• The Journal of Korean Medicine
• /
• v.31 no.5
• /
• pp.82-89
• /
• 2010

Objectives: The aim of this study was to determine distribution patterns of TOAST subtypes of ischemic stroke patients admitted to oriental hospitals and to get a better understanding of present conditions in oriental medicine by comparing with the Korea stroke registry (KSR), the largest and representative data. Methods: Clinical data were collected from acute ischemic stoke patients. MRI studies including vascular images were performed in all cases. TOAST criteria were used to determine subtypes of ischemic stroke patients. According to the duration from disease onset to hospital admission time, patients were assigned to 3 groups (Group I0 to 3 d, Group II4 to 7 d, Group III8 to 28 d) and the distribution of TOAST subtypes were compared among these three groups. Results: We collected 514 sets of clinical data from 10 oriental hospitals between May 2007 and September 2009. Small vessel occlusion (SVO) subtype was the most common (57.62%), followed by large artery atherosclerosis (LAA, 29.98%). Compared with TOAST distribution of KSR, the proportion of ischemic stroke patients with SVO subtype was higher than that of KSR. On the other hand the proportion of patients with stroke of undetermined etiology (SUE) was lower. Distributions of SVO, LAA and cardioembolism (CE) in group were I 66.4%, 23.8% and 8.9%, respectively; those in group IIIwere 51.03%, 34.71% and 11.57%, respectively. Conclusions: In oriental hospitals, the proportion of ischemic stroke patients diagnosed as SVO type was higher than that of KSR. At early stage (from onset to 2 d) proportion of SVO was very high, however after 7 days from onset it decreased with concomitant increases in proportions of LAA and CE. These phenomena may be due to the facts that 1) at early stage emergency treatments are limited in oriental hospitals, 2) after early stage many patients prefer oriental treatments, including rehabilitation.

• Journal of Trauma and Injury
• /
• v.26 no.3
• /
• pp.243-247
• /
• 2013

Introduction: Surgical treatment of subclavian artery (SA) injury is challenging because approaching the lesion directly and clamping the proximal artery is difficult. This can be overcome by using an endovascular technique. Case 1: A 37-year-old male was drawn into the concrete mixer truck. He had a right SA injury with multiple traumatic injuries: an open fracture of the right leg with posterior tibial artery (PTA) injury, a right hemothorax, and fractures of the clavicle, scapula, ribs, cervical spine and nasal bone. The injury severity score (ISS) was 27. Computed tomography (CT) showed a 30-mm-length thrombotic occlusion in the right SA, which was 15 mm distal to the vertebral artery (VA). A self-expandable stent($8mm{\times}40mm$ in size) was deployed through the right femoral artery while preserving VA flow, and the radial pulse was palpable after deployment. Other operations were performed sequentially. He had a viable right arm during a 13-month follow-up period. Case 2: A 25-year-old male was admitted to our hospital due to a motorcycle accident. The ISS was 34 because of a hemothorax and open fractures of the mandible and the left hand. Intraoperative angiography was done through a right femoral artery puncture. Contrast extravasation of the SA was detected just outside the left rib cage. After balloon catheter had been inflated just proximal to the bleeding site, direct surgical exploration was performed through infraclavicular skin incision. The transected SA was identified, and an interposition graft was performed using a saphenous vein graft. Other operations were performed sequentially. He had a viable left arm during a 15-month follow-up period. Conclusion: The challenge of repairing an SA injury can be overcome by using an endovascular approach.

• The Korean Journal of Pain
• /
• v.20 no.2
• /
• pp.83-91
• /
• 2007

Background: Cerebral blood vessels are innervated by sympathetic nerves that originate in the superior cervical ganglia (SCG). This study was conducted to determine the effect of an SCG block on brain injury caused by focal cerebral ischemia/reperfusion in a rat model. Methods: Male Sprague-Dawley rats (270-320 g) were randomly assigned to one of three groups (lidocaine, ropivacaine, and control). After brain injury induced by middle cerebral artery (MCA) occlusion/reperfusion, the animals were administered an SCG bloc that consisted of $30{\mu}l$ of 2% lidocaine or 0.75% ropivacaine, with the exception of animals in the control group, which received no treatment. Twenty four hours after brain injury was induced, neurologic scores were assessed and brain samples were collected. The infarct and edema ratios were measured, and DNA fragmented cells were counted in the frontoparietal cortex and the caudoputamen. Results: No significant differences in neurologic scores or edema ratios were observed among the three groups. However, the infarct ratio was significantly lower in the ropivacaine group than in the control group (P < 0.05), and the number of necrotic cells in the caudoputamen of the ropivacaine group was significantly lower than in the control group (P < 0.01). Additionally, the number of necrotic and apoptotic cells in theropivacaine group were significantly lower than inthe control group in both the caudoputamen and the frontoparietal cortex (P < 0.05). Conclusions: Brain injury induced by focal cerebral ischemia/reperfusion was reduced by an SCG block using local anesthetics. This finding suggests that a cervical sympathetic block could be considered as another treatment option for the treatment of cerebral vascular diseases.

• Journal of Korean Neurosurgical Society
• /
• v.65 no.5
• /
• pp.665-679
• /
• 2022

Objective : Patients with mild ischemic stroke experience various sequela and residual symptoms, such as anxious behavior and deficits in movement. Few approaches have been proved to be effective and safe therapeutic approaches for patients with mild ischemic stroke by acute stroke. Sildenafil (SIL), a phosphodiesterase-5 inhibitor (PDE5i), is a known remedy for neurodegenerative disorders and vascular dementia through its angiogenesis and neurogenesis effects. In this study, we investigated the efficacy of PDE5i in the emotional and behavioral abnormalities in rats with mild ischemic stroke. Methods : We divided the rats into four groups as follows (n=20, respectively) : group 1, naïve; group 2, middle cerebral artery occlusion (MCAo30); group 3, MCAo30+SIL-pre; and group 4, MCAo30+SIL-post. In the case of drug administration groups, single dose of PDE5i (sildenafil citrate, 20 mg/kg) was given at 30-minute before and after reperfusion of MCAo in rats. After surgery, we investigated and confirmed the therapeutic effect of sildenafil on histology, immunofluorescence, behavioral assays and neural oscillations. Results : Sildenafil alleviated a neuronal loss and reduced the infarction volume. And results of behavior task and immunofluorescence shown possibility that anti-inflammation process and improve motor deficits sildenafil treatment after mild ischemic stroke. Furthermore, sildenafil treatment attenuated the alteration of theta-frequency rhythm in the CA1 region of the hippocampus, a known neural oscillatory marker for anxiety disorder in rodents, induced by mild ischemic stroke. Conclusion : PDE5i as effective therapeutic agents for anxiety and movement disorders and provide robust preclinical evidence to support the development and use of PDE5i for the treatment of mild ischemic stroke residual disorders.

• Journal of Chest Surgery
• /
• v.37 no.2
• /
• pp.154-159
• /
• 2004

The arteriovenous fistula (AVF), which maintains satisfactory blood flow, is necessary to the patients of end-stage renal disease for the long term hemodialysis. We performed the snuffbox fistula as the first operation for hemodialysis vascular access. This study was performed to investigate the patency rates, complications, risk factors for occlusion of the AVF, and the types of reoperations. Material and Method: We performed 146 snuffbox fistulas from Jun. 1994 to Dec. 2001 The records of the patients except six patients who were lost from follow up were analyzed retrospectively, Mean age and male:female ratio were 52$\pm$15 years (range, 17∼79 years) and 80 : 60 respectively. Diabetes mellitus and hypertension were combined in 47 patients and 101 respectively. Preoperative levels of creatinine and potassium were 9.09$\pm$3.68 mg/dL (range, 2.55∼20.09 mg/dL) and 4.7$\pm$0.9 mmol/L (range, 2.3∼8.1 mmol/L). One hundred thirteen cases of the snuffbox fistulas were done at left side hand and the others at right hand. Result: Mean follow up period of the patients was 41.8$\pm$31.0 months (range, 0.2∼108,8 months). During the follow up period, 35 occlusions of AVF occurred and these AVFs were patent for 9.8$\pm$10.1 months (range, 0.1∼40.4 months). The patency rates of f month, and 1, 2, 3, 5 years were known as 92.8, 80.2, 73.8, 71.3, 69.6% respectively. Right sided snuffbox fistulas (p-value=0.045) and old age (p-value=0.048) were revealed as significant risk factors for occlusion of AVF. The postoperative complications consisted of occlusions of AVF caused by intimal hyperplasia of vein in 24, thrombosis in nine, stenosis of anastomosis site in three, and venous hypertensions in two. After the first operation 37 patients underwent 86 reoperations. Conclusion: The snuffbox fistulas showed acceptable patency rates and low complication rates. The snuffbox fistulas as the first operation for AVF formation can be a good option for the patients with end-stage renal disease.

• The Korean Journal of Pharmacology
• /
• v.18 no.2
• /
• pp.1-14
• /
• 1982

The effects of xanthine-xanthine oxidase reaction on brain microsomal $Na^+-K^+-ATPase$ activity were studied to see possible involvement of oxygen free radicals in pathologic change occurring in ischemic state of CNS accompanied by cerebral vascular occlusion or impact injury. When microsomal fraction was incubated with xanthine ana xanthine oxidase, $Na^+-K^+-ATPase$ activity of the fraction was markedly inactivated (80% inactivation) whereas btssl $Mg^{++}-ATPase$ was much less sensitive (less than 10% inactivation) compared to that of $Na^+-K^+-ATPase$. The inactivation was observed only in the presence of both xanthine and xanthine oxidase, not either of them alone, and the extent of inactivation was dependent on the concentration of xanthine. In an attempt to determine which of the oxygen species was responsible for the inactivation, the ability of various scavengers to overcome the inactivation was tested. Superoxide dismutase, catalase and 1,4-diazabicyclo(2,2,2)octane were shown to reverse the inactivation of the ATPase in dose-dependent manner. In contrast, mannitol as well as other $OH{\cdot}$quenchers were ineffective in limiting oxygen radical-induced inactivation. Thus $O_{\bar{2}}{\cdot},\;H_2O_2$ and $^1O_2$ were implicated to be mediators involved in the inactivation. Since oxygen radicals are suspected as being a cause of the peroxidative damaging process in train ischemia, the ATPase inactivation by oxygen radicals may be a possible contributing factor which gives rise to functional derangement of nerve cells observed in the pathologic process.

• Korean Journal of Veterinary Research
• /
• v.39 no.5
• /
• pp.878-895
• /
• 1999

Ischemic preconditioing (IPC), i.e., a preliminary brief episode of ischemia and reperfusion, has been shown to reduce the cell damage induced by long ischemia and reperfusion. Superoxide radical which is produced during reperfusion after ischemia was recognized as a factor of the ischemic injury and it is dismutated into $H_2O_2$ and $O_2$ by two types of intracellular superoxide dismutase (SOD), Cu,Zn-SOD in cytoplasm and Mn-SOD in mitochondria. Recently oxygen free radicals are suggested to induce the apoptosis, however mechanism of the reduced apoptosis by ischemic preconditioing was unknown, while many studies performed in mammalian heart indicated that ATP-sensitive $K^+$ ($K_{APT}$) channel activation related with the protective effects. The aim of present study is to investigate 1) whether IP upregulate the Cu,Zn-SOD and Mn-SOD activities, and 2) whether ischemic preconditioning decreases apoptosis via $K_{APT}$ channel activation in timely reperfused skeletal muscle after long ishemia. The experimental animals, Sprague-Dawley rats weighing 250~300g, were divided into 8 groups; 1) control group, 2) ischemic preconditioning only groups, 3) pinacidil, a $K_{APT}$ channel opener, treatment only groups, 4) glibenclamide, a $K_{APT}$ channel blocker, treatment only groups, 5) ischemia groups, 6) ischemia after IPC groups, 7) ischemia and pinacidil treatment groups, and 8) IP and ischemia after glibenclamide pretreatment groups. Animals of the control group were administered with the vehicle (DMSO) alone. Pinacidil (1mg/kg) was administered intravenously 5 minutes after initiation of ischemia, and glibenclamide (0.5mg/kg) was injected intravenously 20 minutes before IPC. In rats that were ischemic preconditioned, the left common iliac artery was occluded for 5 minutes followed by 5 minutes of reperfusion by three times using vascular clamp. Ischemia was done by occlusion of the same artery for 4 hours. The specimens of left rectus femoris muscle were obtained immediately (0 hour), 12 hours, 24 hours after drug administrations, IP or ischemia and reperfusion. The immunoreactivities of SOD and its alterations were observed by use of sheep antihuman Cu,Zn-SOD and Mn-SOD antibodies on the $10{\mu}m$ cryosections. The incidencies of apoptosis were observed by TUNEL methods with in situ apoptosis detection kit on $6{\mu}m$ paraffine section. The results obtained were as follows : 1. After IPC, immunoreactivities of Cu,Zn-SOD mainly in the small-sized fibers were increased by 24 hours, that of Mn-SOD at 0 hour and 24 hours. 2. No significant changes in immunoreactivities of SOD was observed in the pinacidil and in the glibenclamide treatment only groups, and in the ischemia only groups. 3. The immunoreactivities of the Cu,Zn-SOD were increased in the ischemia after IPC groups and the ischemia and pinacidil treatment groups. 4. The immunoreactivities of the Cu,Zn-SOD in the IPC and ischemia after glibenclamide pretreatment groups were not increased except for the 12 hours reperfusion group. But, Mn-SOD immunoreactivities were increased in the 0 hours, 12 hours and 24 hours after reperfusion. 5. In the control group, the IPC only groups, and the pinacidil treatment only groups, negative or trace apoptotic reactions were observed, but the positive apoptotic reaction occured in the glibenclamide treatment groups. 6. Moderate or many number of apoptosis were revealed in the ischemia groups, and also the IPC and ischemia after glibenclamide pretreatment group except for 12 hours and 24 hours after reperfusion. However, the incidence of apoptosis was decreased in the ischemia after IPC groups and in the ischemia and pinacidil treatment groups. 7. There is a coincidence between the increase of Cu,Zn-SOD immunoreactivities and the decrease of apoptosis in the presence of ischemia and reperfusion. These results suggest that the protective effects of ishemic preconditioing may related to the SOD activation, and the ischemic preconditioning decreases the apoptosis partially via $K_{APT}$ channel activation in timely reperfused rat skeletal muscle. It is also suggested that inhibition of apoptosis by IPC may related with the SOD activation.

• Investigative Magnetic Resonance Imaging
• /
• v.7 no.2
• /
• pp.116-123
• /
• 2003

Purpose : The present study was undertaken to evaluate the usefulness of cerebral diffusion (DWI) and perfusion MR imaging (PWI) in rabbit models with hyperacute cerebral ischemic infarction. Materials and Methods : Experimental cerebral infarction were induced by direct injection of mixture of Histoacryl glue, lipiodol, and tungsten powder into the internal cerebral artery of 6 New-Zealand white rabbits, and they underwent conventional T1 and T2 weighted MR imaging, DWI, and PWI within 1 hour after the occlusion of internal cerebral artery. The PWI scan for each rabbit was obtained at the level of lateral ventricle and 1cm cranial to the basal ganglia. By postprocessing using special imaging software, perfusion images including cerebral blood volume (CBV), cerebral blood flow (CBF), and mean transit time (MTT) maps were obtained. The detection of infarcted lesion were evaluated on both perfusion maps and DWI. MTT difference time were measured in the perfusion defect lesion and symmetric contralateral normal cerebral hemisphere. Results : In all rabbits, there was no abnormal signal intensity on T2WI. But on DWI, abnormal high signal intensity, suggesting cerebral infarction, were detected in all rabbits. PWI (rCBV, CBF and MTT map) also showed perfusion defect in all rabbits. In four rabbits, the calculated square of perfusion defect in MTT map is larger than that of CBF map and in two rabbits, the calculated size of perfusion defect in MTT map and CBF map is same. Any rabbits do not show larger perfusion defect on CBF map than MTT map. In comparison between CBF map and DWI, 3 rabbits show larger square of lesion on CBF map than on DWI. The others shows same square of lesion on both technique. The size of lesion shown in 6 MTT map were larger than DWI. In three cases, the size of lesion shown in CBF map is equal to DWI. But these were smaller than MTT map. The calculated square of lesion in CBF map, equal to that of DWI and smaller than MTT map was three. And in one case, the calculated square of perfusion defect in MTT map was largest, and that of DWI was smallest. Conclusion : DWI and PWI may be useful in diagnosing hyperacute cerebral ischemic infarction and in e-valuating the cerebral hemodynamics in the rabbits.

• Journal of Chest Surgery
• /
• v.35 no.6
• /
• pp.407-419
• /
• 2002

Atherosclerosis is a chronic inflammatory disease of the arterial wall characterized by progressive accumulation of lipids, cells, and extracellular matrix. Matrix metalloproteinases(MMPs) and tissue inhibitor of metalloproteinases(TIMPS) contribute to vascular matrix remodeling in atherosclerosis, and some cytokines may play role in the synthesis or activation of MMPs or TIMPs. Material and Method： We produced experimental atherosclerotic plaques in 9 rabbits by atherogenic hypercholesterol diet for 12 weeks, and 10 other rabbits were used as control group with standard laboratory chow, At that time, 19 rabbits were sacrificed and aorta, coronary arteries and blood specimens were prepared. The expressions of MMP-9, TIMP-2 and interleukin(IL)-18, and the bioactivity of IL-6 were investigated with H&E stain, immunohistochemical stain, immunoblotting(Western blot analysis), and bioassay. Result： Serum cholesterol in the experimental group increased up to 1258$\pm$262 mg/dL(control group： 41$\pm$7 mg/dL). All experimental group showed well-developed atherosclerotic plaques in aorta and coronary artery. The expression of MMP-9 in aorta and coronary artery of the experimental group showed significant increase than that of the control group by immunohistochemistry. Among the experimental group, complicated lesions with intimal rupture or complete luminal occlusion, demonstrated stronger expression of MMP-9. Interestingly, there was no difference in expression of TIMP-2 between the experimental and the control group. These findings were confirmed by Western blot analysis. The bioassay revealed significant up-regulation of serum bioactivity of IL-6 in the experimental group(4819.60$\pm$2021.25 IU/$m\ell$) compared to that of IL-6 in the control group(27.20 $\pm$ 12.19 IU/$m\ell$). IL-18 was expressed in all atherosclerotic plaques, whereas little or no expression was detected in the control group. Conclusion： The increased MMP-9 expression along with the unchanged TIMP-2 expression seem to be contributory factors in extracellular matrix degradation in atherosclerosis. Focal overexpression of MMP-9 may promote plaque destabilization and cause complications of atherosclerotic plaques such as thrombosis with/without acute coronary syndrome. Elevation of IL-6 and IL-18 may be more than just markers of atherosclerosis but actual participants in lesion development. Identification of critical regulatory pathway is important to improve the understanding of the cellular and molecular basis of atherosclerosis and may open the way for novel therapeutic strategies.