• The Korean Journal of Pharmacology
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• v.30 no.3
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• pp.273-289
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• 1994

Reversible brain ischemia was produced by occluding both common carotid arteries for 5 min, and the effects of aminoguanidine (AG), $DL-{\alpha}-difluoromethylornithine$ (DFMO), MK-801, and nimodipine (NM) on the ischemia induced changes of the polyamine, glutamate and acetylcholine levels in the hippocampus CA1 subfield and the specific $[^3H]\;MK-801$ binding to the hippocampus synaptosomal membranes were studied with a histological reference of the cresyl violet stained hippocampus. The basal putrescine level $(PT:\;74.4{\pm}8.8\;nM)$ showed a rapid increase (up to 1.7 fold) for 5 min of ischemia, remained significantly increased for 6 h, and then resumed the further increase to amount gradually up to about 3 fold 96 h after recirculation. However, the level of spermidine was little changed, and the spermine level showed a transient increase during ischemia followed by a sustained decrease to about 40% of the preischemic level after recirculation. The increase of PT level induced by brain ischemia was enhanced with AG or MK-801, but it was reduced by DFMO or NM. The basal glutamate level $(GT:\;0.90{\pm}0.l4\;{\mu}M)$ rapidly increased to a peak level of $8.19{\pm}1.14\;{\mu}M$ within 5 min after onset of the ischemia and then decreased to the preischemic level in about 25 min after recirculation. And NM reduced the ischemia induced increase of GT level by about 25%, but AG, DFMO and MK-801 did not affect the GT increase. The basal acetylcholine level $(ACh:\;118.0{\pm}10.5\;{\mu}M)$ did little change during/after brain ischemia and was little affected by AG or NM. But DFMO and MK-801, respectively, produced the moderate decrease of ACh level. The specific $[^3H]\;MK-801$ binding to the hippocampus synaptosomal membrane was little affected by brain ischemia for 5 min. The control value (78.9 fmole/mg protein) was moderately decreased by AG and MK-801, respectively but was little changed by DFMO or NM. The microscopic findings of the brains extirpated on day 7 after ischemia showed severe neuronal damage of the hippocampus, particularly CA1 subfield. NM and AG moderately attenuated the delayed neuronal damage, and DFMO, on the contrary, aggravated the ischemia induced damage. However, MK-801 did not protect the hippocampus from ischemic damage. These results suggest that unlike to the mode of anti-ischemic action of NM, AG might protect the hippocampus from ischemic injury as being negatively regulatory on the N-methyl-D-aspartate (NMDA) receptor function in the hippocampus.

• YAKHAK HOEJI
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• v.43 no.2
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• pp.251-262
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• 1999

In order to investigate pharmacological properties of New Wonbang Woohwangchungsimwon Pill (NSCH) and Wonbang Woohwangchungsimwon Pill (SCH), the effects of NSCH and SCH on cerebral ischemia and central nervous system were compared. Cerebral ischemia insult was performed using unilateral carotid artery occlusion in mongolian gerbils. The histological observations showed preventive effects of NSCH and SCH treatments with ischemia-induced brain damage. The ATP in brain tissue was decreased in vehicle-treated ischemic gerbils. This decrease was prevented by SCH treatment. In contrast to what was inhibited by NSCH and SCH treatments. While NSCH and SCH had no effects on the hexobarbital-induced sleeping time, they prevented the seizures induced by electric shock and strychnine. NSCH and SCH showed sedative effect in rotarod and spontaneous activity test. Furthermore, NSCH and SCH showed anti-stress effect. Our findings suggest that the pharmacological profiles of NSCH on cerebral ischemia and central nervous system are similar to those of SCH.

• Proceedings of the PSK Conference
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• 2001.04a
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• pp.123.2-124
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• 2001

• Advances in Traditional Medicine
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• v.7 no.5
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• pp.564-568
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• 2008

The root of Polygala tenuifolia Willd (PT) is known to have neuroprotective effects and as an antidementic herb in Chinese and Japanese traditional medicine. We examined potential neuroprotective effects of PT using the 4-vessel occlusion model in rats. In this study, the efficacy of PT for the prevention of neuronal damage and for the reduction of memory impairment was investigated. The results indicate that PT confers significant neuroprotection especially for ischemic hippocampal neurons.

• Journal of Chest Surgery
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• v.28 no.12
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• pp.1113-1121
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• 1995

From August, 1986 to December, 1993, mitral valve replacement was performed in 178 patients. Of the valve implanted, 114 were St.Jude Medical, 47 Duromedics, 16 Carpenter-Edward and 1 Ionesc-Shiley. The hospital mortality rate was 2.8%[5 patients and the late mortality rate was 7.5%[13 patients . The causes of hospital death were LV rupture in 1, renal failure in 1, cardiac tamponade in 1, valve malfunction in 1 and hypoxic brain damage in 1. The causes of late death were sudden death in 6, congestive heart failure in 4, brain ischemic injury in 3. Follow-up was done on 155 surviving patients : mean follow-up period was 50.94$\pm$8.04 months. The actual survival rate was 88.2% at 8 years. We concluded, therefore, that good clinical results could be achieved with mitral valve replacement in mid-term follow-up, and long-term follow-up is also necessary.

• Journal of Medicine and Life Science
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• v.16 no.3
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• pp.55-59
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• 2019

Cerebral vessels are functionally and structurally specialized to provide adequate blood flow to brain which shows high metabolic rates. Cerebral hemorrhage or ischemic infarction due to cerebrovascular injury or occlusion can cause the immediate brain damage, and if not treated rapidly, can lead to serious or permanent brain damages, and sometimes life-threatening. Unlike these popular cerebrovascular diseases, there are diseases caused by genetic problems. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is one of them. CADASIL does not show the high incidence, but it is considered to be significantly affected by regional obstructiveness such as islands and therefore, to be an important genetic disease in Jeju. This paper aims to summarize the possibility of animal model research that can provide preclinical data for CADASIL disease research and to evaluate its applicability in future research plans.

• Biomolecules & Therapeutics
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• v.7 no.3
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• pp.234-241
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• 1999

The present study assessed the cerebroprotective effect of platelet-activating factor(PAF) antagonists in transient cerebral ischemia of rats. Right middle cerebral artery (MCA) of Sprague-Dawley rats was occluded for 2 hours using an intraluminal filament technique, and was reperfused for 6 hours following cerebral ischemia. The infarct area of seven coronal brain slices was measured morphometrically following stain ing in the 2% 2,3,5-triphenyltetrazolium chloride solution. The changes in regional cerebral blood flow (rCBF) and pial arteriolar diameter were measured by laser-Doppler flowmetry and by a videomicroscopy, respectively. The infarct size was significantly reduced by PAF antagonists, BN 52021 and CV-6209, which were administered i.p. 10 min before MCA occlusion. Pretreatment with PAF antagonists significantly restored the changes in pial arterial diameter as well as those in rCBF during the period of cerebral ischemia-reperfusion. PAF antagonists significantly inhibited the inducible nitric oxide synthase activity in the pial arteries ipsilateral to ischemia. These results suggest that PAF antagonists exert a cerebroprotective effect against ischemic brain damage through an improvement of postocclusive cerebral blood flow.

• Kidney Research and Clinical Practice
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• v.37 no.4
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• pp.315-322
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• 2018

The high mortality rates associated with acute kidney injury are mainly due to extra-renal complications that occur following distant-organ involvement. Damage to these organs, which is commonly referred to as multiple organ dysfunction syndrome, has more severe and persistent effects. The brain and its sub-structures, such as the hippocampus, are vulnerable organs that can be adversely affected. Acute kidney injury may be associated with numerous brain and hippocampal complications, as it may alter the permeability of the blood-brain barrier. Although the pathogenesis of acute uremic encephalopathy is poorly understood, some of the underlying mechanisms that may contribute to hippocampal involvement include the release of multiple inflammatory mediators that coincide with hippocampus inflammation and cytotoxicity, neurotransmitter derangement, transcriptional dysregulation, and changes in the expression of apoptotic genes. Impairment of brain function, especially of a structure that has vital activity in learning and memory and is very sensitive to renal ischemic injury, can ultimately lead to cognitive and functional complications in patients with acute kidney injury. The objective of this review was to assess these complications in the brain following acute kidney injury, with a focus on the hippocampus as a critical region for learning and memory.

• Annals of Clinical Neurophysiology
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• v.24 no.1
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• pp.30-34
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• 2022

In cases of hyponatremia induced by brain damage, it is important to distinguish between the syndrome of inappropriate anti-diuretic hormone secretion (SIADH) and cerebral salt wasting syndrome. A ventriculoperitoneal (VP) shunt is the standard treatment for hydrocephalus, and external lumbar drainage (ELD) is an option to evaluate the effect of a VP shunt. However, ELD has potential complications, such as subarachnoid hemorrhage, meningitis, and rarely hyponatremia. Therefore, we report a case of a patient with cerebral salt-wasting syndrome resulting from ELD to treat normal-pressure hydrocephalus during the rehabilitation of acute ischemic stroke.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.6
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• pp.673-679
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• 1997

It has been generally accepted that glutamate mediates the ischemic brain damage, excitotoxicity, and induces release of neurotransmitters, including norepinephrine(NE), in ischemic milieu. In the present study, the role of nitric oxide(NO) in the ischemia-induced $[^3H]norepinephrine([^3H]NE)$ release from cortex slices of the rat was examined. Ischemia, deprivation of oxygen and glucose from $Mg^{2+}-free$ artificial cerebrospinal fluid, induced significant release of $[^3H]NE$ from cortex slices. This ischemia-induced $[^3H]NE$ release was significantly attenuated by glutamatergic neurotransmission modifiers. $N^G-nitro-L-arginine$ methyl ester(L-NAME), $N^G-monomethyl-L-arginine$ (L-NMMA) or 7-nitroindazole, nitric oxide synthase inhibitors attenuated the ischemia-evoked $[^3H]NE$ release. Hemoglobin, a NO chelator, and 5, 5- dimethyl-L-pyrroline-N-oxide(DMPO), an electron spin trap, inhibited $[^3H]NE$ release dose-dependently. Ischemia-evoked $[^3H]NE$ release was inhibited by methylene blue, a soluble guanylate cyclase inhibitor, and potentiated by 8-bromo-cGMP, a cell permeable cGMP analog, zaprinast, a cGMP phosphodiesterase inhibitor, and S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide generator. These results suggest that the ischemia-evoked $[^3H]NE$ release is mediated by NMDA receptors, and activation of NO system is involved.