{'fraction_non_alphanumeric': 0.021235521235521235, 'fraction_numerical': 0.0019305019305019305, 'mean_word_length': 5.1726190476190474, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Alterations in L-Arginine Metabolism After Lung Transplantation

Since the discovery of nitric oxide (NO) in biological systems more than 20 years ago, it became widely ac- cepted that endogenous NO plays a key role in the regulation of a variety of physiological processes. NO is involved in reperfusion injury and chronic rejection after solid organ transplantation. Arginase is an enzyme that competes with NO synthases for the common substrate L-arginine. Increased arginase activity alters L-arginine metabolism and reduces sub- strate availability for NO synthases, and thereby contributes to organ dysfunction following transplantation. NO defi- ciency after lung transplantation impacts on perfusion and ventilation of the donor organ. L-ornithine, the product of ar- ginase activity, is precursor for polyamine and proline biosynthesis which are both involved in airway remodeling. The purpose of this review is to summarize the current knowledge on the role of alterations in the L-arginine metabolism in lung transplantation.