Effect of oxygen upon pulmonary circulation in acclimatized man at high altitude

The response to breathing 100% oxygen was studied in 26 acclimatized residents of the Peruvian Andes at altitudes of 12,300 and 14,200 ft. Arterial oxygen saturation increased from 86% to 96%. Mean pulmonary artery pressure decreased by 5 mm Hg and cardiac output did not change. Calculated pulmonary arteriolar resistance was lowered. Pulmonary artery pressure during oxygen breathing was not decreased to normal values observed at sea level. The data suggest the presence of two factors responsible for the increase in pulmonary arteriolar resistance at high altitude: 1) hypoxic vasoconstriction which is reversed by oxygen breathing and 2) anatomic alterations which are not affected by oxygen breathing. Oxygen breathing at high altitude also produced a slowing of the heart rate and increased the relative height of the secondary or tidal wave of the brachial arterial pressure pulse. pulmonary arteriolar resistance and 100% oxygen; arterial pulse contour–effect of 100% oxygen at high altitude; pulmonary arteriolar resistance–nature of in high altitude; hypoxic vasoconstriction at high altitude–reversal by 100% oxygen breathing; oxygen breathing–comparison of effect on pulmonary circulation at high altitude and sea level Submitted on May 8, 1964

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Pulmonary circulation in acclimatized man at high altitude

Journal of Applied Physiology ◽

10.1152/jappl.1965.20.2.233 ◽

1965 ◽

Vol 20 (2) ◽

pp. 233-238 ◽

Cited By ~ 37

Author(s):

H. N. Hultgren ◽

J. Kelly ◽

H. Miller

Keyword(s):

Pulmonary Artery ◽

High Altitude ◽

Sea Level ◽

Pulmonary Artery Pressure ◽

Peruvian Andes ◽

Artery Pressure ◽

Content Difference ◽

Mean Pulmonary Artery Pressure ◽

Arteriolar Resistance ◽

Wedge Pressure

Cardiac catheterization studies have been carried out in 30 acclimatized adults at an altitude of 12,3000 ft in the Peruvian Andes. Mean pulmonary artery pressure was 22 mm. Hg (range 14-31 mm Hg) compared to 15 mm Hg (range 11-17 mm Hg) observed in sea-level subjects. The pulmonary artery wedge pressure was normal and calculated pulmonary arteriolar resistance was increased by 180% over sea-level values. The arteriovenous oxygen content difference and oxygen consumption were slightly greater at high altitude, but the cardiac output was normal. There was no relationship between hematocrit and pulmonary artery pressure or resistance, suggesting that in the high-altitude resident, blood viscosity in a hematocrit range of 40-78% does not significantly affect resistance to blood flow. Nine subjects studied at 14,200 ft had the same mean pulmonary artery pressure (22 mm Hg, range 17-32 mm Hg) as the larger group at 12,300 ft. pulmonary artery pressure Submitted on May 8, 1964

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Effect of altitude relocations upon AaDo2 at rest and during exercise

Journal of Applied Physiology ◽

10.1152/jappl.1975.39.3.469 ◽

1975 ◽

Vol 39 (3) ◽

pp. 469-474 ◽

Cited By ~ 6

Author(s):

J. C. Cruz ◽

L. H. Hartley ◽

J. A. Vogel

Keyword(s):

Gas Exchange ◽

Pulmonary Artery ◽

High Altitude ◽

Sea Level ◽

Pulmonary Artery Pressure ◽

Venous Admixture ◽

Artery Pressure ◽

Altitude Exposure ◽

Cerro De Pasco

The supine pulmonary venous admixture (shunt) has been measured at Cerro de Pasco, 4,350 m altitude in eight subjects native to high altitude (HAN) under resting condition. Alveolar-arterial O2 tension difference (AaDO2) was also determined at rest and during exercise. The same subjects were studied again after 10 days' sojourn at sea level in Lima at 150 m altitude. They were compared with four subjects from sea level (SLN) who were studied first at Lima and after 2 and 10 days at Cerro de Pasco. At altitude, AaDO2 was smaller in HAN than SLN both at rest and during exercise. Shunt was the same in both groups. It is concluded that HAN show more even ventilation/perfusion relationship (VA/Q) at altitude, probably due to their high pulmonary artery pressure. On the contrary, SLN show less even VA/Q on altitude exposure, since their shunt decreased 37%. At sea level, HAN increased their AaDO2 due partially to an increase of 110% in their shunt, and in part due to less even VA/Q as shown by augmented VD/VT ratios. Each group tended to have a more effective gas exchange in its own environment.

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Higher pulmonary artery pressure in children than in adults upon fast ascent to high altitude

European Respiratory Journal ◽

10.1183/09031936.00166407 ◽

2008 ◽

Vol 32 (3) ◽

pp. 664-669 ◽

Cited By ~ 16

Author(s):

S. Kriemler ◽

C. Jansen ◽

A. Linka ◽

A. Kessel-Schaefer ◽

M. Zehnder ◽

...

Keyword(s):

Pulmonary Artery ◽

High Altitude ◽

Pulmonary Artery Pressure ◽

Artery Pressure

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Correlation of Pulse Wave Transit Time with Pulmonary Artery Pressure in a Porcine Model of Pulmonary Hypertension

Biomedicines ◽

10.3390/biomedicines9091212 ◽

2021 ◽

Vol 9 (9) ◽

pp. 1212

Author(s):

Fabian Mueller-Graf ◽

Jonas Merz ◽

Tim Bandorf ◽

Chiara Albus ◽

Maike Henkel ◽

...

Keyword(s):

Pulmonary Hypertension ◽

Pulmonary Artery ◽

Pulmonary Artery Pressure ◽

Transit Time ◽

Pulse Wave ◽

Correlation Coefficients ◽

Physiological Basis ◽

Artery Pressure ◽

Hypoxic Vasoconstriction ◽

Pulse Wave Transit Time

For the non-invasive assessment of pulmonary artery pressure (PAP), surrogates like pulse wave transit time (PWTT) have been proposed. The aim of this study was to invasively validate for which kind of PAP (systolic, mean, or diastolic) PWTT is the best surrogate parameter. To assess both PWTT and PAP in six healthy pigs, two pulmonary artery Mikro-Tip™ catheters were inserted into the pulmonary vasculature at a fixed distance: one in the pulmonary artery trunk, and a second one in a distal segment of the pulmonary artery. PAP was raised using the thromboxane A2 analogue U46619 (TXA) and by hypoxic vasoconstriction. There was a negative linear correlation between PWTT and systolic PAP (r = 0.742), mean PAP (r = 0.712) and diastolic PAP (r = 0.609) under TXA. During hypoxic vasoconstriction, the correlation coefficients for systolic, mean, and diastolic PAP were consistently higher than for TXA-induced pulmonary hypertension (r = 0.809, 0.778 and 0.734, respectively). Estimation of sPAP, mPAP, and dPAP using PWTT is feasible, nevertheless slightly better correlation coefficients were detected for sPAP compared to dPAP. In this study we establish the physiological basis for future methods to obtain PAP by non-invasively measured PWTT.

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Targeted blocking of gene expression for CGRP receptors elevates pulmonary artery pressure in hypoxic rats

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00356.2002 ◽

2003 ◽

Vol 285 (1) ◽

pp. L86-L96 ◽

Cited By ~ 20

Author(s):

Xin Qing ◽

Ingegerd M. Keith

Keyword(s):

Pulmonary Artery ◽

Pulmonary Artery Pressure ◽

Pulmonary Circulation ◽

Protective Role ◽

Cgrp Receptor ◽

Sprague Dawley ◽

Artery Pressure ◽

Receptor Component ◽

Technical Control

We previously described the protection by calcitonin gene-related peptide (CGRP) against hypoxic pulmonary hypertension. Here, we examine the roles of its putative receptor RDC-1 and receptor activity-modifying protein (RAMP) 1 in mediating this protection by selectively inhibiting their synthesis. RAMP1 is an accessory protein for another putative CGRP receptor, calcitonin receptor-like receptor. Antisense oligodeoxyribonucleotides (ASODNs, 5 mg·kg-1·day-1 or 5 and 10 mg·kg-1·day-1 for RDC-1) targeting RAMP1 and RDC-1 mRNAs were chronically infused to the pulmonary circulation of male Sprague-Dawley rats during 7 days of normoxia or hypobaric hypoxia (380 mmHg), and α-CGRP ASODN was used as a technical control. CGRP, RAMP1, and RDC-1 ASODNs significantly elevated pulmonary artery pressure (PPA) in chronic hypoxic rats compared with hypoxic mismatched ASODN (MMODN) and saline vehicle controls. CGRP and RAMP1 ASODNs raised PPA in normoxic rats briefly exposed to 10% O2 above MMODN and saline controls. Moreover, normoxic rats treated with CGRP ASODN had higher basal pulmonary vascular tone compared with controls. These data confirm the protective role of CGRP in the pulmonary circulation and suggest that endogenous RAMP1 and RDC-1 are essential in regulation of PPA in hypoxia. This is the first in vivo evidence supporting RDC-1 and RAMP1 as functional CGRP receptor and receptor component.

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Pulmonary artery pressure and arterial oxygen saturation in people living at high or low altitude: systematic review and meta-analysis

Journal of Applied Physiology ◽

10.1152/japplphysiol.00394.2016 ◽

2016 ◽

Vol 121 (5) ◽

pp. 1151-1159 ◽

Cited By ~ 25

Author(s):

Rodrigo Soria ◽

Matthias Egger ◽

Urs Scherrer ◽

Nicole Bender ◽

Stefano F. Rimoldi

Keyword(s):

Systematic Review ◽

Pulmonary Artery ◽

Oxygen Saturation ◽

High Altitude ◽

Pulmonary Artery Pressure ◽

Meta Analysis ◽

Arterial Oxygen Saturation ◽

Arterial Oxygen ◽

Low Altitude ◽

Apparently Healthy

More than 140 million people are living at high altitude worldwide. An increase of pulmonary artery pressure (PAP) is a hallmark of high-altitude exposure and, if pronounced, may be associated with important morbidity and mortality. Surprisingly, there is little information on the usual PAP in high-altitude populations. We, therefore, conducted a systematic review (MEDLINE and EMBASE) and meta-analysis of studies published (in English or Spanish) between 2000 and 2015 on echocardiographic estimations of PAP and measurements of arterial oxygen saturation in apparently healthy participants from general populations of high-altitude dwellers (>2,500 m). For comparison, we similarly analyzed data published on these variables during the same period for populations living at low altitude. Twelve high-altitude studies comprising 834 participants and 18 low-altitude studies (710 participants) fulfilled the inclusion criteria. All but one high-altitude studies were performed between 3,600 and 4,350 m. The combined mean systolic PAP (right ventricular-to-right atrial pressure gradient) at high altitude [25.3 mmHg, 95% confidence interval (CI) 24.0, 26.7], as expected was significantly (P < 0.001) higher than at low altitude (18.4 mmHg, 95% CI 17.1,19.7), and arterial oxygen saturation was significantly lower (90.4%, 95% CI 89.3, 91.5) than at low altitude (98.1%; 95% CI 97.7, 98.4). These findings indicate that at an altitude where the very large majority of high-altitude populations are living, pulmonary hypertension appears to be rare. The reference values and distributions for PAP and arterial oxygen saturation in apparently healthy high-altitude dwellers provided by this meta-analysis will be useful to future studies on the adjustments to high altitude in humans.

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Inhibition of 20-HETE abolishes the myogenic response during NOS antagonism in the ovine fetal pulmonary circulation

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00315.2004 ◽

2005 ◽

Vol 289 (2) ◽

pp. L261-L267 ◽

Cited By ~ 10

Author(s):

Thomas A. Parker ◽

Theresa R. Grover ◽

John P. Kinsella ◽

John R. Falck ◽

Steven H. Abman

Keyword(s):

Pulmonary Artery ◽

Pulmonary Artery Pressure ◽

Pulmonary Circulation ◽

Ductus Arteriosus ◽

Combined Treatment ◽

Specific Inhibitor ◽

Fetal Lung ◽

Myogenic Response ◽

Fetal Sheep ◽

Artery Pressure

Mechanisms that maintain high pulmonary vascular resistance (PVR) and oppose vasodilation in the fetal lung are poorly understood. In fetal lambs, increased pulmonary artery pressure evokes a potent vasoconstriction, suggesting that a myogenic response contributes to high PVR in the fetus. In adult systemic circulations, the arachidonic acid metabolite 20-hydroxyeicosatetraenoic acid (20-HETE) has been shown to modulate the myogenic response, but its role in the fetal lung is unknown. We hypothesized that acute increases in pulmonary artery pressure release 20-HETE, which causes vasoconstriction, or a myogenic response, in the fetal lung. To address this hypothesis, we studied the hemodynamic effects of N-methylsufonyl-12,12-dibromododec-11-enamide (DDMS), a specific inhibitor of 20-HETE production, on the pulmonary vasoconstriction caused by acute compression of the ductus arteriosus (DA) in chronically prepared fetal sheep. An inflatable vascular occluder around the DA was used to increase pulmonary artery pressure under three study conditions: control, after pretreatment with nitro-l-arginine (l-NA; to inhibit shear-stress vasodilation), and after combined treatment with both l-NA and a specific 20-HETE inhibitor, DDMS. We found that DA compression after l-NA treatment increased PVR by 44 ± 12%. Although intrapulmonary DDMS infusion did not affect basal PVR, DDMS completely abolished the vasoconstrictor response to DA compression in the presence of l-NA (44 ± 12% vs. 2 ± 4% change in PVR, l-NA vs. l-NA + DDMS, P < 0.05). We conclude that 20-HETE mediates the myogenic response in the fetal pulmonary circulation and speculate that pharmacological inhibition of 20-HETE might have a therapeutic role in neonatal conditions characterized by pulmonary hypertension.

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