Methylene Blue and Cirrhosis: Pathophysiologic Insights, Therapeutic Dilemmas
Widespread changes in vascular tone accompany the development of cirrhosis and portal hypertension and contribute to the onset of end-organ complications of liver disease (1). The pulmonary vasculature may be affected, and both vasoconstriction in resistance vessels (which leads to portopulmonary hypertension in approximately 1% to 2% of patients with cirrhosis) (2) and, more commonly, vasodilation in the microcirculation (which leads to the hepatopulmonary syndrome in 8% to 15% of patients with cirrhosis) have been observed. The hepatopulmonary syndrome is defined by intrapulmonary microvascular vasodilation that results in abnormal arterial oxygenation (3). Although the natural history of the syndrome has not been characterized in prospective studies, abnormalities are generally progressive and mortality rates are usually high (4). In addition, because many patients who develop the hepatopulmonary syndrome have well-preserved hepatic synthetic function (5), there is a good chance that pulmonary abnormalities will influence quality of life over time.
The pathogenesis of vasodilation in the lung in the hepatopulmonary syndrome is being actively investigated. Studies in humans (6) and in animal models (7) suggest that elevated nitric oxide production in the lung is an important mediator in the onset of vasodilation. However, many aspects of pathogenesis remain poorly defined, and this lack of information has impeded the development of effective medical therapies. At present, the only clearly successful treatment is liver transplantation, which has significantly improved or reversed vasodilation and gas …
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