Y-D Fan1, M-L Zhu, D Geng, K Zhou, G-J Du, Z-L Wang. 1. Department of Neurosurgery, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, PR China. 276260192@qq.com.
Abstract
OBJECTIVE: We aimed at investigating the pathological mechanism changing of injury during reperfusion injury, reperfusion time correlation and compliance, finding the blood supply and improving the secondary damage. MATERIALS AND METHODS: A total of 180 patients who underwent a surgical procedure and that received normal saline intraperitoneally immediately after the patients' aortic occlusions were investigated. Patients were divided in three groups. Experimental conditions and programs were designed for various approaches. RESULTS: Thirty min after the onset of ischemia, we found a decrease in the local blood flow in the lumbar spinal cord, almost -77.48% of the baseline, which was reversed partially by initial reperfusion, even exceeding the baseline level. However, 1 hour after reperfusion, the blood flow was again decreased to the level below the baseline, followed by a decline to 207.13% ± 38.25 PU for 3 h without any recovery. Attenuating this secondary damage with neuroprotective strategies requires an understanding of these pathophysiologic processes. CONCLUSIONS: This study showed the pathological mechanism changes during reperfusion injury and reperfusion time correlation and compliance, and analyzed some of the important pathophysiologic processes involved in secondary damage after spinal cord injury. Moreover, our research discusses a number of pharmacologic therapies that have either been studied or have future potential for this devastating injury.
OBJECTIVE: We aimed at investigating the pathological mechanism changing of injury during reperfusion injury, reperfusion time correlation and compliance, finding the blood supply and improving the secondary damage. MATERIALS AND METHODS: A total of 180 patients who underwent a surgical procedure and that received normal saline intraperitoneally immediately after the patients' aortic occlusions were investigated. Patients were divided in three groups. Experimental conditions and programs were designed for various approaches. RESULTS: Thirty min after the onset of ischemia, we found a decrease in the local blood flow in the lumbar spinal cord, almost -77.48% of the baseline, which was reversed partially by initial reperfusion, even exceeding the baseline level. However, 1 hour after reperfusion, the blood flow was again decreased to the level below the baseline, followed by a decline to 207.13% ± 38.25 PU for 3 h without any recovery. Attenuating this secondary damage with neuroprotective strategies requires an understanding of these pathophysiologic processes. CONCLUSIONS: This study showed the pathological mechanism changes during reperfusion injury and reperfusion time correlation and compliance, and analyzed some of the important pathophysiologic processes involved in secondary damage after spinal cord injury. Moreover, our research discusses a number of pharmacologic therapies that have either been studied or have future potential for this devastating injury.