The Bronchial Arteries in Pulmonary Emphysema

Cudkowicz, Leon; Armstrong, John

doi:10.1136/thx.8.1.46

Cited by 90 publications

(25 citation statements)

References 18 publications

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“…Because SU5416 increased endothelial cell apoptosis in colon cancer liver metastases (23), we hypothesized that impairment of the VEGF receptor kinase activity may induce endothelial cell apoptosis in the lung. Our finding of alveolar cell apoptosis and emphysema in the lungs of rats chronically treated with a VEGF receptor inhibitor is intriguing in view of the vascular hypothesis of emphysema presented by earlier investigators (4,24,25). A second VEGF receptor blocker, structurally unrelated to SU5416, when administered to rats with an experimental protocol identical to that used for SU5416, confirmed our results of increased lung mean linear intercept as observed in rats treated with SU5416 (R.M.…”

Section: Discussionsupporting

confidence: 79%

Inhibition of VEGF receptors causes lung cell apoptosis and emphysema

Kasahara

Tuder²,

Taraseviciene‐Stewart³

et al. 2000

J. Clin. Invest.

1,005

790

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Section: Discussionsupporting

confidence: 79%

Inhibition of VEGF receptors causes lung cell apoptosis and emphysema

Kasahara

Tuder²,

Taraseviciene‐Stewart³

et al. 2000

J. Clin. Invest.

1,005

790

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“…4. Finally, it is not possible to assess the impression of peripheral arterial changes upon the pulmonary artery pressure, in view of the contradictory evidence relevant to the existence of pulmonary-bronchial artery anastomoses in normal human lungs (21,22). While the absence of correlation between the peripheral and pulmonary arterial pressure changes in the present data (Figure 4) be expected to occur with progressive increases in the cardiac output (24) to a previously established critical limit (1,5), it is an unexpected finding in those situations where the exercise outputs remained steady.…”

Section: Discussionmentioning

confidence: 99%

Response of Pulmonary Artery Pressure and Total Pulmonary Resistance of Untrained, Convalescent Man to Prolonged Mild Steady State Exercise1

Sancetta¹,

Rakita²

1957

J. Clin. Invest.

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Although many published studies relevant to the effects of exercise on the gross pulmonary hemodynamics of patients with heart disease are available in the literature, few data are to be found which deal with normal man (1-6). There have been conflicting claims that there is no increase, no significant increase, a consistent increase, or an occasional decrease in the pulmonary artery pressure of normal man as the result of exercise loads eventuating in oxygen uptakes up to 400 ml. per M.2 per min. (2) and pulmonary blood flows two to three times the resting basal levels (1, 5). Moreover, comparison among the published data is difficult because of variations in the exercise posture, the duration of exercise, the work loads employed, and the timing of blood and pressure sampling, which often are varied in different subjects within the same body of data.Slonim, Ravin, Balchum, and Dressler (6) alone have systematically studied the continuous pulmonary artery pressure variations in 5 normal subjects in the recumbent position over a 7-minute period of exercise, employing an almost uniform work rate between 784 and 840 foot-pounds per minute. These authors noted immediate increases in pulmonary systolic, diastolic and mean pressures, which usually reached a peak between the first and third minutes of exercise with an overall tendency to a slight secondary decline by the sixth minute. A steady state was not achieved.The present report is intended to extend these findings employing a mild and uniform external work load of 850 foot-pounds per minute sustained over a period of 39 minutes. This mild amount of work was selected in order that steady state be attained in a reasonably uniform period of time, 1 Supported by a grant from United Appeal, Lorain County, Ohio. that it be maintained as long as possible, and that some lower limit of valid, measurable change be established for comparison in subjects with heart disease physically unable to exercise at higher work loads and achieve the steady state (7). MATERIALS AND METHODSStudies were conducted on 12 subj ects with normal cardio-respiratory systems who had convalesced from various illnesses (bronchopneumonia, active peptic ulcer, eczematoid dermatitis), or had been admitted for investigation of minor complaints. None were anemic or febrile. All had been ambulatory for several days before the studies were conducted. On the day prior to the experiment the subjects were exercised in the supine position at a standard work rate of 850-foot pounds per minute for a period of 39 minutes. In all but three instances the steady state, as determined by repetitive determinations of the oxygen consumption (8), was attained within 10 to 12 minutes of exercise; in the remaining three, it was attained at the 12 to 14-minute period. The following morning, at an ambient temperature of 23 degrees C., cardiac catheterization was performed in the post-absorptive state with mild sedation (Pentobarbital Sodium, 0.1 Gm.), employing standard No. 7F Cournand catheters. The supine position was...

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“…However, such shunts are not characteristic of the emphysematous lung and, furthermore, would appear to be excluded by the absence of a rapid initial appearance of both tracer electrolytes and albumin-Il31. Bronchial arterial anastomoses with the pulmonary vessels have been described in chronic pulmonary .disease (16)(17)(18), but sinice blood flow through these channels is from left to right no effect on the first circulation transfer would be expected.…”

Section: Resultsmentioning

confidence: 99%

PULMONARY TRANSCAPILLARY EXCHANGE OF Na24 AND P32-LABELED PHOSPHATE IN PULMONARY EMPHYSEMA*

Rothschild¹,

Davis²,

Oratz³

et al. 1959

J. Clin. Invest.

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In previous studies it was observed that 5 to 20 per cent of intravenously administered Na24 and P32-labeled phosphate and other electrolytes escaped from the circulation during a single transit through the cardiopulmonary pool (1). The relatively small transcapillary exchange of electrolytes in the lungs as compared with skeletal muscle and certain other viscera was attributed to a lesser permeability of the pulmonary capillaries (1). The fraction of intravascular tracer electrolyte transferred across the pulmonary capillaries during pulmonary transit was diminished in the presence of a rapid circulation time and increased in patients with congestive heart failure and a prolonged circulation time (1). The present study extends these observations in patients with pulmonary emphysema where the problem of structural and physiological alterations of the pulmonary vascular tree is of particular interest. METHODS

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The Bronchial Arteries in Pulmonary Emphysema

Cited by 90 publications

References 18 publications

Inhibition of VEGF receptors causes lung cell apoptosis and emphysema

Inhibition of VEGF receptors causes lung cell apoptosis and emphysema

Response of Pulmonary Artery Pressure and Total Pulmonary Resistance of Untrained, Convalescent Man to Prolonged Mild Steady State Exercise1

PULMONARY TRANSCAPILLARY EXCHANGE OF Na24 AND P32-LABELED PHOSPHATE IN PULMONARY EMPHYSEMA*

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