = 0.41, p = 0.10) or with FEV1 percent predicted (for RB, r = -0.21, p = 0.42; for MB, r = -0.28, p = 0.28). There was no correlation between emphysema and FEV1 percent predicted (r = -0.13, p = 0.54). CONCLUSIONS: High-resolution CT lung scans are an in vivo surrogate to quantitate moderate to severe morphologic emphysema. Emphysema does not appear to be primarily responsible for severe expiratory airflow limitation in most patients with severe COPD. There was no correlation between severity of small airway histologic condition and emphysema or FEV1 percent predicted. The causes of the lesions responsible for small airways obstruction need to be identified.

Aged↗

PubMed1996

Contribution of lung and chest wall mechanics following emphysema resection.

OBJECTIVE: To determine the contributions of (1) chest wall (Pcw) and (2) lung elastic recoil pressure (PL) to (3) total elastic recoil pressure exerted by the respiratory system (Prs) in 18 patients (12 men) aged 66 +/- 6 years (mean +/- 1 SD) with severe emphysema who underwent video-assisted thoracoscopic bilateral lung volume reduction surgery under paralyzed (vecuronium) general anesthesia (isoflurane). DESIGN: We measured preoperative and 6-week postoperative lung function studies, and intraoperative inspiratory lung conductance (GL), PL, Pcw, and Prs (cm H2O) at end-expiratory lung volume (EELV), EELV plus 0.60 +/- 0.0 L, and EELV plus 1.15 +/- 0.0 L. All values are mean +/- SEM. RESULTS: Preoperative vs postoperative FVC was 1.9 +/- 0.1 L vs 2.3 +/- 0.1 L (p = 0.03); FEV1 was 0.6 +/- 0.1 L vs 0.9 +/- 0.1 L (p < 0.02); total lung capacity was 7.4 +/- 0.4 L vs 5.9 +/- 0.3 L (p < 0.001); functional residual capacity was 5.7 +/- 0.4 L vs 4.4 +/- 0.2 L (p = 0.001). At EELV preoperative vs postoperative, PL was 0.0 +/- 0.3 vs 1.1 +/- 0.05 (p = 0.04), Pcw was 5.0 +/- 0.7 vs 2.4 +/- 0.9 (p = 0.02), and Prs was 5.0 +/- 0.8 vs 3.5 +/- 0.7 (p = 0.08). AT EELV plus 0.60 L, PL was 3.2 +/- 0.6 vs 6.1 +/- 0.9 (p < 0.001), Pcw was 8.8 +/- 0.8 vs 7.0 +/- 0.9 (p = 0.12), and Prs was 12.0 +/- 0.8 vs 13.1 +/- 0.7 (p = 0.80). At EELV plus 1.15 L, PL was 6.8 +/- 0.9 vs 10.3 +/- 1.1 (p < 0.001), Pcw was 13.5 +/- 1.0 vs 11.2 +/- 1.2 (p = 0.12), and Prs was 20 +/- 1.2 vs 21.5 +/- 1.0 p = 0.93). AT EELV plus 0.06 L, GL was 0.09 +/- 0.00 L/S/cm H2O vs 0.16 +/- 0.01 (p < 0.01). At EELV plus 1.15 L, GL was 0.12 +/- 0.01 vs 0.21 +/- 0.03 (p < 0.05) with similar preoperative vs postoperative GL/PL slopes. CONCLUSION: The increase in PL and decrease in Pcw following LVRS for emphysema may be responsible for the increase in spirometry and airway conductance.

Aged↗