Pulmonary gas exchange in humans exercising at sea level and simulated altitude

1986 ◽  
Vol 61 (1) ◽  
pp. 260-270 ◽  
Author(s):  
P. D. Wagner ◽  
G. E. Gale ◽  
R. E. Moon ◽  
J. R. Torre-Bueno ◽  
B. W. Stolp ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Arterial Pressure ◽  
Sea Level ◽  
Pulmonary Arterial Pressure ◽  
Minute Ventilation ◽  
Statistical Significance ◽  
Random Order ◽  
Normal Subjects ◽  
Simulated Altitude ◽  
Pulmonary Arterial

In a previous study of normal subjects exercising at sea level and simulated altitude, ventilation-perfusion (VA/Q) inequality and alveolar-end-capillary O2 diffusion limitation (DIFF) were found to increase on exercise at altitude, but at sea level the changes did not reach statistical significance. This paper reports additional measurements of VA/Q inequality and DIFF (at sea level and altitude) and also of pulmonary arterial pressure. This was to examine the hypothesis that VA/Q inequality is related to increased pulmonary arterial pressure. In a hypobaric chamber, eight normal subjects were exposed to barometric pressures of 752, 523, and 429 Torr (sea level, 10,000 ft, and 15,000 ft) in random order. At each altitude, inert and respiratory gas exchange and hemodynamic variables were studied at rest and during several levels of steady-state bicycle exercise. Multiple inert gas data from the previous and current studies were combined (after demonstrating no statistical difference between them) and showed increasing VA/Q inequality with sea level exercise (P = 0.02). Breathing 100% O2 did not reverse this increase. When O2 consumption exceeded about 2.7 1/min, evidence for DIFF at sea level was present (P = 0.01). VA/Q inequality and DIFF increased with exercise at altitude as found previously and was reversed by 100% O2 breathing. Indexes of VA/Q dispersion correlated well with mean pulmonary arterial pressure and also with minute ventilation. This study confirms the development of both VA/Q mismatch and DIFF in normal subjects during heavy exercise at sea level. However, the mechanism of increased VA/Q mismatch on exercise remains unclear due to the correlation with both ventilatory and circulatory variables and will require further study.

Operation Everest II: pulmonary gas exchange during a simulated ascent of Mt. Everest

1987 ◽  
Vol 63 (6) ◽  
pp. 2348-2359 ◽  
Author(s):  
P. D. Wagner ◽  
J. R. Sutton ◽  
J. T. Reeves ◽  
A. Cymerman ◽  
B. M. Groves ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Sea Level ◽  
Pulmonary Arterial Pressure ◽  
Flow Distribution ◽  
Barometric Pressure ◽  
Normal Subjects ◽  
O2 Uptake ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Eight normal subjects were decompressed to barometric pressure (PB) = 240 Torr over 40 days. The ventilation-perfusion (VA/Q) distribution was estimated at rest and during exercise [up to 80–90% maximal O2 uptake (VO2 max)] by the multiple inert gas elimination technique at sea level and PB = 428, 347, 282, and 240 Torr. The dispersion of the blood flow distribution increased by 64% from rest to 281 W, at both sea level and at PB = 428 Torr (heaviest exercise 215 W). At PB = 347 Torr, the increase was 79% (rest to 159 W); at PB = 282 Torr, the increase was 112% (108 W); and at PB = 240 Torr, the increase was 9% (60 W). There was no significant correlation between the dispersion and cardiac output, ventilation, or pulmonary arterial wedge pressure, but there was a correlation between the dispersion and mean pulmonary arterial pressure (r = 0.49, P = 0.02). When abnormal, the VA/Q pattern generally had perfusion in lung units of zero or near zero VA/Q combined with units of normal VA/Q. Alveolar-end-capillary diffusion limitation of O2 uptake (VO2) was observed at VO2 greater than 3 l/min at sea level, greater than 1–2 l/min VO2 at PB = 428 and 347 Torr, and at higher altitudes, at VO2 less than or equal to 1 l/min. These results show variable but increasing VA/Q mismatch with long-term exposure to both altitude and exercise. The VA/Q pattern and relationship to pulmonary arterial pressure are both compatible with alveolar interstitial edema as the primary cause of inequality.

Pulmonary gas exchange in humans during exercise at sea level

1986 ◽  
Vol 60 (5) ◽  
pp. 1590-1598 ◽  
Author(s):  
M. D. Hammond ◽  
G. E. Gale ◽  
K. S. Kapitan ◽  
A. Ries ◽  
P. D. Wagner
Keyword(s):  
Gas Exchange ◽  
Sea Level ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Inert Gas ◽  
Diffusion Limitation ◽  
O2 Uptake ◽  
Heavy Exercise ◽  
Blood Temperature ◽  
O2 Diffusion

Previous studies have shown both worsening ventilation-perfusion (VA/Q) relationships and the development of diffusion limitation during exercise at simulated altitude and suggested that similar changes could occur even at sea level. We used the multiple-inert gas-elimination technique to further study gas exchange during exercise in healthy subjects at sea level. Mixed expired and arterial respiratory and inert gas tensions, cardiac output, heart rate, minute ventilation, respiratory rate, and blood temperature were recorded at rest and during steady-state exercise in the following order: rest, minimal exercise (75 W), heavy exercise (300 W), heavy exercise breathing 100% O2, repeat rest, moderate exercise (225 W), and light exercise (150 W). Alveolar-to-arterial O2 tension difference increased linearly with O2 uptake (VO2) (6.1 Torr X min-1 X 1(-1) VO2). This could be fully explained by measured VA/Q inequality at mean VO2 less than 2.5 l X min-1. At higher VO2, the increase in alveolar-to-arterial O2 tension difference could not be explained by VA/Q inequality alone, suggesting the development of diffusion limitation. VA/Q inequality increased significantly during exercise (mean log SD of perfusion increased from 0.28 +/- 0.13 at rest to 0.58 +/- 0.30 at VO2 = 4.0 l X min-1, P less than 0.01). This increase was not reversed by 100% O2 breathing and appeared to persist at least transiently following exercise. These results confirm and extend the earlier suggestions (8, 21) of increasing VA/Q inequality and O2 diffusion limitation during heavy exercise at sea level in normal subjects and demonstrate that these changes are independent of the order of performance of exercise.

Chronic activation of neurokinin-1 receptor induces pulmonary hypertension in rats

1999 ◽  
Vol 276 (5) ◽  
pp. H1543-H1551 ◽  
Author(s):  
Li-Wen Chen ◽  
Chau-Fong Chen ◽  
Yih-Loong Lai
Keyword(s):  
Pulmonary Hypertension ◽  
Substance P ◽  
Arterial Pressure ◽  
Sea Level ◽  
Pulmonary Arterial Pressure ◽  
Weight Ratio ◽  
Pulmonary Arterial ◽  
Chronic Activation ◽  
Neurokinin 1 ◽  
Hypoxic Group

In this study we explored the hypothesis that chronic activation of neurokinin-1 (NK-1) receptor induces pulmonary hypertension in Wistar rats. First, the activation of NK-1 receptor on the pulmonary circulation was investigated by use of a chronic injection of NK-1 agonist [Ser9,Met(O2)11]-substance P (1 × 10−9mol/kg) for 2 wk at sea level (rats breathed room air) and during hypoxia (rats were placed in a hypobaric 380-Torr chamber). Second, we studied the effect of NK-1 antagonist (CP-96345) on developing and developed (after 4 wk of chronic hypoxia) pulmonary hypertension. Pulmonary arterial pressure, the weight ratio of right ventricle to left ventricle + septum, hematocrit, and substance P (SP) were measured. We found that NK-1 agonist significantly increased pulmonary arterial pressure in the sea-level but not in the hypoxic group. However, NK-1 agonist induced neither right heart hypertrophy nor polycythemia. CP-96345 significantly decreased pulmonary arterial pressure in the hypoxic group but had no effect in the sea-level group. Furthermore, CP-96345 significantly attenuated the acute SP-induced increase in pulmonary arterial pressure in the sea-level and hypoxic groups, with a larger increase in the hypoxic group. These results suggest that chronic activation of NK-1 receptor induces pulmonary hypertension and that there is an increase in the sensitivity of pulmonary vessels in response to SP in chronically hypoxic rats.

Pulmonary hypertension after postlavage lung injury in rabbits: possible role of polymorphonuclear leukocytes

1991 ◽  
Vol 71 (5) ◽  
pp. 1990-1995 ◽  
Author(s):  
R. Burger ◽  
A. C. Bryan
Keyword(s):  
Pulmonary Hypertension ◽  
Gas Exchange ◽  
Lung Injury ◽  
Arterial Pressure ◽  
Airway Pressure ◽  
Pulmonary Arterial Pressure ◽  
Lung Lavage ◽  
High Frequency Ventilation ◽  
Mean Airway Pressure ◽  
Pulmonary Arterial

Previous studies showed that repeated lung lavage leads to a severe lung injury with very poor gas exchange, a substantial protein leak into the alveoli with hyaline membrane formation, pulmonary hypertension, and migration of granulocytes (PMN) into the alveolar spaces. Depletion of PMN leads to a better gas exchange and a markedly decreased protein leak with only scanty hyaline membranes. In this study we show that there is sustained pulmonary hypertension after the lung lavage, but in PMN-depleted rabbits there is no postlavage increase in pulmonary arterial pressure. Changing the shunt fraction by manipulating mean airway pressure still leads to a hypoxic vasoconstriction with increase of pulmonary arterial pressure. Thus, after lung lavage, pulmonary reactivity to hypoxia is still preserved. Comparisons between high-frequency ventilation and conventional mechanical ventilation at the same mean airway pressures showed that equal mean airway pressure in these two very different modes of ventilation do not translate into the same mean functional lung volumes.

Pulmonary vascular tone is a determinant of basal lung perfusion in normal seated subjects

1983 ◽  
Vol 54 (1) ◽  
pp. 262-266 ◽  
Author(s):  
B. Nemery ◽  
W. Wijns ◽  
L. Piret ◽  
F. Cauwe ◽  
L. Brasseur ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Vascular Tone ◽  
Pulmonary Arterial Pressure ◽  
Normal Subjects ◽  
Lung Perfusion ◽  
Regional Perfusion ◽  
Heart Catheterization ◽  
Pulmonary Vasodilator ◽  
Pulmonary Arterial

In the human upright lung the downward increase in lung perfusion reverses in the lower third, thus giving rise to a zone of reduced basal perfusion (zone 4). The flow in zone 4 is regulated by the extra-alveolar vessels, the diameter of which is determined by lung volume, perivascular interstitial pressure, and vasomotor tone. To estimate the role of pulmonary vascular tone in the formation of zone 4, we infused nitroprusside (NTP), a potent pulmonary vasodilator, in six normal seated subjects. We measured their regional perfusion distribution using 133Xe in control conditions and at two dose levels of NTP (20.8 and 52.1 micrograms/min). Regional perfusion distribution was measured similarly and according to the same protocol in six subjects receiving only a placebo solution. In four of the six subjects receiving NTP, right-heart catheterization allowed simultaneous estimations of cardiac output and pulmonary arterial pressure to be made. NTP slightly decreased the perfusion of the nondependent parts of the lungs and markedly increased the perfusion of the lung bases, thus reducing the extent of zone 4. No changes were observed in the placebo experiments. Cardiac output and indices of ventilation and gas exchange did not change significantly. Peripheral and pulmonary arterial pressure fell slightly but significantly during NTP infusion. We attribute the observed changes in basal perfusion to the vasodilatory effects of NTP on the extra-alveolar vessels. Our findings thus support the hypothesis that in normal subjects zone 4 is partly created by the pulmonary vascular tone.

Severe VA/Q mismatch in perfused lungs evoked by sequential challenge with endotoxin and E. coli hemolysin

1994 ◽  
Vol 76 (3) ◽  
pp. 1020-1030 ◽  
Author(s):  
D. Walmrath ◽  
J. Pilch ◽  
M. Scharmann ◽  
F. Grimminger ◽  
W. Seeger
Keyword(s):  
Pulmonary Hypertension ◽  
Gas Exchange ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Low Doses ◽  
Edema Formation ◽  
Shunt Flow ◽  
E Coli ◽  
Vasoconstrictor Response ◽  
Pulmonary Arterial

Escherichia coli hemolysin (ECH), an important pathogenicity factor in extraintestinal E. coli infections, provokes pulmonary hypertension and microvascular leakage in buffer-perfused rabbit lungs. We investigated gas exchange abnormalities in response to low doses of ECH, lipopolysaccharides (LPS), and sequential and combined application of these bacterial agents by using the multiple inert gas elimination technique. In control lungs and after admixture of 100 ng/ml of LPS, unimodal narrow distribution of perfusion and ventilation to midrange ventilation-perfusion (VA/Q) areas was noted. ECH [0.08 hemolytic units (HU)/ml] caused a moderate increase in pulmonary arterial pressure (< 10 mmHg), progressive lung edema formation (approximately 10 g within 20 min), and a broadening of perfusate and gas flow dispersion. Application of 0.08 HU/ml of ECH in lungs “primed” with 100 ng/ml of LPS in a preceding 125-min perfusion period provoked a large increase in pulmonary arterial pressure (> 50 mmHg within 5 min), rapid edema formation (approximately 10 g within 10 min), and severe VA/Q mismatch with predominance of shunt flow. Vasoconstrictor response and VA/Q mismatch, but not edema formation, were largely inhibited by pretreatment of lungs with acetylsalicylic acid or the thromboxane receptor antagonist BM-13.505. In addition, “rescue” application of BM-13.505 rapidly reversed pressure rise and shunt flow due to sequential LPS and/or ECH stimulation, whereas edema formation was not affected. We conclude that the marked pulmonary hypertension in response to low doses of ECH in LPS-primed lungs is paralleled by severe gas exchange abnormalities with predominance of shunt flow. Both the vasoconstrictor response and the development of shunt are closely related to toxin-induced thromboxane generation.

Effect of Iohexol and Diatrizoate on Pulmonary Arterial Pressure following Pulmonary Angiography

1988 ◽  
Vol 29 (4) ◽  
pp. 487-490 ◽  
Author(s):  
H. Tajima ◽  
T. Kumazaki ◽  
N. Tajima ◽  
K. Ebata
Keyword(s):  
Arterial Pressure ◽  
Contrast Medium ◽  
Pulmonary Arterial Pressure ◽  
Random Order ◽  
Normal Pressure ◽  
Pulmonary Angiography ◽  
Double Blind ◽  
Pulmonary Arterial ◽  
Double Blind Crossover Study ◽  
Made In

A clinical comparison of the effects on pulmonary arterial pressure produced by iohexol and diatrizoate, following selective pulmonary angiography, was made in 17 patients with a normal pressure before the injection of the contrast medium. A double blind crossover study was performed and each contrast medium was administered in random order. The pulmonary arterial pressure was continuously recorded before, during and after the injection for 3 minutes. The effect of iohexol on the pulmonary arterial pressure was significantly less than that of diatrizoate. The results indicated that iohexol should be better tolerated than diatrizoate and therefore a safer contrast medium for selective pulmonary angiography.

Minimal hypoxic pulmonary hypertension in normal Tibetans at 3,658 m

1993 ◽  
Vol 74 (1) ◽  
pp. 312-318 ◽  
Author(s):  
B. M. Groves ◽  
T. Droma ◽  
J. R. Sutton ◽  
R. G. McCullough ◽  
R. E. McCullough ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
High Altitude ◽  
Sea Level ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Maximal Exercise ◽  
Pulmonary Arterial Pressure ◽  
Small Sample ◽  
Ergometer Exercise ◽  
Pulmonary Arterial

Elevated pulmonary arterial pressure in high-altitude residents may be a maladaptive response to chronic hypoxia. If so, well-adapted populations would be expected to have pulmonary arterial pressures that are similar to sea-level values. Five normal male 22-yr-old lifelong residents of > or = 3,600 m who were of Tibetan descent were studied in Lhasa (3,658 m) at rest and during near-maximal upright ergometer exercise. We found that resting mean pulmonary arterial pressure [15 +/- 1 (SE) mmHg] and pulmonary vascular resistance (1.8 +/- 0.2 Wood units) were within sea-level norms and were little changed while subjects breathed a hypoxic gas mixture [arterial O2 pressure (PaO2) = 36 +/- 2 Torr]. Near-maximal exercise [87 +/- 13% maximal O2 uptake (VO2max)] increased cardiac output more than threefold to values of 18.3 +/- 1.2 l/min but did not elevate pulmonary vascular resistance. Breathing 100% O2 during near-maximal exercise did not reduce pulmonary arterial pressure or vascular resistance. We concluded that this small sample of healthy Tibetans with lifelong residence > or = 3,658 m had resting pulmonary arterial pressures that were normal by sea-level standards and exhibited minimal hypoxic pulmonary vasoconstriction, both at rest and during exercise. These findings are consistent with remarkable cardiac performance and high-altitude adaptation.

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