The Small Intestine in the Acute Period of Spinal Injury: Early Metabolic Disorders According to Fluorescence-Lifetime Imaging FLIM

RELEVANCE A special place in the development of enteral insufficiency is given to dysproteinemia, which is one of the leading causes of the development of decubital ulcers in patients with spinal cord injury. Early enteral nutrition partially solved this problem, but the incidence of bedsores still remains high and reaches 68%. The risk of metabolic disorders in the acute period of spinal injury is largely determined by non-occlusive intestinal ischemia against the background of spinal shock, neurohumoral dysregulation; intra-intestinal and intra-abdominal hypertension; change in intestinal microflora. Pathological changes in the intestinal wall occur during the first 20 days after injury and further exacerbate chronic maldigestion, malabsorption, intestinal dyskinesia in patients with traumatic spinal cord disease. New knowledge about the features of early enteral nutrition in patients in the acute period of traumatic spinal cord disease will reduce the risk of decubitus ulcerative defects. AIM OF THE STUDY To study the dynamics of metabolic processes in the tissues of the small intestine in the acute period of spinal injury. MATERIAL AND METHODS Wistar rats (n=22). Spinal injury was simulated by acute complete transection of the spinal cord at the level of Th5–Th6 vertebrae. The assessment of metabolic changes in the cells of the serous membrane of the intestine was performed immediately, 3 and 24 hours after injury. The metabolism was assessed in vivo using fluorescence time-resolved macroimaging technology FLIM by autofluorescence in the spectral channel of the metabolic cofactor nicotinamide adenine dinucleotide (phosphate). RESULTS The acute period of spinal cord injury is accompanied by a change in the endogenous autofluorescence of the serous membrane of the small intestine: a statistically significant decrease in the mean fluorescence lifetime (τm), the lifetime of the long component (τ2), and the relative contribution of the long component (а2) in 24 h after injury was recorded. The changes observed using FLIM confirm the catabolic type of metabolism in the tissues of the small intestine after spinal cord injury. CONCLUSION For the first time in the experiment in vivo it has been shown that the acute period of spinal injury is accompanied by a violation of metabolic processes in the tissues of the small intestine. This fact requires a more balanced approach in calculating the calorie content of nutrients used for early enteral nutrition in patients with spinal cord injury.