Hypoxic pulmonary vasoconstriction and pulmonary gas exchange in normal man

Mélot, Christian; Naeije, Robert; Hallemans, Roger; Lejeune, Philippe; Mols, Pierre

doi:10.1016/0034-5687(87)90073-9

Cited by 58 publications

(39 citation statements)

References 20 publications

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“…Thus, for example, Mélot et al (16), who studied humans by using the multiple inert gas elimination technique, deduced that "in normoxic conditions, active hypoxic regulation of gas exchange results in hardly or nondetectable improvements in arterial blood gases." The weakness of the hypoxic pulmonary vasoconstriction in normoxia was attributed by these authors to the fact that its potential contribution to improving matching of perfusion to ventilation was greatest for values of PA O 2 of ϳ60 Torr, i.e., below the usual range experienced in healthy lungs ventilated with air at sea level.…”

Section: Discussionmentioning

confidence: 99%

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

Balanos

Talbot

Dorrington

et al. 2003

Journal of Applied Physiology

152

101

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Section: Discussionmentioning

confidence: 99%

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

Balanos

Talbot

Dorrington

et al. 2003

Journal of Applied Physiology

152

101

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“…The differences in the lifestyle, extreme obesity [7] or genetic predisposition to excessive hypoxic pulmonary vasoconstriction [21] may also contribute to development of PH in some patients with OSAS.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary haemodynamics in patients with OSAS or an overlap syndrome

Hawryłkiewicz¹,

Sliwiński²,

Górecka³

et al. 2004

Monaldi Arch Chest Dis

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Background. Alveolar hypoxia is the most important mechanism leading to pulmonary arterial vasoconstriction, remodelling and pulmonary hypertension. Patients with Obstructive Sleep Apnoea Syndrome (OSAS) experience multiple short periods of alveolar hypoxia during apnoeic episodes. However, the question as to whether these hypoxic episodes are responsible for the development of permanent pulmonary hypertension is still debatable. We aimed to investigate the relationship between the episodes of nocturnal desaturation and pulmonary haemodynamics in two distinct group patients: with pure OSAS or an overlap syndrome. Methods: We studied 67 patients with severe OSAS (means: age 45±8 years, AHI 62±22, FEV1 3.6±0.8 L = 97±16% of predicted PaO2 72±10 mmHg, PaCO2 40±4 mmHg) and 17 patients with an overlap syndrome (OS), means: age 51±5 years, AHI 64±19, FEV1 1.5±0.7 = 43±16% of predicted PaO2 57±9 mmHg). All subjects underwent pulmonary artery catheterisation with pressure and flow recordings and an overnight full sleep study. Results. On average patients with OSAS had nocturnal desaturation (mean overnight SaO2 = 87±5%) and normal PPA (15.8±4.6 mmHg). Only 11 out of 67 subjects (16%) presented with pulmonary hypertension. Patients with OS had nocturnal desaturation (mean overnight SaO2 = 80.2±8.5%) and mild pulmonary hypertension (PPA 24.2±7.4 mmHg). Only three out of 17 patients had normal pulmonary arterial pressure. Conclusions. In patients with severe OSAS, pulmonary hypertension is rare (16%) and is related best to the severity of the disease and to obesity. In OS patients diurnal pulmonary hypertension is frequent but does not correlate with the severity of nocturnal desaturation.

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“…HPV is a relatively weak mechanism for the homeostatic control of alveolar oxygenation [16]. Several other studies of HPV9s overall efficiency have produced variable results [16][17][18]. ARDS has even been reported to inhibit or abolish HPV.…”

Section: Discussionmentioning

confidence: 99%

“…Increases in shunt have also been reported in patients with ARDS after the administration of other intravenous vasodilators, including nitroprusside [65], isoproterenol, and diltiazem [17].…”

Section: Other Intravenous Vasodilatorsmentioning

confidence: 96%

Pathophysiology and pharmacological treatment of pulmonary hypertension in acute respiratory distress syndrome

Moloney

Evans²

2003

Eur Respir J

112

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Pulmonary hypertension (PH) is a characteristic feature of the acute respiratory distress syndrome (ARDS). The magnitude of PH has been shown to correlate with the severity of lung injury in patients with ARDS independently of the severity of associated hypoxaemia and has an adverse prognostic significance.Early in the histopathological evolution of ARDS, pulmonary vasoconstriction, thromboembolism and interstitial oedema contribute to the development of PH, although pulmonary vascular remodelling probably occurs eventually. Intravenous vasodilator agents lead to an increase in intrapulmonary shunting and systemic hypotension, which can limit their therapeutic use, and have not been shown to improve survival. By contrast, rapidly metabolised vasodilators administered by inhalation induce selective pulmonary vasodilatation and decrease shunting, but again do not appear to confer a survival benefit.Research aimed at further understanding the mechanisms that underlie pulmonary hypertension, a characteristic feature of the acute respiratory distress syndrome, are expected to provide improvements in pharmacological interventions for the treatment of pulmonary hypertension in the acute respiratory distress syndrome.

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Hypoxic pulmonary vasoconstriction and pulmonary gas exchange in normal man

Cited by 58 publications

References 20 publications

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

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

Pulmonary haemodynamics in patients with OSAS or an overlap syndrome

Pathophysiology and pharmacological treatment of pulmonary hypertension in acute respiratory distress syndrome

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