Alveolar resistance to atelectasis

Cavagna, G; Stemmler, Edward J.; DuBois, Arthur B.

doi:10.1152/jappl.1967.22.3.441

Cited by 50 publications

(15 citation statements)

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“…Pulmonary vein pressure was set, and it aver- (24). What effect lung inflation has on arterial, capillary, and venous resistance is not known, although it has been shown that small vessel volume decreases and large vessel volume increases with increasing degrees of lung inflation (25,26).…”

Section: Resultsmentioning

confidence: 99%

Longitudinal distribution of vascular resistance in the pulmonary arteries, capillaries, and veins

Brody¹,

Stemmler²,

DuBois³

1968

J. Clin. Invest.

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A B S T R A C T A new method has been described for measuring the pressure and resistance to blood flow in the pulmonary arteries, capillaries, and veins. Studies were performed in dog isolated lung lobes perfused at constant flow with blood from a donor dog. Pulmonary artery and vein volume and total lobar blood volume were measured by the ether plethysmograph and dyedilution techniques. The longitudinal distribution of vascular resistance was determined by analyzing the decrease in perfusion pressure caused by a bolus of low viscosity liquid introduced into the vascular inflow of the lobe.The pulmonary arteries were responsible for 46% of total lobar vascular resistance, whereas the pulmonary capillaries and veins accounted for 34 and 20% of total lobar vascular resistance respectively. Vascular resistance was 322 dynes * sec* cm-5/ml of vessel in the lobar pulmonary arteries, 112 dynes sec.cm-5/ml in the pulmonary capillaries, and 115 dynes-sec* cm5/ml in the lobar pulmonary veins. Peak vascular resistivity (resistance per milliliter of volume) was in an area 2 ml proximal to the capillary bed, but resistivity was high throughout the pulmonary arterial tree. The pulmonary arteries accounted for approximately 50% of vascular resistance upstream from the sluice point when alveolar pressure exceeded venous pressure.The method described provides the first measurements of pulmonary capillary pressure. Midcapillary pressure averaged 13.3 cm H2O, pulDr. Brody is a postdoctoral fellow of the National Institutes of Health.

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Section: Resultsmentioning

confidence: 99%

Longitudinal distribution of vascular resistance in the pulmonary arteries, capillaries, and veins

Brody¹,

Stemmler²,

DuBois³

1968

J. Clin. Invest.

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“…Assuming a vertical lung length of 30 cm and a P pl gradient of 0.25 cmH 2 O/cm descent (Milic-Emili et al 1964b), the estimated P c,max values at lung bottom correspond to a P L of zero in the old and -1 cmH 2 O in the young subjects. In contrast, according to Cavagna et al (1967), a more negative P L is required to start airway closure in experimental animals. In this elegant study, airway and alveolar collapsibility were assessed in vivo by measuring quasi-static deflation P-V curves of lung during progressive reduction of volume (measured plethysmographically) achieved by gas absorption following tracheal clamping in oxygen filled lungs (case a), or by withdrawing air from the trachea with a syringe (case b).…”

Section: Trapped Gas Volumementioning

confidence: 99%

Closing volume: a reappraisal (1967–2007)

2007

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Measurement of closing volume (CV) allows detection of presence or absence of tidal airway closure, i.e. cyclic opening and closure of peripheral airways with concurrent (1) inhomogeneity of distribution of ventilation and impaired gas exchange; and (2) risk of peripheral airway injury. Tidal airway closure, which can occur when the CV exceeds the end-expiratory lung volume (EELV), is commonly observed in diseases characterised by increased CV (e.g. chronic obstructive pulmonary disease, asthma) and/or decreased EELV (e.g. obesity, chronic heart failure). Risk of tidal airway closure is enhanced by ageing. In patients with tidal airway closure (CV > EELV) there is not only impairment of pulmonary gas exchange, but also peripheral airway disease due to injury of the peripheral airways. In view of this, the causes and consequences of tidal airway closure are reviewed, and further studies are suggested. In addition, assessment of the "open volume", as opposed to the "closing volume", is proposed because it is easier to perform and it requires less equipment.

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“…This reversal of ventilation distribution has been attributed to airway closure (trapping) in the dependent lung zones (4,9). For closure to occur, pleural pressure must be greater than airway pressure (10). As lung volume approaches residual volume (RV), the pleural pressure in the lower lung zones indeed exceeds airway pressure, causing trapping in the dependent lung zones.…”

mentioning

confidence: 99%

Regional distribution of pulmonary ventilation and perfusion in elderly subjects

Holland¹,

Milic–Emili²,

Macklem³

et al. 1968

J. Clin. Invest.

152

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A B S T R A C T Using radioactive xenon, we measured the regional distribution of pulmonary ventilation and blood flow in six normal men, whose ages ranged between 65 and 75 yr. The measurements were made in the standing position. The static volume-pressure relation of the lungs was also measured in five of the subjects. The results indicate that by comparison with normal young men: (a) Blood flow to the upper lung zones was increased, although it still remained predominant in the lower zones. (b) Ventilation distribution during a vital capacity inspiration was similar to that seen in young subjects. (c) In five of the six elderly subjects, however, the distribution of ventilation in the resting tidal volume range was not preferential to the lower zones as it was in young men. This was probably caused by airway closure in the lower lung zones. The elderly subjects thus exhibit during normal tidal volume breathing a ventilation distribution pattern similar to that observed in young subjects when breathing at low lung volumes, i.e., near residual volume. This difference is probably due to the combined effect of the loss in elastic recoil of the lungs observed in the elderly subjects and of a decreased resistance to collapse of the aged airways. These findings suggest that in the elderly subjects there is a significant regional ventilation-perfusion impairment during quiet breathing, which may explain in part Dr. Holland's present address is Cardio-Pulmonary Laboratory, Dalhousie University, Halifax, Canada. Address requests for reprints to Dr.

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Alveolar resistance to atelectasis

Cited by 50 publications

References 0 publications

Longitudinal distribution of vascular resistance in the pulmonary arteries, capillaries, and veins

Longitudinal distribution of vascular resistance in the pulmonary arteries, capillaries, and veins

Closing volume: a reappraisal (1967–2007)

Regional distribution of pulmonary ventilation and perfusion in elderly subjects

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