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PubMed1990

Pulmonary function in infancy and in childhood following mechanical ventilation in the neonatal period.

Pulmonary function was evaluated in both infancy and childhood in the same 19 prematurely born infants, who required mechanical ventilation (MV) during the neonatal period. Results of our patients were compared with those of control subjects. Upon first evaluation, we found that lung resistance (RL) was significantly elevated (24.85 +/- 6.06 vs. 17.77 +/- 2.39 cmH2O/L/s; P less than 0.01). The mean value of dynamic lung compliance (CLdyn) was low, but the difference compared to controls did not reach significance. From infancy to childhood, elevated RL persisted (9.33 +/- 2.51 vs. 6.52 +/- 1.52 cm H2O/L/s; P less than 0.01), and the decrease of CLdyn became significant (46.86 +/- 12.84 vs. 59.34 +/- 15.68 mL/cmH2O; P less than 0.05). In addition, maximum flow at functional residual capacity was significantly decreased (0.824 +/- 0.284 vs. 1.215 +/- 0.358 L/s; P less than 0.01); whereas pulmonary diffusing capacity for carbon monoxide was similar in the patients (7.62 +/- 2.16 mL/min/mm Hg) and in the controls (8.38 +/- 1.6). Pulmonary dysfunction following premature birth, respiratory distress, and prolonged MV may not resolve from infancy to childhood.

Child↗
PubMed1998

Clinical features and serum antinuclear antibodies in 230 Danish patients with systemic sclerosis.

The objective was to investigate the relationship between the presence of different types of antinuclear antibodies (ANA) in patients with systemic sclerosis (SSc) and the presence of clinical features. Sera from 230 patients with SSc were tested for the presence of ANA, including anticentromere antibodies (ab), antitopoisomerase I ab, anti-U1 RNP ab and antinucleolar ab, including anti-Th RNP, anti-U3 RNP and anti-U17 RNP. Clinical features were registered prospectively in a clinical database. Eighty-two per cent of the patients were women. The median age was 58 yr (45-67, quartiles) and median age at disease onset was 44 (30-55) yr. ANA were found in 86% of the patients (anticentromere: 34%; antitopoisomerase I: 14%; anti-U1 RNP: 6.5%; antinucleolar total: 16%; anti-Th RNP: 2.2%; anti-U3 RNP: 3.5%; anti-U17 RNP: 0%). Anticentromere ab were found to be related to a high prevalence of calcinosis, telangiectasia, digital ulcers, acrosclerosis, primary biliary cirrhosis, isolated reduction of pulmonary diffusing capacity, and a low prevalence of radiological evidence of pulmonary fibrosis. Antitopoisomerase I ab were associated with a high prevalence of digital joint deformity, distal osteolysis, radiological signs of pulmonary fibrosis, a low prevalence of calcinosis and late onset of disease. Anti-U1 RNP ab were related to a high prevalence of arthritis and myositis, a low prevalence of calcinosis, and early disease onset. The presence of antinucleolar ab, including anti-U3 RNP and anti-Th RNP, was not significantly related to any particular clinical features in this study; possibly due to the small number of patients with these ab. The presence of anticentromere, antitopoisomerase I and anti-U1 RNP ab in the serum was also found to have previously described clinical correlations in a group of Danish SSc patients.

Adolescent↗
PubMed1987

Impairment of ventilatory function and pulmonary gas exchange in non-smoking coalminers.

Indices of ventilatory function and pulmonary gas exchange in 32 non-smoking coalminers (mean age 38.1) were compared with those of 34 non-smoking steelworkers of similar age. The coalminers had significantly lower forced expiratory volume in 1 s (FEV1) and maximum expiratory flow rates and significantly higher residual volume, but similar vital capacity and indices derived from the single-breath test. Pulmonary diffusing capacity for CO and indices of CO2 exchange were similar in both groups. Arterial partial pressure of O2 (PaO2) was significantly lower and alveolar-arterial O2 difference was significantly higher in coalminers than in controls, both at rest and during exercise. There was no relation between lung function and radiological signs of simple pneumoconiosis (10 coalminers had pneumoconiosis). The differences in FEV1 (0.42 l) and in PaO2 (10 mm Hg) between the two groups are the same or larger than those usually found between smokers and non-smokers. Exposure to coaldust may result in biologically significant alterations of lung function even in the absence of pneumoconiosis.

Adult↗
PubMed1997

A finite-element model of oxygen diffusion in the pulmonary capillaries.

We determined the overall pulmonary diffusing capacity (DL) and the diffusing capacities of the alveolar membrane (Dm) and the red blood cell (RBC) segments (De) of the diffusional pathway for O2 by using a two-dimensional finite-element model developed to represent the sheet-flow characteristics of pulmonary capillaries. An axisymmetric model was also considered to assess the effect of geometric configuration. Results showed the membrane segment contributing the major resistance, with the RBC segment resistance increasing as O2 saturation (SO2) rises during the RBC transit: RBC contributed 7% of the total resistance at the capillary inlet (SO2 = 75%) and 30% toward the capillary end (SO2 = 95%) for a 45% hematocrit (Hct). Both Dm and DL increased as the Hct increased but began approaching a plateau near an Hct of 35%, due to competition between RBCs for O2 influx. Both Dm and DL were found to be relatively insensitive (2-4%) to changes in plasma protein concentration (28-45%). Axisymmetric results showed similar trends for all Hct and protein concentrations but consistently overestimated the diffusing capacities (approximately 2.2 times), primarily because of an exaggerated air-tissue barrier surface area. The two-dimensional model correlated reasonably well with experimental data and can better represent the O2 uptake of the pulmonary capillary bed.

Blood Proteins↗
PubMed1992

Effect of smoking cessation on pulmonary carbon monoxide diffusing capacity and capillary blood volume.

We studied 16 smokers, with a mean age of 41 yr (SD, 12 yr) and a mean DLCO of 81% predicted (SD, 19%), before and after smoking cessation. Two subjects were able to stop smoking for only 24 h, whereas 14 subjects abstained for 1 wk, 11 for 1 month, and five for 3 months. The initial mean DLCO in ml/min/mm Hg was 18.9 (SD, 4.6) after correction for COHb back pressure and the reduction in hemoglobin because of COHb. A week after smoking cessation there was a significant increase in DLCO, to 20.8 (SD, 5.4), p = 0.001. There was no further increase in DLCO at 1 month or at 3 months. In four subjects tested while they were still smoking and 24 h after smoking cessation, there was a significant increase in DLCO after correction for COHb, from 17.4 (SD, 1.5) to 19.8 (SD, 1.3), p = 0.02. These results indicate that after smoking cessation there is a rapid improvement in DLCO, suggesting that smoking had previously decreased DLCO. However, there may also be an irreversible component to the reduction of DLCO in some of the subjects in whom the DLCO remained abnormal even after continued smoking cessation for 1 month.

Adult↗
PubMed1985

Effects of pulmonary hemodynamics on lung function in adult patients with atrial septal defect.

To clarify the relationship of pulmonary function with differing severity of atrial septal defect (ASD) and to assess the effects of pulmonary hemodynamics on these functions, we classified 101 patients with adult ASD by their pulmonary arterial mean pressure (PAm) and pulmonary blood flow (Qp), and compared details of pulmonary functions between pairs of groups. Classification was by drawing lines at the PAm of 20 mmHg and the Qp of 10 L/min. Group I was the low pressure-low flow group, Group II the low pressure-high flow group, Group III the high pressure-low flow group, and Group IV the high pressure-high flow group. Vital capacity as the percentage of predicted (%VC) was low in Groups III and IV. There were no significant differences in the ratio of forced expiratory volume in one second to forced vital capacity (FEV1%), flow at 25% forced vital capacity and closing volume as the percentage of predicted (%V25, %CV/VC) between each group. Both maximum midexpiratory flow rate and flow rate at 50% forced vital capacity as the percentage of predicted (%MMEF, %V50) in Group III with the most severe ASD, were significantly low. Pulmonary diffusing capacities for carbon monoxide as the percentage of predicted (%DLco) exceeded 100% in all groups, and tended to decrease with increases of PAm without relation to Qp. Pulmonary dysfunctions in adult ASD were mainly due to restrictive changes accompanied by obstructive change in proportion to the decrease of VC. Peripheral airway obstructions are mild in ASD and these might be caused by lower pressure of left atrium and no existence of pulmonary venous congestion in ASD, even in the most severe group.

Adolescent↗
PubMed1993

About mechanisms of prostaglandin E1 induced deterioration of pulmonary gas exchange in COPD patients.

Prostaglandin E1 (PGE1) has been reported to attenuate COPD-related pulmonary hypertension and to slightly lower the arterial oxygen tension (PaO2). In order to infer the involved mechanisms, the effects of intravenous infusion of PGE1 on pulmonary haemodynamics, diffusing lung capacity for CO (DLCO), membrane diffusing capacity (Dm), pulmonary capillary blood volume (Vc), physiological shunt (Qps/Qt), arterial blood gases and other lung functional indices were evaluated in 20 COPD patients with pulmonary hypertension and, excluding right catheterization, in 14 control subjects. The examines were studied at baseline and during infusion of 20-30 ng kg-1 min PGE1 or placebo. In control subjects PGE1 only caused systemic arterial pressure decrease (-17.8%). In COPD patients, as expected, PGE1 increased cardiac index (16.2%), but decreased systemic arterial pressure (-21.2%), pulmonary arterial pressure (-27.9%), pulmonary vascular resistance (-45.4%) and PaO2 (-10.4%), worsening their hypoxaemia. However, the effect of PGE1 on DLCO was an increase (11.9%), due to an increase in Vc (15.2%) and less markedly in Dm (4.9%). Physiological and anatomical shunts were increased with PGE1 (20.2% and 14.8%) and the overall ventilation/perfusion ratio decreased from 0.89 to 0.79. Decrements in PaO2 correlated with increments in Qps/Qt (r = 0.86). In conclusion, in COPD patients studied, PGE1 increased DLCO, which compensated for the deleterious effect of increased cardiac output on alveolar-capillary gas equilibration. Therefore, worsening of hypoxaemia during PGE1 infusion was related with increased right-to-left shunt and deterioration of ventilation-perfusion relationship.

Alprostadil↗
PubMed1995

Effect of preinspiratory maneuver on the single-breath DLCO.

We have observed in some patients with pulmonary disease and normal subjects that the difference between two successive measurements for single-breath DLCO amounted to 10%. By scrutinizing data from these subjects, we observed that they spontaneously changed their preinspiratory maneuver just before inhaling the test gas mixture. The purpose of the present work is to assess the influence of five different preinspiratory maneuvers on DLCO. Nine healthy males were investigated. They performed at random the five following maneuvers: (A) rapid exhalation from functional residual capacity (FRC) to residual volume (RV), (B) rapid exhalation from FRC to RV and long apnea at RV, (C) rapid exhalation from FRC to RV and short apnea at RV, (D) slow exhalation at a constant speed from FRC to RV, and (E) curvilinear exhalation from FRC to RV. The DLCO values after maneuver B were higher than those after the four other maneuvers; there was a significant relationship between DLCO and the duration of the preinspiratory maneuver. The data are best explained by an alteration in the distribution of the inspired gas mixture to areas with different diffusing capacities. In conclusion, the preinspiratory maneuvers must be standardized in order to improve the reproducibility of the single-breath DLCO measurements.

Adult↗
PubMed1998

[Studies on pulmonary and systemic hemodynamic changes after transjugular intrahepatic portosystemic shunt (TIPS)].

In 10 patients who underwent transjugular intrahepatic portosystemic shunt (TIPS) at our institution, postoperative pulmonary and systemic hemodynamic changes were compared with those before the procedure. After TIPS, right atrial and pulmonary capillary wedge pressures, cardiac output, and cardiac index increased significantly, and there was a significant decrease in total peripheral resistance. Thus, systemic hemodynamic changes showed evidence of a more hyperdynamic circulation. In addition, right ventricular end-diastolic volume index was significantly increased and this increase was persistent, with maintained right heart strain. With respect to pulmonary hemodynamics, alveolar arterial oxygen difference and right-to-left shunt increased significantly, along with a significant decrease in arterio-venous oxygen content difference, which indicated impairment of pulmonary diffusing capacity. These findings suggest that preoperative evaluation of the cardiac reserve and pulmonary function is important before performing TIPS. After TIPS, patients should be followed carefully because postoperative heart failure or pulmonary edema may occur.

Aged↗
PubMed1999

Acute saline infusion reduces alveolar-capillary membrane conductance and increases airflow obstruction in patients with left ventricular dysfunction.

BACKGROUND: Impaired alveolar-capillary membrane conductance is the major cause for the reduction in pulmonary diffusing capacity for carbon monoxide (DLCO) in heart failure. Whether this reduction is fixed, reflecting pulmonary microvascular damage, or is variable is unknown. The aim of this study was to assess whether DLCO and its subdivisions, alveolar-capillary membrane conductance (DM) and pulmonary capillary blood volume (Vc), were sensitive to changes in intravascular volume. In addition, we examined the effects of volume loading on airflow rates. METHODS AND RESULTS: Ten patients with left ventricular dysfunction (LVD) and 8 healthy volunteers were studied. DM and Vc were determined by the Roughton and Forster method. The forced expiratory volume in 1 second (FEV1), vital capacity, and peak expiratory flow rates (PEFR) were also recorded. In patients with LVD, infusion of 10 mL. kg-1 body wt of 0.9% saline acutely reduced DM (12.0+/-3.3 versus 10.4+/-3.5 mmol. min-1. kPa-1, P<0.005), FEV1 (2.3+/-0.4 versus 2.1+/-0.4 L, P<0.0005), and PEFR (446+/-55 versus 414+/-56 L. min-1, P<0.005). All pulmonary function tests had returned to baseline values 24 hours later. In normal subjects, saline infusion had no measurable effect on lung function. CONCLUSIONS: Acute intravascular volume expansion impairs alveolar-capillary membrane function and increases airflow obstruction in patients with LVD but not in normal subjects. Thus, the abnormalities of pulmonary diffusion in heart failure, which were believed to be fixed, also have a variable component that could be amenable to therapeutic intervention.

Aged↗
PubMed1992

Measurement of alveolar gas mixing in mechanically ventilated patients.

OBJECTIVE: To evaluate a computer-based, real-time, multibreath nitrogen washout technique in mechanically ventilated patients, incorporating an in-line flow measurement device to measure functional residual capacity and two indices of gas mixing, ventilatory efficiency, and alveolar mixing efficiency. SETTING: ICU, Charing Cross Hospital, London. DESIGN: Within-patient reproducibility of a multibreath nitrogen washout technique. PATIENTS: Seven intubated patients requiring mechanical ventilation. One patient completed two sets of readings. INTERVENTIONS: Patients were connected to a pneumatically driven ventilator fitted with a switching device to be operated either by an appropriate oxygen-nitrogen mixture or equivalently blended oxygen-argon mixture. An inspiratory-expiratory, two-way valve was attached to the delivery port of the ventilator, with a pneumotachograph for flow measurement and a gas sampling probe for gas concentration measurement in line with the patient's endotracheal tube. The analog signals were digitized and handled by a microcomputer. MEASUREMENTS AND MAIN RESULTS: No significant differences were found for any index, with coefficients of variation of 1.5%, 2.9%, and 2.1% for functional residual capacity, ventilatory efficiency, and alveolar mixing efficiency, respectively. CONCLUSIONS: This method gives excellent reproducibility for biological measurements in a clinical setting and shows that these measurements can readily be made on mechanically ventilated patients.

Adult↗
PubMed1989

Furnace-generated acid aerosols: speciation and pulmonary effects.

Guinea pigs were exposed to ultrafine aerosols (less than 0.1 micron) of zinc oxide with a surface layer of sulfuric acid. These acid-coated aerosols are typical of primary emissions from smelters and coal combustors. Repeated daily 3-hr exposures for 5 days produce decrements in lung volumes and pulmonary diffusing capacity and elevations of lung weight/body weight ratio, protein, and number of neutrophils in pulmonary lavage fluid at concentrations of 20 micrograms/m3. A single 1-hr exposure to 20 micrograms/m3 causes increased bronchial reactivity. Higher concentrations of conventionally generated sulfuric acid mist are required to produce responses of similar magnitude.

Acid Rain↗
PubMed1996

[Acetylsalicylic acid antagonism vs ACE inhibitor in congestive heart failure as shown by a diminished respiratory and exercise capacity].

Our hypothesis is that regulation of the lung vessel tone and microvascular permeability may be disrupted in chronic heart failure (CHF) and angiotensin converting enzyme (ACE) inhibition may contribute to their readjustment. This hypothesis is based on the fact that KII-ACE, the same enzyme that converts angiotensin I and inactivates bradykinin, is highly concentrated in the luminal surface of the lung vessels and its blockade in CHF may reduce their exposure to an excess of angiotensin II and augment the action of prostaglandins and nitric oxide (NO) deriving from local kinin hyperconcentration. We probed whether ACE-inhibitors influence the pulmonary function; this is peculiar of CHF; they act as KII- or ACE-blockers. Aspirin was utilized as a prostaglandin synthesis inhibitor. We investigated 16 CHF patients and 16 age- and sex-matched normal volunteers or mild untreated hypertensives. All were non-smokers, not taking ACE-inhibitors, aspirin or other cyclooxygenase inhibitors. Pulmonary function tests, exercise testing with respiratory gases and echocardiography were performed in the run-in and repeated at the end of placebo, enalapril (10 mg t.i.d.), enalapril plus aspirin (325 mg/day) and aspirin given in random order and double-blind fashion for 15 days each. Enalapril, as compared to placebo, caused an increase in mean voluntary ventilation (MVV) and alveolar-capillary diffusing capacity for carbon monoxide (DLCO) in CHF, that were counteracted by the addition of aspirin. Aspirin alone was not effective. Enalapril and aspirin were ineffective on the pulmonary function of controls. As to the functional capacity, enalapril increased exercise tolerance time, oxygen consumption (VO2p), minute ventilation (VEp) tidal volume (VTp) and reduced the ratio of volume of dead space gas (VDp) to VTp (VD/VTp), at peak exercise in CHF patients. These effects all were inhibited by the combination of aspirin and were not observed in controls. In CHF VO2p changes from placebo correlated with those in DLCO (r = 0.80, p < 0.0001) and not with those in ejection fraction. This correlation was abolished by aspirin and was not seen in controls. Variations in VD/VTp in CHF patients while on enalapril were related to those in DLCO (r = -0.69, p = 0.003). In CHF the ventilatory equivalent for carbon dioxide production per minute at 1 liter was diminished with enalapril and not in combination with aspirin. Derangements related to CHF are the substrate for benefits of ACE-inhibition on pulmonary function and exercise capacity. Pulmonary diffusion limitation is an important mediator of exercise impairment and its improvement with enalapril goes in parallel with VD/VT, MVV, VT, VE to VCO2 relationship and not with ejection fraction. These patterns reflect changes occurring within the lung that are not related to left ventricular function. The counteracting influence of aspirin on these affects bespeaks a substantial participation of prostaglandins that might readjust capillary permeability and lung interstitial fluid content or alveolar capillary membrane diffusing capacity.

Aged↗