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Objective:To investigate the effects of high thoracic epidural anesthesia (HTEA) on the cerebral blood flow (CBF) and hippocampal apoptosis-related proteins Bcl-2 and Bax during global cerebral ischemia and reperfusion (GCI) in rats.Methods:Fifteen-minute global ischemia was established by 4-vessel occlusion and epidural catheterization was performed through T4-5 intervertebral spaces in adult male Wistar rats.According to the different drugs infused into the epidural space,the rats were randomly divided into four groups:Sham group (0.9 ％ NaC1),Sham-HTEA group (0.25 ％ bupivacaine),GCI group (global cerebral ischemia,0.9 ％ NaC1) and HTEA group (global cerebral ischemia,0.25 ％ bupivacaine).And 0.25 ％bupivacaine or 0.9 ％ saline (20 μL·h-1) was infused continuously to the thoracic epidural space from 15 minutes before ischemia to 24 hours after reperfusion.Mean arterial pressure (MAP),heart rate (HR) and cerebral blood flow (CBF) were determined until 2 hours after reperfusion,and the hippocampal Bcl-2 and Bax proteins at 24 hours after reperfusion were examined by Western-blot.Results:Compared with the GCI group,HTEA group has no significant difference on MAP and HR during ischemia and 2 hours after reperfusion,andcompared with the Sham group,MAP in GCI group increased in ischemia 0 min and decreased in reperfusion 0 min.The CBF in HTEA group was significantly lower than that in GCI group (123.1％± 35.2％ vs 177.5％± 32.4％,P＜0.01) in reperfusion 10 min,and higher than that in GCI group during the hypoperfusion of 60 to 120 minutes after reperfusion (P＜0.05),and the ratio of Bax/Bcl-2 in hippocampus was significantly decreased in HTEA group 24 hours after reperfusion (P＜0.01).Conclusions:Continuous HTEA infusion of 0.25 ％ bupivacaine 20 μL ·h-1 could maintain the hemodynamic stability,and improve the CBF of hypoperfusion period in rats,as well as reduce the ratio of Bax/Bcl-2 at 24 hours after reperfusion.
ABSTRACT
Objective To observe the expression of glial fibrillary acidic protein ( GFAP), and the pathological and ultrastructnral changes of astrocytes in the CA1 subfield of the hippocampus following global cerebral ischemia and reperfusion, and to explore the neuroprotective mechanism of mild hypothermia. Methods Global cerebral ischemia was established in rats by a modified version of Pulsinelli's method. Ninety-six rats were divided into three groups including a sham-operated group, a normothermic ischemic reperfusion (IR) group and a hypothermic ischemic reperfusion (HIR) group. Each group had four subgroups which were sacrificed for 6, 12 or 24 hours, or 4 days after reperfusion (for each subgroup n = 8 ). Hematoxylin-eosin (HE) staining was used to observe morphological changes in neurons in the CA1 subfield of the hippocampus. TUNEL methods were used to detect apoptosis among those neurons. Immunohistochemical staining was used to detect the expression of GFAP in the CA1 subfield and the mechanism of astrocyte pathology. GFAP TUNEL double-labeled immunohistochemistry was used with both the shamoperated and experimental groups. Electron microscopy was also used to evaluate morphological changes in astrocytes 24 hours and 4 days after ischemia and reperfusion. Results Compared with the sham-operated group, expression of GFAP immunoreactive positive cells increased gradually in the CA1 subfield of the IR group rats. Compared with the IR group, expression of GFAP immunoreactive positive cells was significantly lower in the HIR group at all time points. Microscopic observation at the 4th day showed that some astrocytes in the CA1 subfield had died through oncosis. Conclusions Mild hypothermia can significantly decrease the expression of GFAP immunoreactive positive cells and the number of apoptotic neurons in the CA1 subfield of the hippocampus, minimize cell oedema and provide protection for neurons. Oncosis kills astrocytes following global cerebral ischemia and reperfusion.
ABSTRACT
Objective To observe the influence of δ-opioid reperfusion in rats with change in serum protein S-100B level and to explore the neuroprotective effect of DADLE during cerebral resuscitation. Method The model of global cerebral ischemia and reperfusion was induced by bilateral common carol id artery occlusion combined with hypotension. Fifty SD rats were randomly divided into five groups: sham operation group, model group, DADLE pretreated group, DADI.E treated postischemia group, DADLE treatment during reperfusion group ( n = 10 for each group) .In sham operation group,the rats were operated without ischemia and treatment; in model group, rats had global cerebral ischemia and reperfusion model up without any treament; in DADLE pretreated group, rats received DADlE before ischemia; in DADLE treatment postischemia group,rats had DADLE immediately after ischemia; in DADLE treatment during reperfusion group,rats got DADLE during early reperfusion. After the establishment of model, serum protein S-JOOB was measured by using ELlSA.One-way analysis of variance and SNK test were used for comparison between groups. Results The serum protein S-100B level was (475.56±1.93) pg/ml in sham operational group and that was much lower than that in model group and DADLE treatment groups. While the levels of serum protein S-100B in all DADLE treatment groups were reduced significantly in comparison with model group. There were no differences in the levels of serum protein KS-100B between DADLE treatment groups. Conclusions The δ-opioid receptor DADLE exerts neuroprotective effects on global cerebral ischemia and reperfusion in rats.