2026-04-13T02:08:40Zhttps://recercat.cat/oai/request

oai:recercat.cat:2445/1848372025-12-04T19:02:37Zcom_2072_1057col_2072_478777col_2072_478917

00925njm 22002777a 4500 dc Rosales-Antequera, Cristián author Viscor Carrasco, Ginés author Araneda, Oscar F. author 2022-04-07T17:30:21Z 2022-04-07T17:30:21Z 2022-04-01 2022-04-07T17:30:21Z One of the etiopathogenic factors frequently associated with generalized organ damage after spinal cord injury corresponds to the imbalance of the redox state and inflammation, particularly of the respiratory, autonomic, and musculoskeletal systems. Our goal in this review was to gain a better understanding of this phenomenon by reviewing both animal and human studies. At the respiratory level, the presence of tissue damage is notable in situations that require increased ventilation due to lower thoracic distensibility and alveolar inflammation caused by higher levels of leptin as a result of increased fatty tissue. Increased airway reactivity, due to loss of sympathetic innervation, and levels of nitric oxide in exhaled air that are similar to those seen in asthmatic patients have also been reported. In addition, the loss of autonomic control efficiency leads to an uncontrolled release of catecholamines and glucocorticoids that induce immunosuppression, as well as a predisposition to autoimmune reactions. Simultaneously, blood pressure regulation is altered with vascular damage and atherogenesis associated with oxidative damage. At the muscular level, chronically elevated levels of prooxidants and lipoperoxidation associated with myofibrillar atrophy are described, with no reduction or reversibility of this process through antioxidant supplementation Lesions medul·lars Inflamació Estrès oxidatiu Spinal cord injuries Inflammation Oxidative stress Inflammation and oxidative stress as common mechanisms of pulmonary, autonomic, and musculoskeletal dysfunction after spinal cord injury