Importance of hypoxic vasoconstriction in maintaining oxygenation during acute lung injury

Brimioulle, Serge; Julien, Valérie; Gust, R.; Kozlowski, James; Naeije, Robert; Schuster, Daniel P.

doi:10.1097/00003246-200204000-00027

Cited by 54 publications

(42 citation statements)

References 27 publications

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“…Whilst the exact mechanisms of HPV are still being evaluated [20], it is clear that NO attenuates the response of pulmonary arteries to hypoxaemia both in vitro and in vivo [21]. In addition, it was observed recently that the increase in Ppa, in lung injury, is inhibited by low-dose endotoxin and metabolic alkalosis, factors known to inhibit HPV [22]. This inhibition was incomplete, however, which may reflect the effects on the pulmonary circulation, not only of functional (e.g.…”

Section: Discussionmentioning

confidence: 99%

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

Moloney

Evans²

2003

Eur Respir J

115

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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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Section: Discussionmentioning

confidence: 99%

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

Moloney

Evans²

2003

Eur Respir J

115

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“…regions worsened oxygenation (12)(13)(14), whereas perfusion redistribution away from edematous regions ameliorated hypoxemia (13,15). When the loss of aeration is spatially heterogeneous, dissecting the relation between tissue density and global shunt requires determination of both regional shunt fraction and perfusion.…”

Section: What This Study Adds To the Fieldmentioning

confidence: 99%

“…Accordingly, a high shunt fraction or low Pa O 2 /FI O 2 may not be sensitive indicators of loss of aeration and hence may not be suited, for example, to assess lung derecruitment or stratify patients for their risk of ventilator-associated lung injury. Mechanisms such as hypoxic pulmonary vasoconstriction (12)(13)(14)(15) or vascular compression and obstruction (46) may alter the distribution of perfusion and thus be responsible for the global to regional disconnect in ALI.…”

Section: Relation Between Shunt Fraction Aeration and Perfusionmentioning

confidence: 99%

“…Indeed, what is defined as poorly aerated lung over the resolution element, be it a voxel or an ROI, could comprise nonaerated shunting units and units with normal ventilation-to-perfusion ratio. The contribution to global shunt fraction, however, will be a function of the partitioning of perfusion between these two types of units and of total perfusion, both of which may vary depending on several factors (12)(13)(14)(15)46). The systematic relation between regional shunt and gas fractions (Figure 4) is also compatible with the strong correlation reported between fraction of lung with CT attenuation greater than 2300 HU and global shunt fraction (42,43).…”

Section: Relation Between Shunt Fraction Aeration and Perfusionmentioning

confidence: 99%

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Relation between Shunt, Aeration, and Perfusion in Experimental Acute Lung Injury

Musch¹,

Bellani²,

Melo³

et al. 2008

Am J Respir Crit Care Med

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Rationale: In a pulmonary process characterized by spatially heterogeneous loss of aeration, the impairment of gas exchange is expected to depend on the regional distribution of perfusion relative to that of aeration. Objectives: To investigate how regional aeration, shunt, and perfusion are interrelated at different levels of end-expiratory pressure and how their interplay relates to global shunt fraction in acute lung injury. Methods: Regional shunt and perfusion were assessed by imaging with positron emission tomography the pulmonary kinetics of [ 13 N]nitrogen infused in saline solution in five sheep after lung lavage. The lung field was divided in six horizontal regions. Measurements and Main Results: Each animal showed an inverse relation between regional shunt (FS) and gas (FG) fractions: FS 5 2m Á FG 1 FS 0 . This relation was similar among animals (m 5 1.25 6 0.14, FS 0 5 0.75 6 0.15) and invariant with end-expiratory pressure, despite lack of correlation between global shunt and gas fractions and large interanimal variability in global shunt fraction. When this relation was used to estimate global shunt fraction as a perfusion-weighted average of the estimates of regional shunt fraction derived from regional gas fraction, 72% of the interanimal variability in global shunt fraction could be explained. Conclusions: Despite large interanimal variability in global shunt fraction, there was a consistent inverse relation between regional shunt and gas fractions, independent of end-expiratory pressure. Most of the interanimal variability in global shunt fraction could be explained by the combined effect of this relation and the distribution of perfusion on regional shunt, rather than by differences in global aeration.

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“…In a series of previous studies (8,9,11,30,36,37), we have used low-dose Etx in dogs to modify the physiologic and biochemical expression of OA-induced ALI. Low-dose Etx during OAinduced ALI produces severe systemic hypotension, the ablation of hypoxic vasoconstriction, and a failure for pulmonary perfusion to be distributed away from edematous lung regions, which causes profound hypoxemia.…”

Section: The Combination Of Etx With Oamentioning

confidence: 99%

Physiologic, Biochemical, and Imaging Characterization of Acute Lung Injury in Mice

Zhou

Kozlowski

Schuster

2005

Am J Respir Crit Care Med

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Rationale: Most models of acute lung injury in mice have yet to be fully characterized. Objectives: To directly compare and contrast endotoxin and oleic acid models of acute lung injury in mice in terms of their physiologic, biochemical, histopathologic, and imaging manifestations. Methods: Survival studies, lung weights, x-ray computed tomographic scanning, light and electron microscopy, bronchoalveolar lavage, lung uptake of ( In contrast, oleic acid caused severe alveolar damage with the development of alveolar edema of the increased-permeability type with associated abnormalities in gas exchange. When given together, endotoxin and oleic acid acted synergistically to increase pulmonary edema and to worsen gas exchange and hemodynamics, thereby increasing mortality. This synergism was significantly attenuated by the prior administration of the endotoxin antagonist E5564 (eritoran). Conclusions: Under the conditions of these studies, only mice exposed to oleic acid showed both structural and functional characteristics of acute lung injury. Nevertheless, endotoxin had potent synergistic physiologic effects that increased mortality. Overall, these models, which can be translated to genetically altered mice, are amenable to study with state-of-the-art imaging techniques, and with experimental interventions that can probe the underlying mechanisms of injury.

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Importance of hypoxic vasoconstriction in maintaining oxygenation during acute lung injury

Cited by 54 publications

References 27 publications

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

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

Relation between Shunt, Aeration, and Perfusion in Experimental Acute Lung Injury

Physiologic, Biochemical, and Imaging Characterization of Acute Lung Injury in Mice

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