Pulmonary edema and hemorrhage after acute spinal cord injury in rats

Abstract

Background ContextRespiratory complications are a major cause of morbidity and mortality during the first days after acute spinal cord injury (ASCI). However, the pathophysiology of respiratory insufficiency resulting from spinal cord injury that involves lower levels is less well understood. PurposeThe aim of the present study was to investigate pulmonary pathophysiology after ASCI. Study DesignThis is an experimental animal study of ASCI investigating pulmonary pathophysiology after ASCI. MethodsEighty-four (N=84) rats were divided into two groups: a sham surgery (n=42) and an injury group (n=42). In the injury group, ASCI was induced at the level of the tenth thoracic vertebra by a modified Allen method. Rats were sacrificed 6 hours, 12 hours, 24 hours, 3 days, 1 week, 2 weeks, and 4 weeks after surgery. Pulmonary edema was assessed by calculating the ratio of the wet-to-dry lung weight (W:D). Pulmonary edema and hemorrhage were evaluated by observing gross and microscopic morphology. The study was funded by Natural Science Foundation of China (NSFC, 81272172). The funder of the present study had no capacity to influence the scholarly conduct of the research, interpretation of results, or dissemination of study outcomes. ResultsIn the injury group, W:D was significantly increased 12 hours after surgery compared with the sham surgery group; W:D peaked 3 days after ASCI (p<.05). Gross morphologic observations showed hemorrhagic lesions on the lung tissue 12 hours after ASCI and pulmonary edema 24 hours after ASCI. Pulmonary edema peaked 3 days after ASCI and was obviously decreased 1 week after ASCI. Hemorrhage was apparent until 2 weeks after ASCI. Light microscopy showed congestion of pulmonary capillaries 6 hours after ASCI. The pulmonary alveoli were filled with erythrocytes and serous extravasate 12 hours after ASCI. Hemorrhage and edema were observed in the interstitium and lung alveoli 24 hours after ASCI. ConclusionsEarly pathologic changes such as pulmonary congestion, hemorrhage, and edema after injury may be the basis for early respiratory dysfunction following ASCI.