• Proceedings of the PSK Conference
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• 2003.10a
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• pp.104-105
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• 2003

Hypoxic-ischemic (H-I) encephalopathy in the prenatal and perinatal period is a major cause of morbidity and mortality and often results in cognitive impairment, seizures, and motor impairment (cerebral palsy). Many studies of neonatal H-I brain injury have utilized the well characterized Levine model in which unilateral carotid ligation is followed by exposure to hypoxia. (omitted)

• The Journal of Internal Korean Medicine
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• v.28 no.4
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• pp.863-871
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• 2007

Objects : To gain better insights of East-west integrated treatment of ischemic stroke. We analyzed 89 patients with severe acute ischemic stroke who were admitted to the East-west integrated intensive care unit. Methods : Subjects enrollment was from the East-west integrated intensive care unit of Kyung Hee Medical Center from March 2006 to February 2007. Patients were admitted within 14 days after the onset of ischemic stroke. We assessed the subjects' general characteristics, risk factors, admitting routes and periods, diagnostic imaging, process of western treatment and Korean traditional treatment, complication and consequence. Results : The proportion of males was 50.6%, of females 49.4%, average age was male 66.0$\pm$10.3 and female 71.1$\pm$10.5. Average length of hospital stays was 19.5 days. Monthly admissions were highest in November and December. The admission route was through emergency room (61.8%) or ward (34.8%). Mean Glasgow coma scale score was 10.0$\pm$2.5, average time from symptom of onset to hospital admission was 2.3$\pm$2.2 days. Dominant ischemic vascular territory was middle cerebral artery (66.3%). Initial western treatment was argatroban (22.5%), urokinase (28.1%), and heparinization (38.2%). Distribution of Sasang constitution of So-yang to Tae-eum to So-eum was equal to 5.4 to 2.9 to 1.5. Major complications were observed in 40 (42.7%) patients. In hospital mortality was 12.4% (11 deaths), all of them caused by aggravation of neurological deficit and only 3 of them with major complications. There appears to be a significant positive relationship between length of hospital stay and occurrence of complications (P<0.05). After discharge from the ICU, 64 (71.9%) patients were improved, 11 (12.4%) patients had expired, and 14 (15.8%) patients were transferred. Conclusions : From this study, we suggest that patients with severe acute ischemic stroke should be treated with East-west integrated therapy for more favorable consequences and decreased mortality.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.4
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• pp.818-824
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• 2009

This study aimed to evaluate the effect of purgation therapy with Natrii sulfas, a therapy for stroke patients with constipation in the oriental medicine, on the ischemic brain damage of the rats. The ischemic brain damage was induced by the middle cerebral artery occlusion (MCAO), Natrii sulafas was administered once after the MCAO. After 48 hours, expressions of Bax, Bcl-2, c-Fos, and HSP72 on the brain tissues were observed by immunohistochemistrical methods or technique. Purgation therapy with Natrii sulfas attenuated the excess of Bax expression caused by the ischemic brain damage. It was significant statistically in the penumbra of cerebral cortex, but not in the caudate putamen, of the MCAO rats. Purgation therapy with Natrii sulfas did not attenuate the excess of Bcl-2 expression caused by the ischemic brain damage. Purgation therapy with Natrii sulfas did not attenuate the excess of c-Fos expression caused by the ischemic brain damage. Purgation therapy with Natrii sulfas attenuated the excess of HSP72 expression caused by the ischemic brain damage. It was significant statistically in the penumbra of cerebral cortex, but not in the caudate putamen, of the MCAO rats. These results suggest that purgation therapy with Natrii sulfas has a neuroprotective effect on the ischemic brain damage and an anti-apoptotic effect.

• The Journal of Korean Medicine
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• v.30 no.5
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• pp.77-87
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• 2009

Objectives: This study aimed to evaluate the effect of purgation therapy with Natrii sulfas, an oriental medical therapy for stroke patients with constipation, on physiological indexes and the brain edema of rats. Methods: Brain edema was induced by the middle cerebral artery occlusion (MCAO); Natrii sulfas was administered once after the MCAO. At 3, 6, 15, 24, 48 hours after reperfusion, physiological indexes such as fecal weight, urine volume and water content in stool were assessed, and at 48 hours after reperfusion the edema index was measured. Results: 1. Purgation therapy with Natrii sulfas significantly improved the reduction of fecal weight caused by ischemic insult (P<0.05). 2. Purgation therapy with Natrii sulfas significantly improved the reduction of urine volume caused by ischemic insult (P<0.05). 3. Purgation therapy with Natrii sulfas significantly improved the reduction of water content in stool caused by ischemic insult (P<0.05). 4. Purgation therapy with Natrii sulfas did not improve the neurological symptom caused by ischemic insult. 5. Purgation therapy with Natrii sulfas did not attenuate the total infarct volume caused by ischemic insult. 6. Purgation therapy with Natrii sulfas attenuated the brain edema caused by ischemic insult (P<0.05). Conclusions: These results suggest that purgation therapy with Natrii sulfas improves some important symptoms and has a protective effect on the brain edema caused by ischemic insult.

• Journal of Chest Surgery
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• v.33 no.8
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• pp.605-612
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• 2000

Background: Ischemic preconditioning enhances the tolerance of myocardium against ischemia/reperfusion injury, with the enhancement of the recovery of post-ischemic myocardial function. This study was disigned to assess whether the protective effect of ischemic preconditioning could provide one additional hour of myocardial preservation in four hour myocardial ischemia in a rate heart. Material and method: Fourty four Spargue-Dawley rats, weighing 300~450gm, were divided into four groups. Group 1(n=7) and group 3(n=12) were subjected to 30 minutes of aerobic Langendorff perfusion without ischemic preconditioning and then preserved in saline solution at 2~4$^{\circ}C$ for 4 hours and 5 respectively. Group 2(n=7) and group 4(n=18) were perfused in the same way for 20 minutes, followed by 3 minutes of global mormothermic ischemia and 10 minutes of perfusion and then preserved in the same cold saline solution for 4 hours and 5 hours respectively. Heart rate, left ventricular developed pressure(LVDP), and coronary flow were measured at 15 minutes during perfusion as baseline. Spontaneous defibrillation time was measured after reperfusion. Heart rate, LVDP, and coronary flow were also recorded at 15 minutes, 30 minutes, and 45 minutes during reperfusion. Samples of the apical left ventricular wall were studied using a transmission electron microscope. Result: Time of spontaneous defibrillation(TSD) was significantly longer in group 4 than in group 1(p<0.001), and TSD in group 1 was significantly longer in comparision to that of group 2(p<0.05). Heart rate at 45 minutes was significantly higher in group 1 than in group 4(p<0.05). Heart rate at 15 min was significantly higher in group 2 than in group 1(p<0.001) and in group 4 than in group 3(p<0.05). Left ventricular developed pressure(LVDP) at 30 minutes and 45 minutes was higher in group 1 than in group 4(p<0.01), LVDP at 45 minutes was higher in group 4 than in group 3(p<0.05). Rate-pressure product(RPP) at 30 minutes and 45 minutes was higher in group 1 than in group 4(p<0.05). RPP at 15 minutes was higher in group 2 than in group 1(p<0.01). RPP at 30 minutes and 45 minutes was higher in group 4 than in group 3(p<0.05). Group 2 showed relatively less sarcoplasmic edema and less nuclear chromatin clearance than group 1. Group 4 showed less myocardial cell damage than group 3, group 4 showed less myocardial cell damage than group 3, group 4 showed more myocardial cell edema than group 1. Conclusion: Ischemic preconditioning enhanced the recovery of postischemic myocardial function after 4 hours and 5 hours preservation. However, it was not demonstrated that ischemic preconditioning could definitely provide one additional hour of myocardial preservation in four hour myocardial ischemia in a rat heart.

• Archives of Pharmacal Research
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• v.25 no.5
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• pp.697-703
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• 2002

We investigated that the role of nitric oxide (NO) on ischemic rats in brain and heart. Ischemia was induced by both common carotid arteries (CCA) occlusion for 24h following reperfusion. Then tissue samples were removed and measured NOx. In brain, NOx was increased by about 40% vs. normal and it was significantly inhibited by aminoguanidine, selective iNOS inhibitor. This result showed that NOx concentration was increased by iNOS. We investigated the role of $Ca^{2+}$ during ischemia. Nimodipine, L-type calcium channel blocker, didn't inhibit the increases of NOx concentration during ischemia. It suggested that increased NOx was due to calcium-independent NOS. MK-801, which N-methyl-D-aspartate (NMDA) receptor antagonist, didn't significantly prevent the increases of NOx. In heart, ischemia caused NOx decrease and it is inconsistent with NOx increase in brain. Aminoguanidine and nimodipine didnt affect on NOx decrease. But MK-801 more lowered NOx concentration than those of ischemia control group. It seemed that $Ca^{2+}$ influx in heart partially occurred via NMDA receptor and inhibited by NMDA receptor antagonist. The mean arterial pressure (MAP) in ischemic rats after 24h of CCA occlusion was decreased when compared to normal value, whereas the heart rates (HR) was not different between two groups. Aminoguanidine or MK801 had no effect on MAP or HR, but nimodipine reduced MAP. There was no difference the effects of aminoguanidine, nimodipine, or MK-801, on MAP and HR between normal rats and ischemic rats. In summary, ischemic model caused an increase of NOx concentration, suggesting that this may be produced via iNOS, which is calcium independent in brain. However in heart, ischemia decreased NOx concentration and NMDA receptor was partially involved. The basal MAP was decreased in ischemic rats but HR was not different from normal control, suggesting that increased NOx in brain of ischemic rat may result in the hypotension.

• Korean Journal of Clinical Laboratory Science
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• v.54 no.4
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• pp.256-264
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• 2022

Ischemic stroke is caused by an occlusion by a thrombus or embolus in a cerebral artery, preventing oxygenated blood from reaching the brain and causing the necrosis of nerve cells. This paper summarizes the serum candidate markers associated with cardiovascular disease and atrial fibrillation (AF) disease that enable an early diagnosis of ischemic stroke studied thus far and compares the odds ratio (OR) of each marker. This study examined the effect size of these serum candidate markers using meta-analysis techniques. The academic database search screening for articles containing the keywords "cardiovascular disease," "atrial fibrillation," "ischemic stroke," and "serum marker" was limited to results for patients with ischemic stroke. The most derived markers in this study were N-terminal pro-B-type natriuretic peptide (NT-pro-BNP), D-dimer, C-reactive protein (CRP), and glial fibrillary acidic protein (GFAP), the rest being investigated individually. In conclusion, NT-pro-BNP appears to be very useful for the early diagnosis of ischemic stroke. Primarily, it is a marker of AF, and more AF markers will be uncovered and studied in the future.

• YAKHAK HOEJI
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• v.38 no.1
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• pp.57-66
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• 1994

We studied the effect of eicosanoids on the content of energy metabolites and the intrasynaptosomal $Ca^{++}([Ca^{++}]_i)$ concentration in cerebral ischemic rats. An ischemic model was made by bilateral carotid artery ligation (BCAL) and by incubation of synaptosomes under aglycemic and $N_2$ gas bubbling condition. The content of ATP, creatine phosphate and glucose decreased at 15 minutes after BCAL while that of lactate increased in male Wistar rats. Oral administration of EPA(100 mg/ml/Kg/day) or DHA(16 mg/ml/Kg/day) for 6 weeks improved both the decreases and the increase of the cerebral energy metabolites. In addition, the increase of $[Ca^{++}]_i$, under BACL was suppressed by EPA or DHA treatment. When the both Wistar rats and SHR were administered orally with EPA or DHA for 6 weeks, the effect on the increase of $[Ca^{++}]_i$ under ischemia by $N_2$ gas bubbling were protected. From these results, it may be that EPA or DHA treatment were greatly contributed to preservation of ischemic cerebral energy metabolism and $Ca^{++}$ concentration.

• Biomolecules & Therapeutics
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• v.17 no.3
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• pp.270-275
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• 2009

Polyethylene glycol-conjugated hemoglobin (PEG-Hb) has been proposed as a blood substitute for transfusion due to their plasma expansion and oxygen transport capabilities. The protective effect of PEG-Hb on cerebral hypoxic-ischemic injury was investigated in neonatal hypoxia model and adult rat focal cerebral ischemia model. As intravenously administered 30 min before the onset of hypoxia, PEG-Hb markedly protected cerebral hypoxic injury in a neonatal rat hypoxia model. A similar treatment of PEG-Hb largely reduced the ischemic injury ensuing after 2-h middle cerebral artery occlusion followed by 22-h reperfusion. Consistently, neurological disorder was significantly improved by PEG-Hb. The results indicate that the pharmacological blockade of cerebral ischemic injury by using PEG-Hb may provide a useful strategy for the treatment of cerebral stroke.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.1
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• pp.101-110
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• 2018

In this study, we aimed to investigate the neuroprotective effects of caffeic acid phenethyl ester (CAPE), an active component of propolis purified from honeybee hives, on photothrombotic cortical ischemic injury in mice. Permanent focal ischemia was achieved in the medial frontal and somatosensory cortices of anesthetized male C57BL/6 mice by irradiation of the skull with cold light laser in combination with systemic administration of rose bengal. The animals were treated with CAPE (0.5-5 mg/kg, i.p.) twice 1 and 6 h after ischemic insult. CAPE significantly reduced the infarct size as well as the expression of tumor necrosis $factor-{\alpha}$, hypoxiainducible $factor-1{\alpha}$ monocyte chemoattractant protein-1, $interleukin-1{\alpha}$, and indoleamine 2,3-dioxygenase in the cerebral cortex ipsilateral to the photothrombosis. Moreover, it induced an increase in heme oxygenase-1 immunoreactivity and interleukin-10 expression. These results suggest that CAPE exerts a remarkable neuroprotective effect on ischemic brain injury via its anti-inflammatory properties, thereby providing a benefit to the therapy of cerebral infarction.