Nitric Oxide and Impaired Oxygenation before and after Liver Transplantation

  1. Giovanni Rolla, MD;
  2. Luisa Brussino, MD; and
  3. Paola Colagrande, MD
  1. Dr. Rolla: Università di Torino; Torino, Italy Dr. Brussino: Università di Torino; Torino, Italy Dr. Colagrande: Università di Torino; Torino, Italy

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    IN RESPONSE:

    Teramoto and colleagues question our conclusion that most cases of abnormal oxygenation in patients with cirrhosis are reversible after liver transplantation. We defined oxygenation abnormality as an increase in alveolar-arterial oxygen gradient greater than 15 mm Hg, which was present in 11 patients before and in 4 patients after liver transplantation (P < 0.05). We think our data justify this conclusion. Moreover, Battaglia and colleagues (1) have obtained similar results. That some patients with hepatopulmonary syndrome develop profound, early postoperative hypoxemia (which has been reported to improve after NO inhalation) does not contradict the postulated effect of endogenous NO in determining hypoxemia in cirrhosis. Exhaled NO represents endogenous production throughout the respiratory system, whereas NO administered by inhalation may shift blood flow from nonventilated to ventilated lung units accessible to NO (2).

    In a previous study (3), we found a correlation between alveolar-arterial oxygen gradient and respiratory NO output before liver transplantation. Teramoto and colleagues state that this correlation is stronger than the correlation we had previously found between the decrease in alveolar-arterial oxygen gradient and exhaled NO concentration after liver transplantation. To properly make such a comparison, one must consider the different measurement units of exhaled NO used in our two studies. In particular, NO output takes into account minute ventilation, which is increased in liver cirrhosis (particularly in patients with the hepatopulmonary syndrome, who have the worst oxygenation).

    We agree with Teramoto and colleagues that the improvement in oxygenation after liver transplantation depends on the decrease in intrapulmonary vasodilatation and portal hypertension, both of which are related to NO production (4).

    Giovanni Rolla, MD

    Università di Torino; Torino, Italy

    Luisa Brussino, MD

    Università di Torino; Torino, Italy

    Paola Colagrande, MD

    Università di Torino; Torino, Italy

    The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:

    •Include no more than 300 words of text, three authors, and five references

    •Type with double-spacing

    •Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.

    Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.

    Annals welcomes electronically submitted letters.

    References

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