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

Abstract

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.

Small Extracellular Vesicles Derived from Altered Peptide Ligand‐Loaded Dendritic Cell Act as A Therapeutic Vaccine for Spinal Cord Injury Through Eliciting CD4+ T cell‐Mediated Neuroprotective Immunity

“…After SCI, the local tissue structures are disrupted, leading to antigen exposure at the site. [50] MBP, a crucial constituent of the myelin sheath, is frequently exposed after SCI and triggers immune cell activity. [51] A91-DsEVs stimulated the conversion of CD4 + T cells into antigen-specific Th2 and Treg cells, enabling their recruitment to injury sites.…”

Estimation of peak oxygen consumption in individuals with spinal cord injury patients using multiple linear regression analysis: a preliminary study

“…This necessitates the exploration of new predictive factors. In particular, a reduction in sympathetic nervous system stimulation neurons can cause disorders in catecholamine secretion of the adrenal medulla during exercise, leading to decreased levels of blood catecholamines, heart rate, cardiac output, and ventilation, ultimately limiting cardiopulmonary function [ 28 , 29 ]. Therefore, an equation that includes pulmonary function can be considered as a factor for predicting VO 2 peak in individuals with SCI.…”

Systemic and Pulmonary Inflammation/Oxidative Damage: Implications of General and Respiratory Muscle Training in Chronic Spinal-Cord-Injured Patients

“…Several mechanisms explain this behavior; it has been shown that these patients’ airways have a decreased radius, partly due to lower respiratory muscle strength and lower thoracic excursion, as well as the difficulty in mobilizing secretions that affect the airway radius and, ultimately, in many cases, a compromise of the sympathetic nerves that correspond to the main bronchodilator factor through the adrenergic system of the airway’s smooth muscle [ 25 ]. In addition, the increased parasympathetic tone described in some patients further favors bronchial reactivity by increasing the work of breathing [ 26 , 27 ]. Ultimately, the poor pulmonary function described in this group decreases access to the large physiological pulmonary reserve, leaving patients unable to adequately respond to stressful situations.…”