Role of Continuous High Thoracic Epidural Anesthesia in Hippocampal Apoptosis after Global Cerebral Ischemia in Rats

• Main Authors: Xuan Li, Xing Huo, Chongyou Zhang, Xinyu Ma, Fei Han, Guonian Wang
• Format: Article
• Language: English
• Published: Cell Physiol Biochem Press GmbH & Co KG 2014-09-01
• Series: Cellular Physiology and Biochemistry
• Subjects: High thoracic epidural anesthesia (HTEA); Cerebral ischemia; Global; Rats; Apoptosis; Poly (ADP-ribose) polymerase (PARP)
• Online Access: http://www.karger.com/Article/FullText/366334
• ISSN: 1015-8987; 1421-9778

Background: Cervical sympathetic blockade has been found to reduce cerebral vascular resistance and improve focal cerebral ischemia/reperfusion injury. In this study, we tested the hypothesis that the sympathetic blockade of high thoracic epidural anesthesia (HTEA) would reduce hippocampal apoptosis after global cerebral ischemia (GCI) injury. Methods: Fifteen-minute global ischemia was established by 4-vessel occlusion in adult male Wistar rats. And 0.5% bupivacaine or 0.9% saline (20 μl//h) was infused continuously to the thoracic epidural space through the T4-5 intervertebral space from 15 minutes before ischemia to 24 hours or 72 hours after ischemia. Cerebral blood flow (CBF), Mortality, neurodeficit scores (NDS), Nissl and TUNEL staining, hippocampal superoxide dismutase (SOD) activity, malondialdehyde (MDA) concentrations, western blot of poly (ADP-ribose) polymerase (PARP) and immunohistochemical staining (PARP, Bax and Bcl-2) were determined. Results: Both the hyperpefusion and hypoperfusion after reperfusion were improved by HTEA. HTEA decreased the number of apoptotic neurons in cornu ammonis area 1 (CA1), reduced PARP and Bax expressions with a decrease of Bax/Bcl-2 ratio induced by ischemic injury. The upregulation of SOD activity and the downregulation of MDA were obvious in the HTEA group compared with the GCI group. HTEA also improved NDS but not the mortality rate. Conclusion: Our study demonstrated that continuous HTEA attenuates hippocampal apoptosis and a behavioral deficit after global cerebral ischemia, and that these protective effects are associated with the improved microcirculation, reduced oxidative stress and the less activation of PARP.