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Biomedical subjects

G G Weinmann

Publications and source records attributed to G G Weinmann.

At least 19 recordsLinked to original sources
PubMed2000

Race and gender differences in the effects of smoking on lung function.

STUDY OBJECTIVE: To assess the extent to which the relationship between smoking and lung function in adults varies by gender and race/ethnicity. DESIGN: A random-effects metaregression analysis to synthesize results from common cross-sectional regression models fit to participants in each of 10 gender-race strata in each of eight large population-based observational studies or clinical trials. SETTING: Source data collected as part of the most recently completed examination cycle for each of the participating studies. PARTICIPANTS: Participants ranged in age from 30 to 85 years, although the age, race, gender, and general health characteristics of each of the populations varied greatly. INTERVENTIONS: Most of the studies were observational in nature, although some did involve lifestyle interventions. All treatment assignments were ignored in the analysis. MEASUREMENTS AND RESULTS: All studies measured lung function using standardized methods with centrally trained and certified technicians. Study findings confirm statistically significant, dose-related smoking effects in all race-gender groups studied. Significant gender differences in the effects of cigarette smoking were seen only for blacks; black men who smoked had greater smoking-related declines in FEV(1) than did black women. This effect was present in only one of two smoking models, however. Significant racial differences in the effects of smoking were seen only for men, with Asian/Pacific Islanders having smaller smoking-related declines than white men in both models. CONCLUSIONS: In summary, this analysis generally failed to support the hypothesis of widespread differences in the effects of cigarette smoking on lung function between gender or racial subgroups.

Adult↗
PubMed1997

Pulmonary function testing in population-based studies.

A wealth of information on pulmonary function is currently available in NHLBI-sponsored, population-based studies. These data can be used to address critically important questions in pulmonary and cardiovascular disease research, but their potential cannot be realized without the active collaboration of pulmonary- and cardiovascular-disease researchers. Investigators interested in analyzing these data in collaboration with the parent study investigators are invited to contact these investigators directly (see APPENDIX). Results of analyses recommended in the workshop should be used to identify hypotheses for future efforts in collecting data on the epidemiology of pulmonary diseases and their relationship to cardiovascular disease.

Adolescent↗
PubMed1996

An update on air pollution.

Air pollution is associated with adverse health effects. Much of the recent literature, which is the focus of this review, has concentrated on identifying individuals at risk and on the health effects of mixed pollutants. For indoor air, new analyses continue to support the notion that the risk of residential radon exposure is low and that environmental tobacco smoke may cause respiratory symptoms and dysfunction in adults, especially asthmatic adults, as well as in children. For outdoor air, the long-term effects of ozone exposure remain unclear, despite evidence of inflammation and small airway dysfunction after acute exposure. Ozone may increase the sensitivity of asthmatic patients to allergens. Increased morbidity in association with increasing particulate matter levels gives coherence to the argument that the relationship between particulate matter and mortality is causal. However, other investigators note the tight associations among outdoor pollutants and consider particulate matter a marker of air pollution levels.

Adult↗
PubMed1995

Response to acute ozone exposure in healthy men. Results of a screening procedure.

We screened 64 healthy, nonsmoking men, 18 to 35 yr old, for their sensitivity to 0.35 ppm ozone (O3) administered for 130 to 150 min with intermittent exercise. The changes in FVC, FEV1, AND FEF25-75 (p < 0.0001) immediately after O3 exposure varied widely among subjects. Histograms of the percentage changes in FVC and FEV1 did not differ from a unimodal, skewed (gamma) distribution (p = 0.99 and p = 0.17, respectively); the changes in FEF25-75 tended to deviate from a gamma distribution (p = 0.055). To adjust FEF25-75 for the confounding effects of O3 on FVC, we used multiple linear regression analysis with contemporaneous FVC as a covariable, analysis of a subgroup of nine subjects whose O3-induced FVC changes were < or = 5%, and volume correction of FEF25-75 for any changes in FVC after exposure. These analyses showed reductions in FEF25-75 unexplained by and following a different time course than the O3-induced changes in FVC. In 26 subjects also exposed to filtered air, significant effects of O3 on respiratory frequency (p < 0.004) and tidal volume (p < 0.0007) correlated weakly with FVC changes. The results confirm the wide variability in spirometric responsiveness among individuals to O3 and suggest that intrinsic narrowing of the small airways may be a significant component of the functional response.

Adolescent↗
PubMed1995

Evidence for ozone-induced small-airway dysfunction: lack of menstrual-cycle and gender effects.

Recently, we analyzed FEF25-75 isovolumetrically to assess the acute effects of ozone (O3) on small-airway function: the reduction in isovolumetric (isoV) FEF25-75 at end exposure progressed during the next 25 min even as FVC was recovering. To evaluate this effect over a longer period, we measured isovolumetric FEFs, helium-oxygen (He-O2) volume of isoflow (VisoV), the multiple breath nitrogen washout (MBNW) curve, FRC, and RV in 24 subjects 24 h after a 130-min exposure to filtered air (FA) and O3 (0.35 ppm). Men and women were studied to test for gender-based differences in response, after first determining that menstrual-cycle phase did not itself influence response. Isovolumetric FEF25-75, Vmax50, and Vmax75 were reduced about equally at 25 min after O3 exposure (p < or = 0.02) and showed no recovery at 24 h. FVC and FEV1, although still depressed after 24 h (p < 0.05), showed substantial recovery (p < 0.01). FRC, RV, and VisoV showed no effect of O3 exposure. No gender differences in O3 responsiveness were found. In summary, O3-induced reductions in isovolumetric flow rates, suggestive of small-airway dysfunction, may persist for 24 h following acute exposure to O3, a time-course consistent with inflammation.

Adolescent↗
PubMed1995

Ozone exposure in humans: inflammatory, small and peripheral airway responses.

We exposed eight normal adults to filtered air (FA) and 0.35 ppm ozone (O3) and compared responses in spirometry, including isovolume (isoV) flows at intermediate-to-low lung volumes, against levels of inflammatory markers in bronchoalveolar lavage fluid (BALF) and peripheral lung resistance (Rp) measured through a wedged bronchoscope. Spirometry was performed at the end, 25 min and 24 h after exposure, bronchoscopy at 24 h after exposure. The percentages of neutrophils, fibrinogen, albumin, PGE2, PGF2 alpha, and kinins were elevated in BALF after O3 compared with FA. The percentage reduction in (isoV) FEF25-75 at 25 min and 24 h after administration of O3 correlated closely with the rise in fibrinogen concentrations in BALF, a marker of altered vascular permeability. Rp, a measurement dominated by very small or peripheral airways, was unaffected in 7 of 8 subjects. The absence of change in Rp might have reflected insufficient penetration of O3 into these airways to produce or sustain an effect for 24 h; alternatively, the bronchoscopic procedure which included atropine and lidocaine pretreatment may have reversed an O3 effect. An unexpected finding was the significant association between baseline Rp (after FA) and the magnitude of the spirometric response to O3. Our results suggest that small airway dysfunction in the immediate post-O3 period is a marker of lung inflammation.

Adult↗
PubMed1991

Use of collateral airways to assess airway reactivity.

We investigated the correlation between collateral airway reactivity and other indexes of lung reactivity in response to aerosol and intravenous (iv) challenges. In four anesthetized mongrel dogs, we measured the peripheral airway resistance (Rp) to gas flow out of a wedged lung segment in different lobes on multiple occasions. We obtained dose-response curves of peripheral airways challenged with iv histamine or aerosols through the bronchoscope. During the same iv bolus challenge, whole lung airway pressure (Paw) responses to histamine were also measured. On separate occasions, changes in lung resistance (RL) were measured after the whole lung was challenged with a histamine aerosol. Reactivity was assessed from the dose-response curves for Rp and RL as the PD50 (dose required to produce a 50% increase); for changes in Paw we calculated the PD15 (dose required to produce a 15% increase over baseline). Results for Rp showed considerably more variability among different lobes in a given animal with the aerosol challenge through the bronchoscope than with the iv challenge. With aerosol challenge there were no significant differences in the mean PD50 for Rp among any of the animals. However, with the iv challenge two of the dogs showed significant differences from the others in reactivity assessed with Rp (P less than 0.01). Moreover, the differences found in the peripheral airways with iv challenge reflected differences found in whole lung reactivity assessed with either iv challenge (Paw vs. Rp, r2 = 0.96) or whole lung aerosol challenge (RL vs. Rp, r2 = 0.84). We conclude that the measurement of the collateral resistance response to iv challenge may provide a sensitive method for assessing airway reactivity.

Aerosols↗
PubMed1990

In vitro tracheal responses from mice chosen for in vivo lung cholinergic sensitivity.

We selected two inbred strains of mice based on their different in vivo lung responses to intravenous acetylcholine for studies on the in vitro tracheal responses to contractile and relaxing agents. In addition, we studied the role of cyclooxygenase products on the in vitro responses. Tracheal rings were contracted with increasing concentrations of carbachol and KCl and relaxed with increasing concentrations of isoproterenol after contraction with carbachol at the concentration that produced 30, 50, and 70% of the maximal contraction (EC30, EC50, and EC70, respectively) and KCl at the EC50. Half the tracheae simultaneously underwent the same protocols after pretreatment with indomethacin (3 X 10(-6) M). Despite a severalfold difference in the maximal response to cholinergic agents in vivo, there were no significant differences between the strains in the tracheal responses to carbachol (P = 0.78) or KCl (P = 0.13) in vitro. Both strains showed inhibition of the isoproterenol relaxation by carbachol (P less than 0.0001). Multiple linear regression analysis showed that the strain that was more sensitive to carbachol in vivo was also more sensitive to isoproterenol in vitro after carbachol contraction (P = 0.014). The greater isoproterenol sensitivity of the tracheae from this strain was not present after contraction with KCl, nor were these tracheae more sensitive to relaxation with sodium nitroprusside. Indomethacin pretreatment of the tissues in vitro augmented the maximal response and the sensitivity to carbachol (P less than 0.001) and KCl (P = 0.0006), and this effect was similar in both strains. Evaluation of isoproterenol relaxation after indomethacin pretreatment was confounded by the lower concentrations of carbachol needed for contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1990

Succinylcholine potentiates responses to intravenous acetylcholine in the canine lung periphery.

Using the wedged bronchoscope technique to measure collateral resistance (Rcs), we evaluated the effect of succinylcholine (SCh) on the response to acetylcholine (ACh) and methacholine (MCh) in the lung periphery in six mongrel dogs. Dogs were anesthetized, intubated, and mechanically ventilated. After a stable baseline Rcs was obtained, responses to intravenous ACh (25-200 micrograms), intravenous MCh (3-30 micrograms), and aerosolized ACh (30-100 micrograms/ml for 15 s) were measured. We compared the Rcs responses with 1) ACh alone, 2) ACh 2 min after SCh (0.5 mg/kg), 3) ACh 2 min after SCh and during hexamethonium infusion (5 mg/kg + 10 mg.kg-1.h-1), 4) MCh 2 min after SCh, and 5) ACh aerosol 2 min after SCh. SCh did not significantly alter baseline airway tone. SCh increased the Rcs response to ACh by 48 +/- 17% (SE) (P less than 0.01). SCh in the presence of hexamethonium increased the Rcs response by 10 +/- 3% (P less than 0.05), while hexamethonium itself increased the response to ACh by 69 +/- 27%. Because SCh did not increase the Rcs response to intravenous MCh or to aerosolized ACh, SCh probably enhances airway reactivity to intravenous ACh by competing for pseudocholinesterase in plasma. We conclude that the level of muscle relaxant must be taken into account in interpreting studies of airway reactivity when intravenous ACh is employed.

Acetylcholine↗
PubMed1990

Peripheral lung resistance in normal and asthmatic subjects.

In obstructive lung disease, peripheral airways are a major site of pathologic abnormalities. However, resistance to airflow in small airways in the periphery of the lung accounts for only a small fraction of total airway resistance. Consequently, abnormalities of small airway function may not be readily detected using routine pulmonary function testing. In the present study, resistance of the peripheral lung was examined directly in six normal subjects and nine mildly asthmatic subjects. There were no significant differences between the normal and asthmatic groups in pulmonary function assessed by spirometry (FEV1, FVC) and body plethysmography (specific airway conductance). Direct measurements of peripheral lung function were made using a fiberoptic bronchoscope wedged into a subsegmental, right upper lobe bronchus. Using a double-lumen catheter inserted into the instrument channel of the bronchoscope, pressures (PB) produced by three or more different levels of gas flow (V) (5% CO2 in air) between 50 and 500 ml/min were measured. All pressure measurements were made at a constant lung volume (i.e., functional residual capacity) confirmed by monitoring transpulmonary pressure with an esophageal balloon. The pressure-flow relationship in both normal and asthmatic subjects could be approximated by a straight line through the origin, demonstrating these airways to be relatively nondistensible. Peripheral lung resistance (Rp) was defined by PB/V and averaged for three or more levels of flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗
PubMed1988

Effect of tidal volume and frequency on the temporal fall in lung compliance.

In this study we have investigated how changes in respiratory frequency and tidal volume in anesthetized dogs affect the fall in dynamic compliance (Cdyn) that occurs with time after a hyperinflation. Results showed that increasing frequency [at controlled arterial (PaCO2)] PCO2 from 16 to 32 breaths/min had no effect on either the rate of fall or the magnitude of the fall up to 1 h after the hyperinflation. However, increasing the tidal volume from 300 to 750 ml abolished the fall in Cdyn from 10 to 50 min after the hyperinflation; the fall within the first 10 min remained unchanged. We also examined the effect of a simulated "hyperinflation" on the compliance of strips of parenchymal tissue in vitro. This result indicated that in the absence of surface forces, parenchymal tissue demonstrates a fall in compliance, which is complete within 10 min. Overall our findings are consistent with the hypothesis that the fall in Cdyn after hyperinflation is a two-phase process. The initial rapid fall in Cdyn (i.e., within 10 min) may simply represent a passive recovery process from the hyperinflation stress on the parenchymal tissue. The slower fall occurring after 10 min likely results from progressive increases in surface tension, and this increase can apparently be blocked by increases in tidal volume.

Animals↗
PubMed1987

Interaction between high frequency jet ventilation and cardiovascular function.

We have studied the interaction of high frequency jet ventilation with cardiovascular pressures and flows. Results in dogs show that the amplitude of all intrathoracic pressures and flows fluctuate with a frequency equal to the difference between the heart rate and ventilator rate. The magnitude of this amplitude variation may be sufficient to obliterate periodically the pulsations in pulmonary artery and right atrial pressures. It is also shown that these cardiovascular beats can occur when the ventilator rate is close to integral multiples of the heart rate. Direct measurement of pleural pressure and the observation that the beats are markedly reduced when the chest is open support the hypothesis that the primary mechanism responsible for these beats is the interaction of the respiratory fluctuations in pleural pressure with the cardiac-generated pressure pulsations.

Animals↗
PubMed1987

Absence of changes in airway responsiveness during the menstrual cycle.

The effect of sex hormones on airway function has not been well studied in spite of much evidence to suggest that they are important. We asked if the normal physiologic variation in hormone levels during the menstrual cycle resulted in changes in airway responsiveness and pulmonary function that were not clinically apparent. Nine women with asthma and with normal menstrual cycles but not taking systemic asthma medication were asked to chart temperatures, asthma attacks, and use of asthma medication for four menstrual cycles. We measured baseline spirograms, skin and airway responsiveness to histamine, and serum levels for estradiol, progesterone, and testosterone on approximately day 7 and day 24 of two consecutive cycles. None of the women reported cyclic asthma symptoms, and review of subjects' charts demonstrated no menstrual variation in asthma attacks or use of asthma medications. We found no differences in forced vital capacity or FEV1 early compared to late in the menstrual cycle. Neither did we find a change in airway responsiveness, as indicated by the histamine dose causing a 15% fall in FEV1 or a 35% fall in specific airway conductance. Skin responsiveness as indicated by the wheal response to intradermal histamine was also unchanged. We conclude that physiologic changes in hormone levels during the menstrual cycle are not in themselves associated with changes in airway or skin responsiveness to histamine.

Adrenal Cortex Hormones↗
PubMed1987

Effect of high-frequency ventilation on lung mechanics at high transpulmonary pressure.

The different tidal volumes and frequencies of high-frequency ventilation (HFV) compared with conventional mechanical ventilation (CMV) may have different effects on lung mechanics. To test this hypothesis, we compared the effects of 3 h of HFV and CMV on total lung capacity (TLC), functional residual capacity (FRC), the shape of the pressure-volume (PV) curve (%V10), and dynamic compliance (Cdyn), as well as venous admixture and alveolar-arterial O2 gradient. We studied a total of 12 dogs at lung inflations equivalent to 15 cmH2O positive end-expiratory pressure (PEEP) (group I) and 8 dogs at lung inflations equivalent to 0 cmH2O PEEP (group II). For CMV, we used a standard-volume ventilator at a mean tidal volume of 13.8 ml/kg. For HFV, we used an oscillator-type ventilator at 15 Hz and an average tidal volume of 4.3 ml/kg. Our results showed that ventilation with 3 h of PEEP raised lung volume, and lung volumes on HFV were higher than those on CMV in both groups. Specifically, in group I, the volume during ventilation rose on both CMV (150 ml) and HFV (250 ml). These volume changes persisted beyond the ventilation period, such that TLC was unchanged on CMV but had risen 200 ml on HFV. FRC also rose 200 and 300 ml after HFV and CMV, respectively. In group II, the volume during ventilation fell 100 ml on CMV and rose slightly (40 ml) on HFV. TLC and FRC both tended to fall more on CMV.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Nifedipine overdose.

A 59-year-old man ingested 900 mg of nifedipine. Profound hypotension, sinus and atrioventricular node dysfunction, and hyperglycemia resulted. The patient's condition responded favorably to aggressive treatment with intravenous fluids, calcium, and dopamine. Similar effects and response to therapy have been reported in 17 cases of verapamil overdose and are briefly summarized. The effects of nifedipine overdose are discussed, and preliminary recommendations about its management are offered. With increasing use of nifedipine and other calcium channel blockers, more incidents of overdose can be expected.

Atropine↗
PubMed1985

Effect of high-frequency ventilation on histamine-induced lung injury in dogs.

We compared the effects of high-frequency oscillation (HFO) and conventional mechanical ventilation (CMV) on dynamic lung compliance (Cdyn), venous admixture (Qsp/Qt), cardiac output, and total lung resistance (RL) in seven mongrel dogs with histamine-induced lung injury. Baseline measurements during CMV were followed by iv infusion of histamine at 100 micrograms/min. Cdyn, Qsp/Qt, cardiac output, and RL were measured in triplicate during CMV and then during HFO. Subsequently, at least one complete set of measurements was recorded again on CMV. During HFO, animals were ventilated at 15 Hz with a tidal volume of 70 to 80 ml. CMV was delivered at 15 to 18 breath/min with a tidal volume of 15 ml/kg. Histamine infusion produced a marked fall in Cdyn, a variable rise in RL, an inconsistent but usually progressive rise in Qsp/Qt, and hypotension. A period of ventilation with HFO made no difference in the Cdyn, Qsp/Qt, or cardiac output changes produced by histamine infusion.

Animals↗