Inflammation and Oxidative Stress as Common Mechanisms of Pulmonary, Autonomic and Musculoskeletal Dysfunction after Spinal Cord Injury

Simple Summary When a spinal cord injury occurs, the neurons that regulate our voluntary movements, those involved in environment and somatic perception and those that regulate vegetative functions are affected. Once neuronal damage is established, the cells of other tissues are also affected in their functions, altering the interaction between organs and altering the proper functioning of the organism. Multiple studies in animal models, as well as in humans, have recognized as factors involved in organ damage the imbalance between the formation of highly reactive molecules called pro-oxidants and defensive mechanisms called antioxidants. Closely associated with this phenomenon, the inflammatory response is also pathologically activated. In this narrative review, we have analyzed the information involving these pathological processes at the level of the lung, the autonomic nervous system and the skeletal musculature after spinal cord injury. Knowing the abnormal functioning mechanisms that occur after a spinal cord injury not only offers a better understanding of the organic events but also offers future possibilities for therapeutic interventions that may benefit the thousands of patients suffering this pathology. 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.