Altitude and the Human Pulmonary Circulation

Lockhart, A; Saiag, B.

doi:10.1042/cs0600599

Cited by 35 publications

(12 citation statements)

References 65 publications

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“…Specifically, histologic evidence of interstitial edema is lacking in the ovine species after hypoxia, and a report in newborn lambs actually showed hypoxia-induced decreases in extravascular lung water (7). In contrast, other species including the rat demonstrate endothelial injury and edema formation similar to findings reported in human cases of high altitude pulmonary edema (2,3,15,16,17,30). The failure of hypoxia to increase vascular permeability in the sheep and lamb thus may not be applicable to other animals species or man.…”

Section: Methodsmentioning

confidence: 67%

“…Species differences may also contribute to reported discrepancies as past studies suggesting that hypoxia does not lead to an increase in lung vascular permeability have all been carried out in the ovine species. Considerable evidence exists that suggests that the pulmonary vascular response to hypoxia in sheep may differ from those of other mammalian species (2,8,33,34). Specifically, histologic evidence of interstitial edema is lacking in the ovine species after hypoxia, and a report in newborn lambs actually showed hypoxia-induced decreases in extravascular lung water (7).…”

Section: Methodsmentioning

confidence: 99%

“…Increases in vascular permeability in hypoxia could contribute to the development of high-altitude pulmonary edema and endogenous glucocorticoids may have an important influence on pulmonary vascular permeability in hypoxia. Introduction Rapid ascent to high altitude may be associated with the development of pulmonary edema (HAPE)' (1,2 Despite this, attempts to demonstrate hypoxia-induced changes in permeability in the laboratory have produced conflicting results. Bland et al (5) and Landolt et al (6) failed to detect increases in lung lymph flow in adult sheep during hypoxia, even with the added stress of increased blood flow.…”

Section: Introductionmentioning

confidence: 99%

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Hypoxia-induced increases in pulmonary transvascular protein escape in rats. Modulation by glucocorticoids.

Stelzner¹,

O'Brien²,

Sato³

et al. 1988

J. Clin. Invest.

111

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Pulmonary edema after ascent to altitude is well recognized but its pathogenesis is poorly understood. To determine whether altitude exposure increases lung vascular permeability, we exposed rats to a simulated altitude of -14,500 feet (barometric pressure [Pbi 450 Torr) and measured the pulmonary transvascular escape of radiolabeled '25l-albumin corrected for lung blood content with 51Cr-tagged red blood cells (protein leak index = PLI). Exposures of 24 and 48 h caused significant increases in PLI (2.30±0.08 and 2.40±0.06) compared with normoxic controls (1.76±0.06), but brief hypoxic exposures of 1-13 h produced no increase in PLI, despite comparable increases in pulmonary artery pressure. There were associated increases in gravimetric estimates of lung water in the altitude-exposed groups and perivascular edema cuffs on histologic examination. Normobaric hypoxia (48 h; fractional inspired oxygen concentration [FI021 = 15%) also increased lung transvascular protein escape and lung water.Dexamethasone has been used to prevent and treat altitude-induced illnesses, but its mechanism of action is unclear. Dexamethasone (0.5 or 0.05 mg/kg per 12 h) started 12 h before and continued during 48 h of altitude exposure prevented the hypoxia-induced increases in transvascular protein escape and lung water. Hemodynamic measurements (mean pulmonary artery pressure and cardiac output) were unaffected by dexamethasone, suggesting that its effect was not due to a reduction in pulmonary artery pressure or flow. The role of endogenous glucocorticoid activity was assessed in adrenalectomized rats that showed augmented hypoxia-induced increases in transvascular protein escape, which were prevented by exogenous glucocorticoid replacement. In summary, subacute hypoxic exposures increased pulmonary transvascular protein escape and lung water in rats. Dexamethasone prevented these changes independent of reductions of mean pulmonary artery pressure or flow, whereas adrenalectomy increased pulmonary vascular permeability and edema at altitude. Increases in vascular permeability in hypoxia could contribute to the development of high-altitude pulmonary edema and endogenous glucocorticoids may have an important influence on pulmonary vascular permeability in hypoxia. Introduction Rapid ascent to high altitude may be associated with the development of pulmonary edema (HAPE)' (1,2 Despite this, attempts to demonstrate hypoxia-induced changes in permeability in the laboratory have produced conflicting results. Bland et al. (5) and Landolt et al. (6) failed to detect increases in lung lymph flow in adult sheep during hypoxia, even with the added stress of increased blood flow. In contrast, other studies have demonstrated increases in lymph flow in newborn lambs (7) and dogs (8-10) after hypoxia. Furthermore, studies in isolated perfused dog lungs have revealed increased filtration and reflection coefficients consistent with increased vascular permeability after brief exposures to anoxic gas (1 1, 12). Differences in both species and ...

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Section: Methodsmentioning

confidence: 67%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Hypoxia-induced increases in pulmonary transvascular protein escape in rats. Modulation by glucocorticoids.

Stelzner¹,

O'Brien²,

Sato³

et al. 1988

J. Clin. Invest.

111

View full text Add to dashboard Cite

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“…Numerous studies have examined the effects of altitude, both acute and long term; these are well reviewed [16][17][18][19][20] and are summarised in table 3. Many of the effects of altitude have been learnt from the study of the physiology of travellers (usually adults) to high altitude regions, and comparing this with the physiology of high and low altitude residents.…”

Section: Physiological Effects Of Altitudementioning

confidence: 99%

The effects of flight and altitude

Samuels

2004

Archives of Disease in Childhood

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“…resistance of the pulmonary vessels and, thus, results in a significant rise of pulmonary artery pressure (PAP) and right heart load [1][2][3]. Recently, several studies investi gated the effects of pulmonary hypertension on LV dia stolic function [4][5][6][7][8][9], Altered septal motion [5,7] and…”

Section: Introductionmentioning

confidence: 99%

Abnormal Left Ventricular Diastolic Filling Patterns in Acute Hypoxic Pulmonary Hypertension at High Altitude

Ritter¹,

Jenni²,

Maggiorini³

et al. 1993

Am J Noninvas Cardiol

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In order to evaluate left ventricular (LV) diastolic filling properties at high altitude, 19 healthy mountaineers were studied by Doppler echocardiography in a high altitude research laboratory at 4,559 m above sea level. Baseline examinations were carried out at 490 m. Measurements comprised mitral inflow velocity parameters and pulmonary artery pressure (PAP, mm Hg). The two-dimensional (2-D) cross-sectional parasternal short axis view of the left ventricle revealed a characteristic bulging of the interventricular septum towards the LV cavity in all subjects at high altitude. Accordingly, end-diastolic and end-systolic excentricity indexes B/A from 2-D parasternal short axis view increased significantly. Heart rate, M-mode LV fractional shortening (FS, %), and PAP increased significantly at 4,559 m. Isovolumic relaxation time (IVRT, ms), early LV diastolic filling velocity (E, cm/s), deceleration time of early LV diastolic filling (DT, ms) and late LV diastolic flow velocity (A, cm/s), all normalized for the corresponding diastolic time interval, increased significantly at 4,559 m. E/A ratio was significantly depressed at 4,559 m. PAP correlated significantly with LV end-diastolic excentricity index (r = 0.54, p < 0.001), LV end-systolic excentricity index (r = 0.53, p < 0.01), IVRT (r = 0.55, p < 0.001) and E/A (r = -0.37, p < 0.05). It is concluded that the acute rise in PAP at 4,559 m leads to a significant alteration in LV diastolic mitral inflow velocity properties which is associated to the concomitant change in LV geometry and the consecutively prolonged LV isovolumic relaxation.

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Altitude and the Human Pulmonary Circulation

Cited by 35 publications

References 65 publications

Hypoxia-induced increases in pulmonary transvascular protein escape in rats. Modulation by glucocorticoids.

Hypoxia-induced increases in pulmonary transvascular protein escape in rats. Modulation by glucocorticoids.

The effects of flight and altitude

Abnormal Left Ventricular Diastolic Filling Patterns in Acute Hypoxic Pulmonary Hypertension at High Altitude

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