• Journal of Chest Surgery
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• v.41 no.2
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• pp.229-238
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• 2008

Background: Protection of the brain is a major concern during thoracic aortic surgery using hypothermic circulatory arrest (HCA). This study compares the surgical outcomes of two different cerebral protection methods in thoracic aortic surgery using HCA: retrograde cerebral protection (RCP) and antegrade cerebral protection (ACP). Material and Method: We retrospectively reviewed data on 146 patients who underwent thoracic aortic surgery from May 1995 to February 2007 using either RCP (114 patients, Group 1) or ACP (32 patients, Group 2) during HCA. There were 104 dissections (94 acute and 10 chronic) and 42 aneurysms (41 true aneurysms and 1 pseudoaneurysm), and all patients underwent ascending aortic replacement. There were 33 cases of hemiarch replacement, 5 of partial arch replacement, and 21 of total arch replacement. Result: The two groups were similar in preoperative and operative characteristics, but Group 2 had more elderly (over 70 years old) patients (34.4% vs. 10.5%), more coronary artery diseases (18.8% vs. 4.4%), more total arch replacements (46.9% vs. 5.3%) and longer HCA time ($50{\pm}24$ minutes vs. $32{\pm}17$ minutes) than Group 1. The operative mortality was 4.4% (5/114) and 3.1% (1/32), the incidence of permanent neurologic deficits was 5.3% (6/114) and 3.1% (1/32), and the incidence of temporary neurologic deficits was 1.8% (2/114) and 9.4% (3/32) in Groups 1 and 2, respectively. There were no statistical differences between the two groups in operative mortality, postoperative bleeding, or neurologic deficits (permanent and temporary). Conclusion: The early outcomes of aortic surgery using HCA were favorable and showed no statistical difference between RCP and ACP. However, the ACP patients endured longer HCA times and more extended arch surgeries. ACP is the preferred brain protection technique when longer HCA time is expected or extended arch replacement is needed.

• Journal of Yeungnam Medical Science
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• v.12 no.2
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• pp.260-268
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• 1995

Ischemia results when the decrease in tissue perfusion exceeds the tissues ability to increase an oxygen extraction from the blood. Brain edema has been defined as an abnormal accumulation of fluid within brain parenchyma associated with a volumetric enlargement of the brain tissue. In most instances, the labelling of edema as vasogenic or cytotoxic is only relative. For cerebral protection, there were many possible techniques which could increase or maintain cerebral perfusion and reduce cerebral metabolic demand for oxygen. This study was carried out the effect of mild brain hypothermia which was induced by infusion with cold saline into the carotid artery, during brief episodes of transient global ischemia on postischemic brain edema in rabbit. Eight rabbits were anesthetized with halothane and mechanically ventilated with oxygen. For isolated cerebral perfusion, polyethylene catheter was inserted left carotid artery for infusion of cold saline, external carotid artery was ligated, vertebral arteries were cautherized, right carotid artery was snared for ischemia and femoral artery and vein were also canulated for monitoring and drug treatment. At 3 hours After transient global ischemia, specific gravity of cerebral cortex and hippocampus was compared with no-perfusion group , perfusion with cold saline group and normal group. There was no significant differences in physiologic variables among the groups before transient global ischemia. But during transient global ischemia, brain temperature of perfusion group was decreased when compared to no perfusion group. Specific gravity of cerebral cortex and hippocampus of no-perfusion group and perfusion group was statistically significant when compared to normal group (p<0.01). The results of this study suggested that mild brain hypothermia with intracarotid cold saline infusion during brief episodes of transient global ischemia had decreased postischemic brain edema in rabbit.

• The Journal of Internal Korean Medicine
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• v.30 no.4
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• pp.674-684
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• 2009

Objectives : In conditions of brain infarction, irreversible axon damage occurs in the central nerve system (CNS), because gliosis becomes a physical and a mechanical barrier to axonal regeneration. Reactive gliosis induced by ischemic injury such as middle cerebral artery occlusion is involved with up-regulation of GFAP and CD81. This study was undertaken to examine the effect of the Gongjin-dan (GJD) on CD81 and GFAP expression and its pathway in the rat brain following middle cerebral artery occlusion (MCAO). Methods : In order to study ischemic injuries on the brain, infarction was induced by MCAO using insertion of a single nylon thread, through the internal carotid artery, into a middle cerebral artery. Cresyl violet staining, cerebral infarction size measurement, immunohistochemistry and microscopic examination were used to detect the expression of CD81 and GFAP and the effect on the infarct size and pyramidal cell death in the brain of the rat with cerebral infarction induced by MCAO. Also, c-Fos and ERK expression were measured to investigate the signaling pathway after GJD administration in MCAO rats. Results : Measuring the size of cerebral infarction induced by MCAO in the rat after injection of GJD showed the size had decreased. GJD administration showed pyramidal cell death protection in the hippocampus in the MCAO rat. GJD administration decreased GF AP expression in the MCAO rat. GJD administration decreased CD81 expression in the MCAO rat. GJD administration induced up-regulation of c-FOS expression compared with MCAO. GJD administration induced down-regulation of ERK expression compared with MCAO. Conclusion : We observed that GJD could suppress the reactive gliosis, which disturbs the axonal regeneration in the brain of a rat with cerebral infarction after MCAO by controlling the expression of CD81 and GFAP. The effect may be modulated by the regulation of c-Fos and ERK. These results suggest that GJD can be a candidate to regenerate CNS injury.

• Journal of Korean Neurosurgical Society
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• v.63 no.4
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• pp.463-469
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• 2020

Objective : This study aimed to investigate the changes and significance of microRNA155 levels in serum of patients with cerebral small vessel disease (CSVD). Methods : Thirty patients with CSVD who met the inclusion criteria were selected and divided into eight patients with lacunar infarction (LI) group and 22 patients with multiple lacunar infarction (MLI) combined with white matter lesions (WML) group according to the results of head magnetic resonance imaging (MRI). Thirty samples from healthy volunteers without abnormalities after head MRI examination were selected as the control group. The levels of serum microRNA155 in each group were determined by real-time polymerase chain reaction, and the correlation between microRNA155 in the serum of patients with CSVD and the increase of imaging lesions was analyzed by Spearman correlation analysis. Results : Compared with the control group, the serum microRNA155 level in the LI group, MLI combined with WML group increased, the difference was statistically significant (p<0.05); serum microRNA155 level was positively correlated with the increase of imaging lesions (p<0.05). Conclusion : The change of serum microRNA155 level in patients with CSVD may be one of its self-protection mechanisms, and the intensity of this self-protection mechanism is positively correlated with the number of CSVD lesions.

• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2017.05a
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• pp.179-182
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• 2017

Cerebral nervous system intervention procedures have been reported frequently due to radiation exposure such as skin baldness, hair loss, and redness due to prolonged procedures. Therefore, the bismuth shield designed to reduce the radiation exposure of the target organ located in the anterior part of the human body sensitive to skin and radiation sensitivity during CT (computed tomography) scan is applied to the cerebral vascular system intervention by ergonomic design, To reduce the radiation dose of sensitive scalp, we propose a study.

• The Journal of Internal Korean Medicine
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• v.21 no.2
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• pp.319-327
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• 2000

To evaluate the effect of Bangpungdangkwi-eum extracts on reperfusion following the middle cerebral artery occulsion in Sprague Dawley rats, the neuron protection effect were investigated through examining the size of cerebral infarction, cerebral edema, and the morphologic change of neuron. The results were obtained as follows; 1. The size of cerabral infarction in sample group is significantly decreased compared with that in control group. Sample group has approximately 17% cerebral infarction parts induced by ischemia in cerebrum while control group has approximately 22%. 2. The volume of cerebral edema in sample group is significantly decreased compared with that in control group. The volumn in sample group is increased by approximately 4.4% compared with that in normal group while that in control group is increased by approximately 7.7%. 3. The optical microscopic examination reveals that the damage of neurons in the ischemic parts and CA1 and CA3 region of hippocampus in the same side of the ischemic parts was the most high and the damage in sample group is decreased compared with that in control group.

• Journal of Korean Neurosurgical Society
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• v.39 no.1
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• pp.46-51
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• 2006

Objective : An Intracranial aneurysm is an important acquired cerebrovascular disease that can cause a catastrophic subarachnoid hemorrhage. Atherosclerosis is one of possible mechanism, but its contribution to aneurysm formation is unclear. Human apolipoprotein E[apoE] is best known for its arterial protection from atherosclerosis. In this study we observe apoE expression in experimental cerebral aneurysms of rats to elucidate the role of apoE in the process of cerebral aneurysm formation. Methods : Twenty-four male 7-week-old Sprague-Dawley strain rats received a cerebral aneurysm induction procedure. One month[12] and three months[12] after the operation, the rats were killed, their cerebral arteries were dissected, and the regions of the bifurcation of the right anterior cerebral artery-olfactory artery [ACA-OA] bifurcations were examined histologically and immunohistochemically. Results : In the 1 month group [n=12], the ACA-OA bifurcation showed no aneurysmal change in 7 rats and early aneurysmal change in 5 rats. In the 3 months group (n=12), the bifurcation showed no aneurysmal change in 2 rats and an advanced aneurysm in 10 rats. ApoE expression were in 3 specimen in early aneurysmal change, but not in advanced aneurysms. Conclusion : ApoE expression in early aneurysmal wall suggests a possible role for apoE in early events leading to aneurysm formation. Further studios are necessary to elucidate the exact role of apoE in the pathophysiology of cerebral aneurysm.

• The Journal of Korean Medicine
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• v.22 no.4
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• pp.142-150
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• 2001

Objectives : The purpose of this investigation is to evaluate and compare the effects of Sunghyangjunggi-san (SH) and Gwackhyangjunggi-san (GH) extracts on reperfusion following the MCA occlusion in rats. Methods : To evaluate the effect of Sunghyangjunggi-san (SH) and Gwackhyangjunggi-san (GH) extracts on reperfusion following the MCA occlusion, the volume of cerebral infarction and edema were measured and the change of the CA1 pyramidal neurons in the hippocampus were investigated by light microscopy. Results : 1. The infarction volume of the control group was 23.6%, that of the GH group was 23.7%, and that of the SH group was 18.5%. 2. The brain edema volume of the control group increased by 16% compared with that of the normal group, that of the GH group increased by 14%, and that of the SH group increased by 9%. 3. The number of surviving pyramidal neurons in the CAI area of the hippocampus was investigated under light microscopy. In the control group, few surviving pyramidal neurons excisted (mean 6.4) and similarly in the GH group (mean 8.5), but in the SH group, the number of surviving pyramidal neurons was significantly higher, to the mean 18.4. Conclusions : According to the above results, in regard to the damage of neurons following cerebral ischemia, the GH group has little effect of the protection of neurons compared to the control group, but the SH group has a remarkable effect.

• The Journal of Korean Medicine
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• v.28 no.3 s.71
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• pp.216-231
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• 2007

Objectives : Chengsimyeunja-eum and Sunghyangjungi-san are prescriptions used for cerebral infarction clinically; it is known that these formulas reduce ischemic damage. According to previous research data, controlling certain types of glucose is considered to decrease the risk of cerebral infarction. Based on this fact, we investigated the effects of Chengsimyeunja-eum and Sunghyangjungi-san extracts on reperfusion following ischemic damage to diabetic rats, the change of c-FOS and Bax positive neurons in the hippocampus and cerebral cortex and protein through immunohistochemical methods, changes of serum glucose level, serum triglyceride level, and hepatic glucokinase activity. Methods : We induced ischemic damaged in diabetic rats, and the rats were administered Chengsimyeunja-eum and Sunghyangjungi-san extracts. Results : Chengsimyeunja-eum demonstrated significant decrease of c-Fos positive neurons in both hippocampus and cerebral cortex as well as a significant decrease of Bax positive neurons in hippocampus after ischemic damage on diabetic rats and decrease of serum glucose level after ischemic damage on diabetic rats. Sunghyangjungi-san demonstrated significant decreases of c-Fos and Bax positive neurons in both hippocampus and cerebral cortex after ischemic damage on diabetic rats. Conclusions : Chengsimyeunja-eum, effect on glucose level control, has a remarkable effect of protection of neurons not effective on glucose level. Sunghyangjungi-san showed neuroprotective effect through preventing neuronal cell death.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.5
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• pp.515-521
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• 1997

Endothelial cells play a central role in the inflammatory processes, and activation of nuclear factor kappa B ($NF-_{\kappa}B$) is a key component in that inflammatory processes. Previously, we reported that tumor necrosis factor alpha($TNF{\alpha}$) had protective effect of cell death induced by serum deprivation and this protection was related to $NF-_{\kappa}B$ activation. Inducible nitric oxide synthase (iNOS) is a member of the molecules which transcription is regulated mainly by $NF-_{\kappa}B$. And the role of nitric oxide (NO) generated by iNOS on cell viability is still controversial. To elucidate the mechanism of $TNF{\alpha}$ and $NF-_{\kappa}B$ activation on cell death protection, we investigate the effect of NO on the cell death induced by serum- deprivation in bovine cerebral endothelial cells in this study. Addition of $TNF{\alpha}$, which are inducer of iNOS, prevented serum-deprivation induced cell death. Increased expression of iNOS was confirmed indirectly by nitrite measurement. When selective iNOS inhibitors were treated, the protective effect of $TNF{\alpha}$ on cell death was partially blocked, suggesting that iNOS expression was involved in controlling cell death. Exogenously added NO substrate (L-arginine) and NO donors (sodium nitroprusside and S-nitroso-N-acetylpenicillamine) also inhibited the cell death induced by serum deprivation. These results suggest that NO has protective effect on bovine cerebral endothelial cell death induced by serum-deprivation and that iNOS is one of the possible target molecules by which $NF-_{\kappa}B$ exerts its cytoprotective effect.