The Effects of Superior Cervical Sympathetic Ganglion Block on the Acute Phase Injury and Long Term Protection against Focal Cerebral Ischemia/Reperfusion Injury in Rats.
10.3344/kjp.2008.21.2.119
- Author:
Hae Young JEON
1
;
Kyoung Woon JOUNG
;
Jae Moon CHOI
;
Yoo Kyung KIM
;
Jin Woo SHIN
;
Jeong Gill LEEM
;
Sung Min HAN
Author Information
1. Department of Anesthesiology and Pain Medicine, University of Ulsan College of Medicine, Seoul, Korea. jgleem@amc.seoul.kr
- Publication Type:Original Article
- Keywords:
cerebral ischemia/reperfusion;
rat;
superior cervical sympathetic ganglion block
- MeSH:
Amides;
Animals;
Apoptosis;
Blood Vessels;
Brain;
Brain Injuries;
Caspase 3;
DNA Nucleotidylexotransferase;
Ganglia, Sympathetic;
Humans;
In Situ Nick-End Labeling;
Infarction;
Male;
Middle Cerebral Artery;
Neurons;
Neuroprotective Agents;
Rats;
Rats, Sprague-Dawley;
Reperfusion;
Superior Cervical Ganglion
- From:The Korean Journal of Pain
2008;21(2):119-125
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Cerebral blood vessels are innervated by sympathetic nerves from the superior cervical ganglia (SCG), and these nerves may influence the cerebral blood flow. The purpose of the present study was to evaluate the neuroprotective effect of superior cervical sympathetic ganglion block in rats that were subjected to focal cerebral ischemia/reperfusion injury. METHODS: Eighty male Sprague-Dawley rats (270-320 g) were randomly assigned to one of two groups (the ropivacaine group and a control group). In all the animals, brain injury was induced by middle cerebral artery (MCA) reperfusion that followed MCA occlusion for 2 hours. The animals of the ropivacaine group received 30microl of 0.75% ropivacaine, and their SCG. Neurologic score was assessed at 1, 3, 7 and 14 days after brain injury. Brain tissue samples were then collected. The infarct ratio was measured by 2.3.5-triphenyltetrazolium chloride staining. The terminal deoxynucleotidyl transferase mediated dUTP-biotin nick-end labeled (TUNEL) reactive cells and the cells showing caspase-3 activity were counted as markers of apoptosis at the caudoputamen and frontoparietal cortex. RESULTS: The death rate, the neurologic score and the infarction ratio were significantly less in the ropivacaine group 24 hr after ischemia/reperfusion injury. The number of TUNEL positive cells in the ropivacaine group was significantly lower than those values of the control group in the frontoparietal cortex at 3 days after injury, but the caspase-3 activity was higher in the ropivacaine group than that in the control group at 1 day after injury. CONCLUSIONS: The study data indicated that a superior cervical sympathetic ganglion block may reduce the neuronal injury caused by focal cerebral ischemia/reperfusion, but it may not prevent the delayed damage.
