ERJ
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via ISI Web of Science (1)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hughes, J. M. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hughes, J. M. B.
Eur Respir J 2005; 25:211-212
Copyright ©ERS Journals Ltd 2005

The hepatopulmonary syndrome: NO way out?

J. M. B. Hughes

National Heart and Lung Institute, Hammersmith Hospital Campus, Imperial College School of Medicine, London, UK.

To the Editors:

The hepatopulmonary syndrome (HPS) is defined by the triad of chronic liver disease, abnormal pulmonary gas exchange (low arterial oxygen tension (Pa,O2) and transfer factor of the lung for carbon monoxide), and intrapulmonary vascular dilatation 1. The recent editorial on HPS 2 suggests that "hunting endogenous vasodilators that reduce pulmonary vascular tone logically became a sound strategy for those whose quest was to unravel the missing ‘molecular’ link between the diseased liver and the affected lung". But, is this strategy actually so logical? The key feature of the intrapulmonary vascular dilatation in HPS is the intrapulmonary shunt shown physiologically by a low Pa,O2 after 100% oxygen breathing, and anatomically by the passage of radiolabelled albumin macroaggregates (20–60 µm in diameter), or echobubbles, through the pulmonary capillary bed 3. The striking feature pathologically is gross dilatation of capillaries in the alveolar septum, diameters of 100 µm, as compared with the normal 7–15 µm being described 4. Is it likely that endogenous vasodilators are responsible for "relaxing" alveolar capillaries to such an extent? Of course, endogenous vasodilators may play a part in "remodelling" these capillaries.

With regard to pulmonary gas exchange, two factors seem to operate in severe hepatopulmonary syndrome: 1) a hyperdynamic state with low pulmonary vascular resistance and rapid microvascular transit, and 2) vascular remodelling with dilatation of capillaries and a low transfer factor of the lung for carbon monoxide. After liver transplantation, arterial oxygen tension improves, but transfer factor of the lung for carbon monoxide often remains low 5, implying improvement in process 1 more than process 2. Since pulmonary nitric oxide levels return to normal after orthotopic liver transplantation 6, nitric oxide is an unlikely cause of the pulmonary capillary dilatation. Figure 1 in the European Respiratory Journal editorial 2 focuses on pulmonary vascular smooth muscle, but it cannot be the only factor.

REFERENCES

  1. Lange PA, Stoller JR. The hepatopulmonary syndrome. Ann Intern Med 1995;122:521–529.[Abstract/Free Full Text]
  2. Dinh-Xuan AT, Naeije R. The hepatopulmonary syndrome: NO way out? Eur Respir J 2004;23:661–662.[Free Full Text]
  3. Whyte MKB, Hughes JMB, Peters AM, Ussov W, Patel S, Burroughs AK. Analysis of intrapulmonary right to left shunt in the hepatopulmonary syndrome. J Hepatol 1998;29:85–93.[CrossRef][ISI][Medline] [Order article via Infotrieve]
  4. Davis HA, Schwartz DJ, Lefrak SS, Susman N, Schainker BA. Alveolar-capillary oxygen disequilibrium in hepatic cirrhosis. Chest 1978;73:507–511.[Abstract/Free Full Text]
  5. Ewert R, Mutze S, Schachschal G, Lochs H, Plauth M. High prevalence of pulmonary diffusion abnormalities without interstitial changes in long-term survivors of liver transplantation. Transpl Int 1999;12:222–228.[CrossRef][ISI][Medline] [Order article via Infotrieve]
  6. Rolla G, Brussino L, Coloagrande P, et al. Exhaled nitric oxide and impaired oxygenation in cirrhotic patients before and after liver transplantation. Ann Intern Med 1998;129:375–378.[Abstract/Free Full Text]




This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via ISI Web of Science (1)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hughes, J. M. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hughes, J. M. B.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS