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W W Wagner

Publications and source records attributed to W W Wagner.

At least 55 records · Page 3Linked to original sources
PubMed1989

Fate of air emboli in the pulmonary circulation.

The lung serves an important nonrespiratory function by trapping and excreting venous air emboli. The site of trapping and the mechanism of excretion, however, are uncertain. To observe the behavior of bubbles in the pulmonary circulation, we injected venous air emboli into anesthetized dogs and videotaped their elimination from the pulmonary microcirculation by using in vivo microscopy. Small intravenous bubbles lodged exclusively in pulmonary arterioles and were eliminated from that site. To determine whether the gas was dissolving into nearby blood and then was carried to the capillaries for excretion, the rate of bubble radius change was measured during nonperfused conditions produced by balloon occlusion of lobar blood flow and compared with perfused conditions. Bubble volume decreased at the same rate during perfused and nonperfused conditions and thus was independent of regional blood flow. Molecular diffusion of gas directly across the arteriolar wall into alveolar spaces was the most likely mechanism of elimination because calculations based on the Fick equation for molecular diffusion predict an elimination rate nearly identical with those observed experimentally.

Animals↗
PubMed1989

[Physiology of pulmonary capillary recruitment].

At the apices of the lungs in man there is a poorly perfused zone (zone 2) which in certain circumstances can be recruited. The pulmonary capillary recruitment in this zone has been studied in the anaesthetised and ventilated dog. Following a thoracotomy a metal window with a small transparent viewing area was applied to the surface of the right lung, and the dog was placed in the left lateral decubitus position. The sub-pleural pulmonary microcirculation which is in this case in zone 2 was examined using a microscope. Alveolar hypoxaemia led to an increase in the number of pulmonary capillaries that were perfused. This recruitment of the pulmonary capillaries was independent of the cardiac output, the left auricular pressure and the pulmonary venous pressure. The recruitment disappeared if the rise in hypoxic pulmonary artery pressure was prevented using prostaglandin E1. There is a very good correlation between pulmonary arterial pressure and capillary recruitment. The hypoxic capillary recruitment is associated with a rise in capillary volume measured by DLCO. This capillary recruitment observed in the upper part of the lung is linked to a redistribution of the blood flow from the bases towards the apices of the lung as is shown in studies using radioactive microspheres. In conclusion, the response of the pulmonary circulation to generalised alveolar hypoxaemia may be outlined as follows: diffuse pulmonary arterial vasoconstriction leads to a rise in pulmonary artery pressure, which redistributes the blood flow towards the upper part of the lung recruiting capillaries and also increasing the pulmonary surface available for gas exchange.

Alprostadil↗
PubMed1987

Comparison of direct and indirect measurements of pulmonary capillary transit times.

Using in vivo microscopy, we made direct measurements of pulmonary capillary transit time by determining the time required for fluorescent dye to pass from an arteriole to a venule on the dependent surface of the dog lung. Concurrently, in the same animals, pulmonary capillary transit time was measured indirectly in the entire lung using the diffusing capacity method (capillary blood volume divided by cardiac output). Transit times by each method were the same in a group of five dogs [direct: 1.75 +/- 0.27 (SE) s; indirect: 1.85 +/- 0.33 s; P = 0.7]. The similarity of these transit times is important, because the widely used indirect determinations based on diffusing capacity are now shown to coincide with direct measurements and also because it demonstrates that measurements of capillary transit times on the surface of the dependent lung bear a useful relationship to measurements on the capillaries in the rest of the lung.

Animals↗
PubMed1987

Physiological neutrophil sequestration in the lung: visual evidence for localization in capillaries.

Although the lung is known to be a major site of neutrophil margination, the anatomic location of these sequestered cells within the lung is controversial. To determine the site of margination and the kinetics of neutrophil transit through the pulmonary microvasculature, we infused fluorescein isothiocyanate-labeled canine neutrophils into the pulmonary arteries of 10 anesthetized normal dogs and made fluorescence videomicroscopic observations of the subpleural pulmonary microcirculation through a window inserted into the chest wall. The site of fluorescent neutrophil sequestration was exclusively in the pulmonary capillaries with a total of 951 labeled cells impeded in the capillary bed for a minimum of 2 s. No cells were delayed in the arterioles or venules. Transit times of individual neutrophils varied over a wide range from less than 2 s to greater than 20 min with an exponential distribution skewed toward rapid transit times. These observations indicate that neutrophil margination occurs in the pulmonary capillaries with neutrophils impeded for variable periods of time on each pass through the lung. The resulting wide distribution of transit times may determine the dynamic equilibrium between circulating and marginated neutrophils.

Animals↗
PubMed1987

Pulmonary arterial transit times.

To begin to characterize the pulmonary arterial transport function we rapidly injected a bolus containing a radiopaque dye and a fluorescence dye into the right atrium of anesthetized dogs. The concentrations of the dye indicators were measured in the main pulmonary artery (fluoroscopically) and in a subpleural pulmonary arteriole (by fluorescence microscopy). The resulting concentration vs. time curves were subjected to numerical deconvolution and moment analysis to determine how the bolus was dispersed as it traveled through the arteriole stream tube from the main pulmonary artery to the arteriole. The mean transit time and standard deviation of the transport function from the main pulmonary artery to the arterioles studied averaged 1.94 and 1.23 s, respectively, and the relative dispersion (ratio of standard deviation to mean transit time) was approximately 64%. This relative dispersion is at least as large as those reported for the whole dog lung, indicating that relative to their respective mean transit times the dispersion upstream from the arterioles is comparable to that taking place in capillaries and/or veins. The standard deviations of the transport functions were proportional to their mean transit times. Thus the relative dispersion from the main pulmonary artery to the various arterioles studied was fairly consistent. However, there were variations in mean transit time even between closely adjacent arterioles, suggesting that variations in mean transit times between arteriole stream tubes also contribute to the dispersion in the pulmonary arterial tree.

Animals↗
PubMed1987

Athletic amenorrhea, major affective disorders, and eating disorders.

While studying amenorrheic runners, the authors became aware of psychiatric differences between them. Psychiatric interviews of 13 amenorrheic and 19 regularly menstruating runners revealed that of the amenorrheic runners, 11 reported major affective disorders in themselves or in first- and second-degree relatives and eight reported eating disorders in themselves. Among the regularly menstruating runners, however, there were no eating disorders or major affective disorders, and only one had first-degree relatives with major affective disorders. These data suggest a link between athletic amenorrhea in runners, major affective disorders, and eating disorders.

Adult↗
PubMed1987

Athletic amenorrhea: lack of association with body fat.

The most commonly tested hypothetical cause of athletic amenorrhea has been low body fat. Test results have conflicted because of mixed groups of athletes and methodologic problems. In this study, we measured body fat only in distance runners (greater than 53 km X wk-1) of the same somatotype who clearly had regular menses or secondary amenorrhea; this permitted more valid group comparison of body fat using hydrostatic weighing. The regularly menstruating group (N = 7) had 12 periods X yr-1 at intervals of 26.5 +/- 1.0 (SE) days with a duration of 4.1 +/- 0.4 days. In the athletic amenorrhea group (N = 7), menstrual periods had been absent for 1 to 10 yr (average = 3.9 +/- 1.3 yr); they were gynecologically evaluated to restrict the group to those with athletic amenorrhea. The groups were similar in a number of categories: weight, height, age, menarcheal age, weekly training mileage, days/week training, years of training, and maximum oxygen uptake. Percent body fat for the two groups was the same: 17.7 +/- 2.1% for the amenorrheic athletes and 17.4 +/- 1.2% for the regularly menstruating athletes (P = 0.91). These data do not support the idea that low body fat per se causes athletic amenorrhea.

Adipose Tissue↗
PubMed1986

Vertical gradient of pulmonary capillary transit times.

The key determinants of alveolar capillary perfusion are transit times and the extent of recruitment. Capillaries are known to be heavily recruited in the dependent lung, but there are no direct data that bear on how capillary transit times might be affected by gravity. We directly determined mean capillary transit times on the surface of the upper, middle, and lower lung by measuring the passage of fluorescent dye through the capillaries using in vivo television microscopy. In anesthetized dogs, mean capillary transit times averaged 12.3 s in the upper lung, 3.1 s in the midlung, and 1.6 s in the lower lung. This near order of magnitude variation in speed of blood transit establishes that there is a vertical gradient of capillary transit times in the lung. As expected, dependent capillary networks were nearly fully recruited, whereas relatively few capillaries were perfused in the upper lung. The lengthy transit times and sparsely perfused capillary beds in the upper lung combine to provide a substantial part of pulmonary gas exchange reserve.

Animals↗
PubMed1984

Role of collateral ventilation in ventilation-perfusion balance.

Species with collateral ventilation have an auxiliary respiratory mechanism that could protect them, under certain circumstances, from regional alveolar hypoxia. Species without collateral ventilation may have a greater potential for routinely experiencing regional hypoxia; to maintain ventilation-perfusion balance they would have to rely on pulmonary vasoconstriction. We tested these ideas by ventilating a sublobar region of pig lung (no collateral ventilation) with 13% O2 while the rest of the lung was ventilated with 30% O2. Blood flow, as measured by radioactive microsphere distribution to the sublobar region, was reduced 50% during hypoxia. The hypoxia-induced vasoconstriction effectively defended arterial PO2. When a vasodilator was infused, regional blood flow increased to control levels; shunt fraction rose, and arterial PO2 fell. In dogs (collateral ventilation present) the same experimental maneuvers had no significant effect on regional end-tidal gases or on microsphere distribution, indicating that collateral ventilation was able to maintain ventilation-perfusion balance. When regional hypoxia was created in dogs by overcoming collateral ventilation with slightly positive airway pressure in the sublobar region, the dog acted like the pig and used hypoxic vasoconstriction to shift approximately 30% of the blood flow away from the hypoxic alveoli.

Animals↗
PubMed1983

Thermodilution method overestimates low cardiac output in humans.

We compared 57 cardiac output measurements by the thermodilution and Fick methods in 26 patients and found that thermodilution values were higher in all 16 cases in which Fick outputs were less than 3.5 l/min. In 10 cases where Fick values were less than or equal to 2.5 l/min, thermodilution and Fick measurements differed by an average of 35%. When combined with the results of previous studies comparing the thermodilution, dye dilution, and Fick techniques, these findings suggest that the thermodilution method overestimates true cardiac output in the low output range. This overestimation probably is due to heat loss under conditions of low flow. Because the thermodilution method is used widely in patients with low output states, these findings have potentially important clinical implications.

Adolescent↗
PubMed1983

Lung vessel leak precedes right ventricular hypertrophy in monocrotaline-treated rats.

Monocrotaline induces microvascular leak and pulmonary hypertension in rats. We have hypothesized that the leak is related in some way to the pulmonary hypertension and precedes it. In rats given 40 mg monocrotaline/kg body wt subcutaneously, lung wet weight-to-dry weight ratios and lung albumin content began to increase within the first 3 days and became maximal at 1 wk. Alveolar lavage fluid showed little or no increase in protein. Right ventricular hypertrophy increased progressively from 2 through 3 wk. An increase in lung dry weight paralleled the right ventricular hypertrophy. The amount of blood retained in the lung did not account for the increased lung water, albumin, or weight. We considered that microvascular leak without leak into the alveolar space preceded pulmonary hypertension, right ventricular hypertrophy, and increased lung dry weight. In rats not given monocrotaline but exposed for 3 wk to hypobaric hypoxia, lung albumin, lung dry weight, and right ventricular weight increased. Increased lung dry weight probably reflects hyperplasia of lung cells. If so, an association of microvascular leak, lung cell hyperplasia, and right ventricular hypertrophy may occur in both monocrotaline- and hypoxia-induced pulmonary hypertension.

Albumins↗
PubMed1983

Abnormal alveolar cells in monocrotaline induced pulmonary hypertension.

Monocrotaline given to rats causes lung injury which is followed by pulmonary hypertension. A large, abnormal intraalveolar cell has been repeatedly observed. The purpose of the present study was to define the nature of the cell and to determine how it related to the lung injury. As observed by electron microscopy, the intraalveolar cell contained numerous large, dense granules, as well as lipid whorls, extensive Golgi complexes, and many small vesicles. These cells appeared to be macrophages, possibly altered by ingestion of lipid-like material which was free in the alveolar space. Enlarged type II pneumonocytes and mast cells were seen in the alveolar walls but their appearance differed from that of the free alveolar cells. The electron microscopic findings plus the presence of Fc and C3b receptors on the cells indicated they were alveolar macrophages. When the severity of pulmonary hypertension was varied by a) giving monocrotaline to rats of varying age, b) by varying the dose of monocrotaline, or c) by varying the time interval after monocrotaline administration, the number of abnormal alveolar macrophages related to the severity of the pulmonary hypertension. When we reduced the number of circulating leukocytes by whole body radiation, monocrotaline administration was followed both by accelerated pulmonary hypertension and increased numbers of abnormal alveolar macrophages. The abnormal macrophage appeared to be a marker of the monocrotaline induced pulmonary hypertension. However, neither the abnormal macrophage nor the monocrotaline injury appeared to depend on circulating leukocytes.

Animals↗
PubMed1982

Direct measurement of pulmonary capillary transit times.

Direct measurements of capillary transit times in dog lungs were made by using in vivo television microscopy. Mean transit times were unexpectedly long. As pulmonary artery pressures were raised, transit times decreased, suggesting that the normally existing hydrostatic pressure gradient in the lung causes a vertical distribution of transit times. The more rapid transit times approached the minimum time required for complete oxygenation.

Animals↗
PubMed1982

Intrapulmonary blood flow redistribution during hypoxia increases gas exchange surface area.

We have previously shown that airway hypoxia causes pulmonary capillary recruitment and raises diffusing capacity for carbon monoxide. This study was designed to determine whether these events were caused by an increase in pulmonary vascular resistance, which redistributed blood flow toward the top of the lung, or by an increase in cardiac output. We measured capillary recruitment at the top of the dog lung by in vivo microscopy, gas exchange surface area of the whole lung by diffusing capacity for carbon monoxide, and blood flow distribution by radioactive microspheres. During airway hypoxia recruitment occurred, diffusing capacity increased, and blood flow was redistributed upward. When a vasodilator was infused while holding hypoxia constant, these effects were reversed; i. e., capillary "derecruitment" occurred, diffusing capacity decreased, and blood flow was redistributed back toward the bottom of the lung. The vasodilator was infused at a rate that left hypoxic cardiac output unchanged. These data show that widespread capillary recruitment during hypoxia is caused by increased vascular resistance and the resulting upward blood flow redistribution.

Alprostadil↗
PubMed1981

Diffusing capacity of the lung during hypoxia: role of capillary recruitment.

We have used in vivo microscopy to show that airway hypoxia caused pulmonary capillary recruitment. To determine whether the recruited capillaries add to the surface area for gas exchange, we measured the diffusing capacity of the lung for carbon monoxide before and after inducing recruitment with hypoxia. Diffusing capacity increased during hypoxia. However, some increase in diffusing capacity was expected, since there were fewer oxygen molecules to compete with carbon monoxide for hemoglobin-binding sites. To determine the effect of capillary recruitment alone on diffusing capacity, we held hypoxia constant while infusing a vasodilator to diminish recruitment. Diffusing capacity decreased concomitantly as recruitment diminished. These results indicate that our microscopic observations reflect a widespread recruitment that increases the gas exchange surface area.

Animals↗