Human pulmonary vascular response to 4 h of hypercapnia and hypocapnia measured using Doppler echocardiography

2003 ◽  
Vol 94 (4) ◽  
pp. 1543-1551 ◽  
Author(s):  
George M. Balanos ◽  
Nicholas P. Talbot ◽  
Keith L. Dorrington ◽  
Peter A. Robbins
Keyword(s):  
Pulmonary Hypertension ◽  
Pressure Gradient ◽  
Doppler Echocardiography ◽  
Time Course ◽  
Vascular Tone ◽  
Animal Experiments ◽  
Vascular Response ◽  
Circulatory Response ◽  
Breathing Control ◽  
End Tidal

Hypercapnia has been shown in animal experiments to induce pulmonary hypertension. This study measured the sensitivity and time course of the human pulmonary vascular response to sustained (4 h) hypercapnia and hypocapnia. Twelve volunteers undertook three protocols: 1) 4-h euoxic (end-tidal Po 2 = 100 Torr) hypercapnia (end-tidal Pco 2 was 10 Torr above normal), followed by 2 h of recovery with euoxic eucapnia; 2) 4-h euoxic hypocapnia (end-tidal Pco 2 was 10 Torr below normal) followed by 2 h of recovery; and 3) 6-h air breathing (control). Pulmonary vascular resistance was assessed at 0.5- to 1-h intervals by using Doppler echocardiography via the maximum tricuspid pressure gradient during systole. Results show progressive changes in pressure gradient over 1–2 h after the onset or offset of the stimuli, and sensitivities of 0.6 to 1 Torr change in pressure gradient per Torr change in end-tidal Pco 2. The human pulmonary circulatory response to changes in Pco 2 has a slower time course and greater sensitivity than is commonly assumed. Vascular tone in the normal pulmonary circulation is substantial.

Two temporal components within the human pulmonary vascular response to ∼2 h of isocapnic hypoxia

2005 ◽  
Vol 98 (3) ◽  
pp. 1125-1139 ◽  
Author(s):  
Nick P. Talbot ◽  
George M. Balanos ◽  
Keith L. Dorrington ◽  
Peter A. Robbins
Keyword(s):  
Cardiac Output ◽  
Time Course ◽  
Vascular Tone ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Initial Response ◽  
Plateau Phase ◽  
Vascular Response ◽  
Pulmonary Vasoconstriction ◽  
End Tidal ◽  
Underlying Processes

The time course of the pulmonary vascular response to hypoxia in humans has not been fully defined. In this investigation, study A was designed to assess the form of the increase in pulmonary vascular tone at the onset of hypoxia and to determine whether a steady plateau ensues over the following ∼20 min. Twelve volunteers were exposed twice to 5 min of isocapnic euoxia (end-tidal Po2 = 100 Torr), 25 min of isocapnic hypoxia (end-tidal Po2 = 50 Torr), and finally 5 min of isocapnic euoxia. Study B was designed to look for the onset of a slower pulmonary vascular response, and, if possible, to determine a latency for this process. Seven volunteers were exposed to 5 min of isocapnic euoxia, 105 min of isocapnic hypoxia, and finally 10 min of isocapnic euoxia. For both studies, control protocols consisting of isocapnic euoxia were undertaken. Doppler echocardiography was used to measure cardiac output and the maximum tricuspid pressure gradient during systole, and estimates of pulmonary vascular resistance were calculated. For study A, the initial response was well described by a monoexponential process with a time constant of 2.4 ± 0.7 min (mean ± SE). After this, there was a plateau phase lasting at least 20 min. In study B, a second slower phase was identified, with vascular tone beginning to rise again after a latency of 43 ± 5 min. These findings demonstrate the presence of two distinct phases of hypoxic pulmonary vasoconstriction, which may result from two distinct underlying processes.

Desferrioxamine elevates pulmonary vascular resistance in humans: potential for involvement of HIF-1

2002 ◽  
Vol 92 (6) ◽  
pp. 2501-2507 ◽  
Author(s):  
George M. Balanos ◽  
Keith L. Dorrington ◽  
Peter A. Robbins
Keyword(s):  
Pressure Gradient ◽  
Continuous Infusion ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Gene Activation ◽  
Maximum Pressure ◽  
Vascular Response ◽  
Vascular Regulation ◽  
End Tidal

Hypoxia-inducible factor (HIF)-1 is stabilized by hypoxia and iron chelation. We hypothesized that HIF-1 might be involved in pulmonary vascular regulation and that infusion of desferrioxamine over 8 h would consequently mimic hypoxia and elevate pulmonary vascular resistance. In study A, we characterized the pulmonary vascular response to 4 h of isocapnic hypoxia; in study B, we measured the pulmonary vascular response to 8 h of desferrioxamine infusion. For study A, 11 volunteers undertook two protocols: 1) 4 h of isocapnic hypoxia (end-tidal Po2= 50 Torr), followed by 2 h of recovery with isocapnic euoxia (end-tidal Po2= 100 Torr), and 2) 6 h of air breathing (control). For study B, nine volunteers undertook two protocols while breathing air: 1) continuous infusion of desferrioxamine (4 g/70 kg) over 8 h and 2) continuous infusion of saline over 8 h (control). In both studies, pulmonary vascular resistance was assessed at 0.5- to 1-h intervals by Doppler echocardiography via the maximum pressure gradient during systole across the tricuspid valve. Results show a progressive rise in pressure gradient over the first 3–4 h with both isocapnic hypoxia ( P < 0.001) and desferrioxamine infusion ( P < 0.005) to increases of ∼16 and 4 Torr, respectively. These results support a role for HIF-regulated gene activation in human hypoxic pulmonary vasoconstriction.

Time course of the human pulmonary vascular response to 8 hours of isocapnic hypoxia

1997 ◽  
Vol 273 (3) ◽  
pp. H1126-H1134 ◽  
Author(s):  
K. L. Dorrington ◽  
C. Clar ◽  
J. D. Young ◽  
M. Jonas ◽  
J. G. Tansley ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Time Course ◽  
Healthy Adult ◽  
Slow Component ◽  
Adult Males ◽  
Vascular Response ◽  
Slow Time ◽  
Carbon Dioxide Concentrations ◽  
End Tidal ◽  
Forearm Vein

To examine the hypothesis that the human pulmonary vascular response to hypoxia has a component with a slow time course, we measured pulmonary vascular resistance (PVR) in six healthy adult males during 8 h of isocapnic hypoxia. A balloon-tipped pulmonary artery catheter with thermistor was introduced via a forearm vein and used to derive PVR. The subjects were seated in a chamber in which the oxygen and carbon dioxide concentrations were adjusted to maintain an end-tidal Po2 of 50 Torr and an end-tidal Pco2 equal to the subject's normal prehypoxic value. PVR was measured before and at 0.5-h intervals during 8 h of hypoxia, the following 3 h of isocapnic euoxia (end-tidal Po2 100 Torr), and a subsequent 1-h reexposure to hypoxia. PVR rose from 1.23 +/- 0.26 (SE) Torr-min.1(-1) under euoxia [time (t) = 0] to 1.77 +/- 0.21 Torr.min.1(-1) at t = 0.5 h, reached a maximum at 2 h (2.91 +/- 0.33 Torr.min.1(-1)), and remained fairly constant between 2 and 8 h. Restoration of euoxia at 8 h led to a reduction in PVR with a slow component. Reexposure to hypoxia at 11 h resulted in a greater increase in PVR than at 1 h. Systemic vascular resistance had a similar slow component to its response, falling from 18.6 +/- 1.3 Torr.min.1(-1) at t = 0 to 17.3 +/- 1.4 Torr.min.1(-1) at t = 0.5 h, 14.4 +/- 0.6 Torr.min.1(-1) at t = 4 h, and 13.8 +/- 0.8 Torr.min.1(-1) at t = 8 h. The human pulmonary and systemic vascular responses to hypoxia extend over at least several hours.

scholarly journals Sex difference in pulmonary hypertension in the evaluation by exercise echocardiography

2021 ◽  
Vol 11 (1) ◽  
pp. 204589402098845
Author(s):  
Toru Takase ◽  
Mitsugu Taniguchi ◽  
Yutaka Hirano ◽  
Gaku Nakazawa ◽  
Shunichi Miyazaki ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pressure Gradient ◽  
Tricuspid Regurgitation ◽  
Cox Proportional Hazards ◽  
Heart Catheterization ◽  
Exercise Echocardiography ◽  
Poor Survival ◽  
Men And Women ◽  
Low Load ◽  
Male Patients

Male patients with pulmonary hypertension have poor survival than their female counterparts. Poor right ventricular function in men may be one of the major determinants of poor prognosis. This study aimed to investigate the difference in hemodynamics during exercise between men and women by exercise echocardiography. Consecutive patients with pulmonary hypertension who underwent right heart catheterization were enrolled, and survival was analyzed. In patients who underwent exercise echocardiography, the change in tricuspid regurgitation pressure gradient during exercise was calculated at multiple stages (low-, moderate-, and high-load exercise), and the mortality was also recorded. In a total of 93 patients, although there were no differences in pulmonary artery pressure and vascular resistance between sexes, male patients showed poor survival. In patients with exercise echocardiography, change in tricuspid regurgitation pressure gradient at low-load (25 W) exercise was significantly lower in men, although that at maximum-load exercise was not different between men and women. In the Kaplan–Meier analysis, in a median follow-up duration of 1760 days, male patients and those with lower change in tricuspid regurgitation pressure gradient at low-load exercise showed poorer survival ( P = 0.002 and 0.026, respectively). In the Cox proportional hazards analysis, the change in tricuspid regurgitation pressure gradient at low-load exercise was independently associated with poor survival after adjustment for age and sex. In conclusion, a lower change in tricuspid regurgitation pressure gradient at low-load exercise was observed in male patients and was a prognostic marker, which may be associated, at least in part, with poorer prognosis in male patients with pulmonary hypertension.

scholarly journals Echocardiographic and invasive measurements of pulmonary artery pressure correlate closely at high altitude

2000 ◽  
Vol 279 (4) ◽  
pp. H2013-H2016 ◽  
Author(s):  
Yves Allemann ◽  
Claudio Sartori ◽  
Mattia Lepori ◽  
Sébastien Pierre ◽  
Christian Mélot ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
High Altitude ◽  
Doppler Echocardiography ◽  
Systolic Pulmonary Arterial Pressure ◽  
Wide Range ◽  
High Altitude Pulmonary Edema ◽  
Reproducible Method ◽  
Pulmonary Arterial ◽  
Spearman Test ◽  
Invasive Measurement

Exaggerated hypoxia-induced pulmonary hypertension is a hallmark of high-altitude pulmonary edema (HAPE) and plays a major role in its pathogenesis. Many studies of HAPE have estimated systolic pulmonary arterial pressure (SPAP) with Doppler echocardiography. Whereas at low altitude, Doppler echocardiographic estimation of SPAP correlates closely with its invasive measurement, no such evidence exists for estimations obtained at high altitude, where alterations of blood viscosity may invalidate the simplified Bernoulli equation. We measured SPAP by Doppler echocardiography and invasively in 14 mountaineers prone to HAPE and in 14 mountaineers resistant to this condition at 4,559 m. Mountaineers prone to HAPE had more pronounced pulmonary hypertension (57 ± 12 and 58 ± 10 mmHg for noninvasive and invasive determination, respectively; means ± SD) than subjects resistant to HAPE (37 ± 8 and 37 ± 6 mmHg, respectively), and the values measured in the two groups as a whole covered a wide range of pulmonary arterial pressures (30–83 mmHg). Spearman test showed a highly significant correlation ( r = 0.89, P < 0.0001) between estimated and invasively measured SPAP values. The mean difference between invasively measured and Doppler-estimated SPAP was 0.5 ± 8 mmHg. At high altitude, estimation of SPAP by Doppler echocardiography is an accurate and reproducible method that correlates closely with its invasive measurement.

Plasma Catecholamine Levels and Vascular Response in Deoxycorticosterone Acetate Hypertension of Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 315s-317s ◽  
Author(s):  
W. Rascher ◽  
R. Dietz ◽  
A. Schomig ◽  
J. Weber ◽  
F. Gross
Keyword(s):  
Hind Limb ◽  
Vascular Tone ◽  
Plasma Concentrations ◽  
Plasma Catecholamine ◽  
Vascular Response ◽  
Deoxycorticosterone Acetate ◽  
Pronounced Increase ◽  
Basal Plasma ◽  
Noradrenaline And Adrenaline ◽  
Catecholamine Levels

1. In rats with deoxycorticosterone acetate (DOCA) hypertension basal plasma concentrations of noradrenaline and adrenaline correspond to those of sham-treated controls. 2. In DOCA-treated rats frusemide caused a more pronounced increase in plasma noradrenaline than in control rats. This difference was not observed for adrenaline. 3. In the isolated perfused hind-limb preparation the sensitivity to noradrenaline was already enhanced before blood pressure was elevated. 4. These results suggest that the adrenergic vascular tone is increased in DOCA hypertension in rats.

Intrapleural liquid flow down a gravity-dependent hydraulic pressure gradient

1988 ◽  
Vol 64 (2) ◽  
pp. 577-584 ◽  
Author(s):  
G. Miserocchi ◽  
D. Negrini ◽  
M. Pistolesi ◽  
C. R. Bellina ◽  
M. C. Gilardi ◽  
...  
Keyword(s):  
Pressure Gradient ◽  
Time Course ◽  
Sudden Change ◽  
Vertical Movement ◽  
Rate Of Change ◽  
Large Field ◽  
Liquid Volume ◽  
Hydraulic Pressure ◽  
Albumin Clearance ◽  
Turning Maneuver

We studied the vertical movement of 2 mg technetium-labeled albumin injected intrapleurally in 0.5 ml saline (15% of pleural liquid volume) in eight spontaneously breathing anesthetized dogs subject to a sudden change in posture (prone to supine or vice versa). The albumin movements were evaluated through a large field gamma camera placed laterally to the animal and detecting total (AT) and regional activities from two superimposed equal areas (At and Ab, top and bottom, respectively). The At/Ab ratio decreased from 2.1 to 1.3 in four animals up to 20 min from the change in posture and from 0.9 to 0.5 in four more animals studied from 50 to 90 min from turning maneuver. The rate of change in At and Ab was similar in the two groups of animals and unaffected by the acquisition posture. AT decreased by 7.7 and 3.5% for the two groups, respectively, reflecting albumin clearance from the pleural space. The opposite time course of regional activities and the independence of their rate of change of the At/Ab ratio and of the animal posture suggest a top-to-bottom albumin transfer occurring through a bulk flow of liquid estimated at 0.006 ml.kg-1.h-1. The data are consistent with a measured vertical pleural liquid pressure gradient that does not reflect a hydrostatic condition.

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