Hepatopulmonary Syndrome: Oxidative Stress and Physical Exercise

Abstract

Hepatopulmonary syndrome (HPS) may be defined by hepatic disease, gas exchange abnormalities that may lead to hypoxaemia, and the presence of pulmonary vascular dilations. The balance between the many substances involved in vasodilation and vasoconstriction is regulated by the liver; thus, liver damage may generate systemic changes throughout the body. The pulmonary tissue may be damaged by reactive oxygen species or nitric oxide. Dyspnoea is the most frequent pulmonary symptom, caused by tissue damage, and may become worse when an individual exercises. In experimental research the surgical model of bile duct ligation is the optimal model to simulate the typical lung alterations present in HPS, which results in an increase in oxidative stress in hepatic and pulmonary tissues. In liver injury, the muscular system may also be damaged, for example sarcopenia may seriously aggravate cirrhosis and is associated with cirrhotic patient mortality. Muscular changes can be explained by the actions of myostatin and insulin-like growth factor and the increase in body levels of ammonia. As a result of impaired cardiopulmonary and muscular conditions, HPS patients may exhibit a low exercise tolerance, low muscle strength, and low functionality. Liver disease can contribute to HPS oxidative stress and is one of the main factors responsible for the reduction of gas exchange. Physical exercise can be performed as a way of modifying this pathophysiological state. Studies that have investigated physical exercise as a therapy for cirrhosis suggest that this approach may be beneficial for cirrhotic patients, primarily with regard to muscular and cardiorespiratory injuries.