• Title/Summary/Keyword: Ischemic damage

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Experimental Study on Cavo-Pulmonary Anastomosis (상공정맥-우폐동맥 문합에 관한 실험적 연구)

  • 양기민
    • Journal of Chest Surgery
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    • v.10 no.2
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    • pp.281-294
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    • 1977
  • Superior vena cava to pulmonary arterial shunting operation was made between the superior vena cava and the right pulmonary artery in the fashion of end-to-end anastomosis in 20 mongrel dogs. The experimental animals were divided into three group and blood flow in the superior vena cava was occluded for 20, 30 and 60 minutes respectively, and observations were made for the changes in caval pressure and cerebrospinal fluid pressure. And pathologic examinations were also performed. On occluding the caval blood flow, the superior vena caval pressure was sharply and immediately elevated from $103.5{\pm}19.8mmH_2O$ at thoracotomy to $556.4{\pm}86.lmmH_2O$ within 2 minutes to make its plateau thereafter, and the cerebrospinal fluid pressure followed closely the changes of the superior vena caval pressure in its level and pattern being elevated from $102.0{\pm}19.9mmH_2O$ to $490.5{\pm}79.9mmH_2O$. The drops of both the caval and cerebrospinal fluid pressures were definite and marked on opening the shunt flow through the anastomosis, but these postoperative pressures retained still higher ones above their levels measured at thoracotomy. The pathological examinations of the brain and the spinal cord were also performed in six animals. Characteristic changes uniformly seen in all area and in all animals were the findings of capillary congestion and perivascular edema. On the other hand, ischemic nerve cell changes were rather evident, revealing their degrees and extents being related to the prolongation of the time of caval occlusion which has followed by the sustained high pressures in both the superior vena and the cerebrospinal fluid. The experiment suggests the safety of this surgical procedure with minimal, if any, permanent damage as long as the occlusion of the caval blood flow is not prolonged beyond the expected.

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The Case-Control Study of Risk Factors of Silent Cerebral Infarction (무증상 뇌경색의 위험요인에 대한 환자;대조군 연구)

  • Baek, Hye-Ki;Ko, Mi-Mi;Yu, Byeong-Chan;Bang, Ok-Sun;Oh, Yeong-Seon;Kim, Yeon-Jin;Kim, Jung-Hyun;Kim, Yoon-Sik;Seol, In-Chan
    • The Journal of Internal Korean Medicine
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    • v.28 no.4
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    • pp.850-862
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    • 2007
  • Background : Cerebrovascular disease is a major cause of death and disability in adults. Silent cerebral infarction (SCI) portends more severe cerebral infarction or may lead to insidious progressive brain damage resulting in vascular dementia. Known cardiovascular risk factors, such as arterial hypertension, diabetes mellitus, smoking, hyperlipidemia and ischemic heart disease may increase the risk of SCI. This study was designed to evaluate the risk factors of SCI in an apparently normal adult population. Methods : We divided 340 neurologically normal adults (mean age=59.90$\pm$8.30, men:women = 146:194) who underwent brain computed tomography (CT) or magnetic resonance imaging (MRI) at the Stroke Medical Center in Daejeon University Oriental Medicine Hospital in two groups, Silent inf. and Controls,and analyzed risk factors of SCI by interview, physical examination and blood test. Risk factors of SCI were assessed by interview, physical examination and blood test. We performed Pearson's chi-square test and two-sample t-test for univariate analysis and multiple logistic regressions for multivariate analysis to evaluate risk factors of SCI. Results : Old age, diabetes mellitus, and high lactate dehydrogenase (LDH) levels were associated with SCI on univariate analysis. Diabetes mellitus was demonstrated to be an independent risk factor for SCI on multivariate analysis. Conclusions : Advanced age, diabetes mellitus, and LDH levels are associated with SCI.

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Shiga toxin-associated hemolytic uremic syndrome complicated by intestinal perforation in a child with typical hemolytic uremic syndrome

  • Chang, Hye Jin;Kim, Hwa Young;Choi, Jae Hong;Choi, Hyun Jin;Ko, Jae Sung;Ha, Il Soo;Cheong, Hae Il;Choi, Yong;Kang, Hee Gyung
    • Clinical and Experimental Pediatrics
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    • v.57 no.2
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    • pp.96-99
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    • 2014
  • Hemolytic uremic syndrome (HUS) is one of the most common causes of acute renal failure in childhood and is primarily diagnosed in up to 4.5% of children who undergo chronic renal replacement therapy. Escherichia coli serotype O157:H7 is the predominant bacterial strain identified in patients with HUS; more than 100 types of Shiga toxin-producing enterohemorrhagic E. coli (EHEC) subtypes have also been isolated. The typical HUS manifestations are microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency. In typical HUS cases, more serious EHEC manifestations include severe hemorrhagic colitis, bowel necrosis and perforation, rectal prolapse, peritonitis, and intussusceptions. Colonic perforation, which has an incidence of 1%-2%, can be a fatal complication. In this study, we report a typical Shiga toxin-associated HUS case complicated by small intestinal perforation with refractory peritonitis that was possibly because of ischemic enteritis. Although the degree of renal damage is the main concern in HUS, extrarenal complications should also be considered in severe cases, as presented in our case.

The Effect of Urinary Trypsin Inhibitor Against Neuropathic Pain in Rat Models

  • Jung, Ki Tae;Lee, Hyun Young;Yoon, Myung Ha;Lim, Kyung Joon
    • The Korean Journal of Pain
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    • v.26 no.4
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    • pp.356-360
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    • 2013
  • Background: Nerve injury sometimes leads to chronic neuropathic pain associated with neuroinflammation in the nervous system. In the case of chronic neuropathic pain, the inflammatory and algesic mediators become predominant and result in pain hypersensitivity following nervous system damage. It is well known that urinary trypsin inhibitor (ulinastatin, UTI) has an anti-inflammatory activity. Recently, the neuroprotective action of UTI on the nervous system after ischemic injury has been reported. Thus, we evaluated the neuroprotective effect of ulinastatin in a rat model of neuropathic pain. Methods: Neuropathic pain was induced with L5 spinal nerve ligation (SNL) in male Sprague-Dawley rats weighing 100-120 g. The rats were divided into 3 groups, with n = 8 in each group. The rats in the control group (group 1) were administered normal saline and those in group 2 were administered UTI (50,000 U/kg) intravenously through the tail vein for 3 days from the day of SNL. Rats in group 3 were administered UTI (50,000 U/kg) intravenously from the $5^{th}$ day after SNL. The paw withdrawal threshold was measured using the von Frey test for 3 days starting from the $5^{th}$ day after SNL. Results: The paw withdrawal thresholds were significantly increased in the rats of group 2 compared to the other groups (P < 0.05). Conclusions: Ulinastatin, which was administered for 3 days after SNL, increased the paw withdrawal threshold and it could have a neuroprotective effect in the rat model of neuropathic pain.

Emergency Trephination Site of Acute Subdural Hematoma (급성 경막하 혈종에서 응급 두개골 천공의 위치)

  • Moon, Soo-Hyeon;Kim, Geun-Hoe;Kwon, Taek-Hyun;Park, Youn-Kwan;Chung, Hung-Seob;Suh, Jung-Keun
    • Journal of Korean Neurosurgical Society
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    • v.29 no.5
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    • pp.659-663
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    • 2000
  • The motality rate of acute subdural hematoma(ASDH) associated with closed head injury is high in spite of recent advances in neurosurgery. Many variables in regard to outcome of ASDH have been assessed. But among them, intracranial pressure(ICP) control and the time interval between injury and operative evacuation are the only things that can be affected by doctor. We introduced a simple method to the management of ASDH for reducing the time interval between injury and operation. When the immediate decompressive operation of ASDH was impossible by any causes, we made a burr hole at the center of hematoma, usually on 2-3cm above temporal squama and 1-2cm behind coronal suture under local anesthesia before main operation. Partial hematoma evacuation was achieved through the burr hole and it was effective in preventing further worsening of patients neurological status before main operation. Prompt hematoma evacuation through the burr hole seemed to be effective in delaying secondary ischemic brain damage and made easy to closing the dura opening and replacement of the bone flap at the end of main decompressive operation. This easy method may reduce the time interval between injury and operation. We represent surgical technique with two cases of ASDH managed with this simple method.

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The neuroprotective mechanism of ampicillin in a mouse model of transient forebrain ischemia

  • Lee, Kyung-Eon;Cho, Kyung-Ok;Choi, Yun-Sik;Kim, Seong Yun
    • The Korean Journal of Physiology and Pharmacology
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    • v.20 no.2
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    • pp.185-192
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    • 2016
  • Ampicillin, a ${\beta}$-lactam antibiotic, dose-dependently protects neurons against ischemic brain injury. The present study was performed to investigate the neuroprotective mechanism of ampicillin in a mouse model of transient global forebrain ischemia. Male C57BL/6 mice were anesthetized with halothane and subjected to bilateral common carotid artery occlusion for 40 min. Before transient forebrain ischemia, ampicillin (200 mg/kg, intraperitoneally [i.p.]) or penicillin G (6,000 U/kg or 20,000 U/kg, i.p.) was administered daily for 5 days. The pretreatment with ampicillin but not with penicillin G significantly attenuated neuronal damage in the hippocampal CA1 subfield. Mechanistically, the increased activity of matrix metalloproteinases (MMPs) following forebrain ischemia was also attenuated by ampicillin treatment. In addition, the ampicillin treatment reversed increased immunoreactivities to glial fibrillary acidic protein and isolectin B4, markers of astrocytes and microglia, respectively. Furthermore, the ampicillin treatment significantly increased the level of glutamate transporter-1, and dihydrokainic acid (DHK, 10 mg/kg, i.p.), an inhibitor of glutamate transporter-1 (GLT-1), reversed the neuroprotective effect of ampicillin. Taken together, these data indicate that ampicillin provides neuroprotection against ischemia-reperfusion brain injury, possibly through inducing the GLT-1 protein and inhibiting the activity of MMP in the mouse hippocampus.

Clinical Significance of Bifrontotemporal Decompressive Craniectomy in the Treatment of Severe Refractory Posttraumatic Brain Swelling (중증 외상성 뇌부종 환자에서 양측 전두-측두부 감압적 개두술의 의의)

  • Shin, Hyung Shik;Kim, Jin Yong;Kim, Tae Hong;Hwang, Yong Soon;Kim, Sang Jin;Park, Sang Keun
    • Journal of Korean Neurosurgical Society
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    • v.29 no.9
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    • pp.1179-1183
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    • 2000
  • Objective : The treatment of malignant posttraumatic brain swelling remains a frustrating endeavor for neurosurgeon. Mortality and morbidity rates remain high depite advances in medical treatment of increased intracranial pressure. If conventional therapy fails in patients suffering from intracranial hypertension, there is only small number of second-tier option left including decompressive craniectomy. The role of decompressive craniectomy in posttraumatic brain swelling remains controversial. We assessed the efficacy and indications of decompressive craniectomy. Methods : The authors performed decompressive bifrontotemporal craniectomy in 22 patients with malignant posttraumatic brain swelling. Epidural pressure monotoring was performed in all patients. The clnical data and surgical outcomes were reviewed retrospectively. Result : The favorable outcome(GOS score 4-5) was 59%(13 of 22 patients), whereas the mortality rate was 32% (7 of 22 patients). Two patients(9%) remained in severely disabled state. Increased rate of favorable outcome was seen in the patients who had 8 or more of GCS score at admission and exhibited B wave in ICP monitoring and who showed steady state or slow deterioration in clinical course. Conclusion : If conservative therapy fails, decompressive bifrontotemporal craniectomy should be considered in the management of malignant posttraumatic brain swelling before irreversible ischemic brain damage occur.

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The Effects of Difumarate Salt S-15176 after Spinal Cord Injury in Rats

  • Erdogan, Hakan;Tuncdemir, Matem;Kelten, Bilal;Akdemir, Osman;Karaoglan, Alper;Tasdemiroglu, Erol
    • Journal of Korean Neurosurgical Society
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    • v.57 no.6
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    • pp.445-454
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    • 2015
  • Objective : In the present study we analyzed neuroprotective and antiapoptotic effect of the difumarate salt S-15176, as an anti-ischemic, an antioxidant and a stabilizer of mitochondrial membrane in secondary damage following spinal cord injury (SCI) in a rat model. Methods : Three groups were performed with 30 Wistar rats; control (1), trauma (2), and a trauma+S-15176 (10 mg/kg i.p., dimethyl sulfoxide) treatment (3). SCI was performed at the thoracic level using the weight-drop technique. Spinal cord tissues were collected following intracardiac perfusion in 3rd and 7th days of posttrauma. Hematoxylin and eosin staining for histopatology, terminal deoxynucleotidyl transferase dUTP nick end labeling assay for apoptotic cells and immunohistochemistry for proapoptotic cytochrome-c, Bax and caspase 9 were performed to all groups. Functional recovery test were applied to each group in 3rd and 7th days following SCI. Results : In trauma group, edematous regions, diffuse hemorrhage, necrosis, leukocyte infiltration and severe degeneration in motor neurons were observed prominently in gray matter. The number of apoptotic cells was significantly higher (p<0.05) than control group. In the S-15176-treated groups, apoptotic cell number in 3rd and 7th days (p<0.001), also cytochrome-c (p<0.001), Bax (p<0.001) and caspase 9 immunoreactive cells (p<0.001) were significantly decreased in number compared to trauma groups. Hemorrhage and edema in the focal areas were also noticed in gray matter of treatment groups. Results of the locomotor test were significantly increased in treatment group (p<0.05) when compared to trauma groups. Conclusion : We suggest that difumarate salt S-15176 prevents mitochondrial pathways of apoptosis and protects spinal cord from secondary injury and helps to preserve motor function following SCI in rats.

The Protective Effect of Black Ginseng Against Transient Focal Ischemia-induced Neuronal Damage in Rats

  • Park, Hyun-Jung;Shim, Hyun-Soo;Kim, Kyung-Soo;Shim, In-Sop
    • The Korean Journal of Physiology and Pharmacology
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    • v.15 no.6
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    • pp.333-338
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    • 2011
  • Black ginseng (BG) has been widely used as herbal treatment for improving physiological function. In order to investigate the neuroprotective action of this herbal medicine, we examined the influence of BG on the learning and memory of rats using the Morris water maze, and we studied the effects of BG on the central cholinergic system and neural nitric oxide synthesis in the hippocampus of rats with neuronal and cognitive impairment. After middle cerebral artery occlusion was applied for 2h, the rats were administered BG (100 or 400 $mgkg^{-1}$, p.o.) daily for 2 weeks, followed by training and performance of the Morris water maze test. The rats with ischemic insults showed impaired learning and memory on the tasks. Treatment with BG produced improvement in the escape latency to find the platform. Further, the BG groups showed a reduced loss of cholinergic immunoreactivity and nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d)-positive neurons in the hippocampus compared to that of the ISC group. These results demonstrated that BG has a protective effect against ischemia-induced neuronal and cognitive impairment. Our results suggest that BG might be useful for the treatment of vascular dementia.