Ventilation-perfusion relationships during high-altitude adatation.

Haab, P; Held, D.R.; Ernst, H; Farhi, Leon E.

doi:10.1152/jappl.1969.26.1.77

Cited by 33 publications

(10 citation statements)

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“…Haab et al measured alveolar to arterial differences for N2 and CO2 in nine subjects at 2000 ft and for 5 days after ascent to 11,500 ft (10). On the basis of calculated predicted values for these variables, they suggested that ventilation/perfusion abnormalities persisted throughout the 5 days of altitude exposure.…”

Section: Discussionmentioning

confidence: 99%

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Pulmonary Artery Pressure and Alveolar Gas Exchange in Man during Acclimatization to 12,470 ft

Kronenberg¹,

Šafář²,

Leej³

et al. 1971

J. Clin. Invest.

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A B S T R A C T Pulmonary hemodynamics and Rotta, Canepa, Hurtado, Velasquez, and Chavez in 1956 (1) and has been confirmed many times since, both in acclimatized natives (2, 3) and in newcomers (4). The relationship of this pulmonary hypertension to the development of high altitude pulmonary edema (HAPE) is uncertain, but pulmonary artery pressure is higher during episodes of HAPE than during control observations in the same individuals (5), and persons who have had such episodes previously have higher pulmonary artery pressures when reexposed to altitude than nonsusceptible individuals under the same conditions (6). Although it is recognized that the peak incidence of HAPE occurs 1-3 days after entry to high altitude (7), it has not been established whether pulmonary arterial pressure rises in a progressive fashion over the same time course. A progressive rise in pulmonary arterial pressure during a 6 wk period at 12,700 ft has been reported in steers, apparently associated with the right heart failure termed "brisket disease" (8), but was not observed in lambs in a matched experiment (9). Therefore, we decided to investigate in ourselves the time course of the pulmonary arterial pressure both at rest and during exercise at 12,470 ft and to examine other aspects of cardiovascular function over the same time span. We also explored the possibility suggested by Haab, Held, Ernst, and Farhi (10) and Reeves, Halpin, Cohn, and Daoud (11) that hypoxia widens the alveolar to arterial 02 difference.

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Section: Discussionmentioning

confidence: 99%

“…Therefore, we decided to investigate in ourselves the time course of the pulmonary arterial pressure both at rest and during exercise at 12,470 ft and to examine other aspects of cardiovascular function over the same time span. We also explored the possibility suggested by Haab, Held, Ernst, and Farhi (10) …”

Section: Introductionmentioning

confidence: 99%

Pulmonary Artery Pressure and Alveolar Gas Exchange in Man during Acclimatization to 12,470 ft

Kronenberg¹,

Šafář²,

Leej³

et al. 1971

J. Clin. Invest.

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show abstract

“…In support of this theory Haab et a/. (15) analyzed alveolararterial gradients for nitrogen and found that hypoxia exaggerates ventilation-perfusion imbalances. Viswanathan et al (42) did perfusion lung scans of adults who had experienced high altitude pulmonary edema and found a patchy distribution of perfusion during hypoxia.…”

Section: Discussionmentioning

confidence: 91%

Lung Fluid Balance in Hypoxic Lambs

et al. 1984

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SummaryIn spontaneously breathing newborn lambs, alveolar hypoxia increases lung microvascular pressure, which causes lung lymph flow to increase and the concentration of protein in lymph to decrease. To see if this response derives from hypoxia itself rather than from the change in breathing pattern that occurs during hypoxia, we measured lung vascular pressures, pleural pressure, cardiac output, and lung lymph flow in 12 anesthetized lambs that were ventilated at a fixed rate and tidal volume, first with air, then with 10-14% O2 in nitrogen. Alveolar hypoxia did not affect pleural pressure, but pulmonary arterial pressure increased from 19 to 32 torr, lung lymph flow increased from 2.20 to 3.83 ml/h and lymph protein concentration decreased from 3.4 to 2.8 g/dl. To be certain that the increased lymph flow associated with hypoxia is not simply the result of an acute release of fluid from the lungs and to assess the effects of carbon dioxide on lymph flow during hypoxia, we next studied six unanesthetized lambs kept hypoxic for a total of 12 h. After a 2-4-h period in air the lambs breathed 9-11% 0 2 in nitrogen for 2-4 h, then 8-11% O2 and 3-5% C02 in nitrogen for 8-10 h. In these lambs we injected intravenously radioactive albumin and measured its uptake in lymph to see if sustained hypoxia alters microvascular permeability to protein in the lungs. In these experiments pulmonary arterial pressure increased from 17 to 37 torr, lung lymph flow increased from 1.74 to 3.28 ml/h, and lymph protein concentration decreased from 3.8 to 3.1 g/dl during hypoxia. Addition of C02 to the inspired gas did not affect steady state lung lymph flow. Lymph flow remained elevated throughout the 12 h of alveolar hypoxia, and postmortem lung water determinations were not different from those of controls (4.65 f 0.28 versus 4.72 f 0.14 g/g dry bloodless lung). The time required for radioactive albumin to equilibrate in lymph at one-half the specific activity of plasma was no different before and during hypoxia (130 + 7 versus 125 f 11 min). We conclude that in the newborn lamb, alveolar hypoxia increases transvascular fluid filtration by increasing microvascular hydraulic pressure without altering microvascular permeability to protein. This response is independent of changes in pleural pressure or inspired carbon dioxide. Bressack and Bland (5,6) showed that alveolar hypoxia increases lung lymph flow and decreases lymph protein concentration in newborn lambs. They concluded that alveolar hypoxia increases transvascular fluid filtration in the lung by increasing filtration pressure without altering microvascular permeability to protein.At least two issues were unanswered by the previous studies. First, because Bressack and Bland used unanesthetized lambs that breathed spontaneously, hypoxia caused hyperventilation and a resultant decrease in arterial Pco2 and pleural pressure. Arterial Pco2 may influence pulmonary vascular tone (20,25) and pleural pressure may influence lung interstitial fluid pressure (1 4,2 I, 27,38,45); it is poss...

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“…Haab et al (32) analyzed alveolar-arterial gradients for nitrogen and found that hypoxia exaggerates ventilation perfusion imbalances. Viswanathan et al (33) performed perfusion lung scans on adults who had experienced high altitude pulmonary edema and found a patchy redistribution of perfusion during hypoxia.…”

Section: Discussionmentioning

confidence: 99%