• Journal of Acupuncture Research
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• v.20 no.2
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• pp.173-183
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• 2003

이 논문(論文)은 활성 산소(ROS)의 작용(作用)을 규명하고 호도약침액(胡桃藥鍼液)이 인간의 신경교종 세포인 A172에서 화학적(化學的) 저산소증(低酸素症)으로 유발된 세포 사멸에 대해 효능이 있는지를 연구(硏究)한 것이다. 화학적(化學的) 저산소증(低酸素症)은 세포내 미토콘드리아의 전자 수송을 방해하는 antimycin A를 가진 배양세포에 의해 유발(誘發)하였다. 화학적(化學的) 저산소증(低酸素症)에 노출된 세포(細胞)는 시간과 그 양에 따라서 세포 사멸의 결과(結果)가 다르게 나타난다. 화학적 저산소증에 의해서 ROS의 생산이 증가하는데 이것은 $H_2O_2$ 소거(消去) Catalase(과산화수소를 물과 산소로 분해하는 효소)에 의해 방지(防止)된다. Catalase는 화학적 저산소증에 의해 유발(誘發)된 세포 사멸을 방지하는데 비해 DMTU는 효과적이지 않다. 지질(脂質)에 녹는 산화방지제 DPPD와 물에 녹는 산화방지제 Trolox는 세포사멸을 방지하는데 효과(效果)가 없다. 호도약침액(胡桃藥鍼液)은 그 양(量)에 의존적으로 저산소증에 의해 유발된 세포 사멸을 방지하는 효과가 있다. 즉 화학적 저산소증으로 유도된 ROS의 발생을 막고, $H_2O_2$로 유도된 세포사멸을 방지하는데 이것은 화학적 저산소증과 $H_2O_2$의해 유도된 세포사멸에 대해 호도약침액(胡桃藥鍼液)이 방지효과(防止效果)가 있다는 것을 의미한다. 이러한 결과(結果)들은 $H_2O_2$가 지질 과산화와는 무관한 메카니즘으로 저산소증(低酸素症)으로 유발(誘發)된 세포사멸을 중재하고, 따라서 호도약침액(胡桃藥鍼液)은 지질막의 과산화를 방지하기 보다는 ROS를 직접적으로 소거(消去)함으로써 방지 효과가 있다는 것을 의미한다. 더구나 화학적(化學的) 저산소증(低酸素症)은 caspase와 무관한 메카니즘으로 apoptosis를 유발(誘發)한다.

• Journal of Chest Surgery
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• v.42 no.5
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• pp.588-596
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• 2009

Background: To clarify the effect of hypoxia on vascular contractility, we tried to show whether hypoxia induced the release of endothelium-derived relaxing factor (EDRF) and the nature of the underlying mechanism for this release. Material and Method: Isometric contractions were observed in rabbit aorta, and the released EDRF from the rabbit aorta was bioassayed by using rabbit denuded carotid artery. The intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) in the cultured rabbit aortic endothelial cells was recorded by a microfluorimeter with using Fura-2/AM. Hypoxia was evoked to the blood vessels or endothelial cells by eliminating the $O_2$ in the aerating gases in the external solution. Chemical hypoxia was evoked by applying deoxyglucose or $CN^-$. Result: Hypoxia relaxed the precontracted rabbit thoracic aorta that had its endothelium, and the magnitude of the relaxation was gradually increased by repetitive bouts of hypoxia. In contrast, hypoxia-induced relaxation was not evoked in the aorta that was denuded of endothelium. In a bioassay experiment, hypoxia released endothelium-derived relaxing factor (EDRF) and the release was inhibited by L-NAME or the $K^+$ channel blocker tetraethylammonium (TEA). In the cultured endothelial cells, hypoxia augmented the ATP-induced increase of the intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) and this increase was inhibited by TEA. Furthermore, chemical hypoxia also increased the $Ca^{2+}$ influx. Conclusion: From these results, it can be concluded that hypoxia might induce the release of NO from rabbit aortic endothelial cells by increasing $[[Ca^{2+}]_i$.

• Journal of Life Science
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• v.19 no.5
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• pp.598-606
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• 2009

Oxidative stress by free radicals is a major cause of neuronal cell death. Excitotoxicity in hypoxia/ischemia causes an increase in reactive oxygen species (ROS) and a loss of mitochondrial membrane potential (MMP), resulting in dysfunction of the mitochondria and cell death. Pinelliae Rhizoma (PR) is a traditional medicine for incipient stroke. We investigated the effects of PR Water-Extract on the modulation of ROS and MMP in a hypoxic model using cultured rat cortical cells. PR Water-Extract was added to the culture medium at various concentrations (0.25${\sim}$5, 5.0 ${\mu}g/ml$) on day in vitro 12(DIV12), given a hypoxic shock (2% $O_2$/5% $CO_2$, $37^{\circ}C$, 3 hr), and cell viability was assessed on DIV15 by Lactate Dehydrogenase Assay (LDH assays). PR Water-Extract showed a statistically significant effect on neuroprotection (10${\sim}$15% increase in viability; p<0.01) at 1.0 and 2.5 ${\mu}g/ml$ in normoxia and hypoxia. Measurement of ROS production by $H_2DCF-DA$ stainings showed that PR Water-Extract efficiently reduced the number and intensity of ROS-producing neurons, especially at 1 hr post shock and DIV15. When MMP was measured by JC-1 stainings, PR Water-Extract efficiently maintained high-energy charged mitochondria. These results indicate that PR Water-Extract protects neurons in hypoxia by preventing ROS production and preserving the cellular energy level.

• Clinical and Experimental Pediatrics
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• v.45 no.9
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• pp.1106-1113
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• 2002

Purpose : Nuclear ($factor-{\kappa}BNF-{\kappa}B$) is now recognized as playing a potential role in programmed cell death and the adaptive response to various stress. Cellular hypoxia is a primary manifestation of many cardiovascular diseases. It seems that vascular endothelial growth factor (VEGF) and insulin like growth factor-I(IGF-I) have a function as a protective molecule in the heart against several stress including hypoxia. In this study, the role of $NF-{\kappa}B$ to the cellular response and regulation of protective molecules against the acute hypoxia in the heart was studied. Methods : To cause acute hypoxic stress to the heart, Sprague Dawley rats were exposed to hypoxic chamer($N_2$ 92% and $O_2$ 8%). After the hypoxic exposure, nuclear proteins, total proteins and mRNA were isolated from heart. Translocation of the transcription factors $NF-{\kappa}B$, NF-ATc, AP-1 and NKX-2.5 were evaluated by electrophoretic mobility shift assay(EMSA). The expression of IGF-I and VEGF were studied before and after the hypoxic stress by competitive-PCR, Northern hybridization and Western hybridization. To confirm the role of the $NF-{\kappa}B$ in the heart, the rats also were pretreated with diethyl-dithiocarbamic acid(DDTC) into peritoneal cavity to block $NF-{\kappa}B$ translocation into nucleus. Results : The expression of $NF-{\kappa}B$, AP-1 and NF-ATc were increased by the hypoxic stress. Increased expression of the VEGF and IGF-I were also observed by the hypoxic stress. However, the blocking of the $NF-{\kappa}B$ translocation reduced those expressions of VEGF and IGF-I. Conclusion : These results suggest that $NF-{\kappa}B$ has a protective role against the acute hypoxia through several gene expression, especially VEGF and IGF-I in heart muscle.

• The Journal of Internal Korean Medicine
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• v.22 no.4
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• pp.537-546
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• 2001

목적: 고양이 대뇌피질 절편을 사용하여 저산소 발작을 유발한 뒤, 성향정기산이 세포의 이온 환경과 대사의 변화와 관련하여 어떤 영향을 미치는지 연구하였다. 방법: 고양이의 대뇌 피질 절편에 저산소 발작을 유발한 뒤 flame photometry scintillation, Spectrophotometry, method of Jorgensen and Skou, method of Fiske and Subbarow, oxygen monitor, luciferin-luciferase assay 등을 이용하여 세포내 이온함량과 세포대사를 측정하였다. 결과: 성향정기산은 저산소증으로 유발된 세포내의 $K^+$와 $Na^+$의 함량의 변화를 현저하게 지연시켰다. 성향정기산은 Na-K-ATPase의 억제제인 와바인 또는 대사억제제인 2.4-DNP로 유발된 세포내 $K^+$함량의 변화에 어떤 효과도 보이지 않았다. 또한, 정상 상태의 절편뿐만 아니라 저산소 상태의 절편에서 분리된 과립체의 분설에 있어서 Na-K-ATPase의 활동도에 영향을 미치지 않았다. 성향정기산은 저산소 발작하에서 산소 소비량과 세포의 ATP함량이 떨어지는 것을 현저하게 막았다. 또한 ATP를 생산하는 기능을 보호하는 저산소 조직의 사립체를 돕는데 효과적이었다. 결론: 성향정기산은 대뇌 조직의 저산소 발작하에서 세포의 이온 환경과 대사를 보호하는 유익한 효과가 있음을 알 수 있다.

• Journal of Biomedical Engineering Research
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• v.23 no.4
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• pp.295-300
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• 2002

Localized hypoxia, due to the diminished $O_2$supply, is reported to cause necrosis of the arterial cell and to significantly decrease resistances to physiologic distending pressures. In the present study, in order to understand the mechanism of localized hypoxia which might result in the rupture of the aneurysm. $O_2$ transport phenomena across intraluminal thrombus in axisymmetric aneurysms under steady laminar flow condition were numerically analyzed using the Fick's law and the analogy with the fluid-solid heat transfer. For computational models, varying the thickness of intraluminal thrombus, numerical results showed that for the axisymmetric aneurysm with intraluminal thrombus. $O_2$ concentration became minimal at the aneurysm wall. With increased thickness of the intraluminal thrombus in the aneurysm. regions of low $O_2$ concentration were widely distributed near the aneurysm wall, which resulted in the possibility of localized hypoxia. The present study verifis that intraluminal thrombus influences $O_2$ transport to the aneurysm wall. depending on its size and structure.

• Journal of the korean academy of Pediatric Dentistry
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• v.28 no.3
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• pp.337-344
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• 2001

The combination of chloral hydrate and hydroxyzine is one of the safest and most commonly used drug regimens for sedating young, uncooperative pediatric dental patients. The continuous monitoring of respiratory function and early recognition of respiratory difficulties are essential for the successful management of sedated dental patients. The purpose of this study was to evaluate the success rate of the sedation and the hypoxia through monitoring the oxygen desaturation in the pulse oximeter in pediatric dental patients sedated with 60mg/kg chloral hydrate and 25mg hydroxyzine. The following results were obtained : 1. The success rate of the sedation was 69.6% and there was no statistically significant difference among the groups based on the ages, weight and duration of the operative time. 2. Forty two percentage of the sedated patients showed the temporary hypoxia state and there was no statistically significant difference based on the ages and weights of the patients. But there was a statistically significant difference on the duration of the operative time.

• Neonatal Medicine
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• v.18 no.2
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• pp.320-327
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• 2011

Purpose: To determine the effect of changing practice guidelines designed to avoid hyperoxia or hypoxia in very low birth weight or very preterm infants. Methods: We analyzed a database of <1,500 g birth weight or <32 weeks of gestation infants who were born and admitted to the neonatal intensive care unit of Chungnam National University Hospital from January 2007 to July 2010. First, we defined the relationship between arterial partial pressure of oxygen ($PaO_2$) and pulse oxygen saturation ($SpO_2$). When we evaluated 96 pairs of $PaO_2$ and $SpO_2$ measurements, oxygen saturation was 90-94% at a $PaO_2$ of 43-79 mmHg on the oxyhemoglobin dissociation curve, according to pulse oximetry. Based on this observation, a change in practice was instituted in August 2008 with the objective of avoiding hypoxia and hyperoxia in preterm infants with targeting a $SpO_2$ 90-94% (period II). Before the change in practice, high alarms for $SpO_2$ were set at 100% and low alarms at 95% (period I). Results: Sixty-eight infants the met enrollment criteria and 38 (56%) were born during period II, after the change in $SpO_2$ targets. Demographic characteristics, except gender, were similar between the infants born in both periods. After correcting for the effect of confounding factors, the rates for mortality, severe retinopathy of prematurity, and IVH attended to be lower than those for infants in period II. No difference in the rate of patent ductus arteriosus needed to treat was observed. Conclusion: A change in the practice guidelines aimed at avoiding low oxygen saturation and hyperoxia did not increase neonatal complication rates and showed promising results, suggesting decreased mortality and improvements in short term morbidity. It is still unclear what range of oxygen saturation is appropriate for very preterm infants but the more careful saturation targeting guideline should be considered to prevent hypoxemic events and hyperoxia.

• Tuberculosis and Respiratory Diseases
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• v.41 no.5
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• pp.504-512
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• 1994

Background: It is well known that severe hypoxemia is often associated with liver cirrhosis without preexisting cardiac or pulmonary diseases. Pulmonary vascular impairments, more specifically, intrapulmonary shunting have been considered as a major mechanism. Intrapulmonary shunting arises from pulmonary vascular dilatation at the precapillary level or direct arteriovenous communication and has relationship with the characteristic skin findings of spider angioma. However, these results are mainly from Western countries where alcoholic and primary biliary cirrhosis are dominant cuases of cirrhosis. It is uncertain that the same is true in viral hepatitiss associated liver cirrhosis, which is dominant causes of liver cirrhosis in Korea. We investigated the incidences of hypoxemia and orthodeoxia in Korean cirrhotic patients dominantly composed of postnecrotic cirrhosis and the significance of intrapulmonary shunting as the suggested mechanism of hypoxemia, Method: We performed the arterial blood gas analysis separately both at the supine and errect position in 48 stable cirrhotic patients without the evidences of severe complications such as ascites, variceal bleeding, and hepatic coma. According to the results of arterial blood gas analysis, all patients were divided into hypoxemic and normoxemic group. In each group, pulmonary function test and Tc-99m-MAA whole body scan were performed. The shunting fraction was calculated based on the fact that the sum of cerebral and bilateral renal blood flow is 32% of the systemic blood flow. Results: The hypoxemia of $PaO_2$ less than 80 mmHg was observed in 9 patients(18.8%) and Orthodeoxia more than 10 mmHg was observed in 8 patients(16.7%). But there was no patient with significant hypoxemia of $PaO_2$ less than 60 mmHg. $PaO_2$ was significantly decreased in the patients with spider angioma than the pathients without spider angioma and showed no correlation with the serologic type and severities of liver function test findings. Any parameters of pulmonary function test did not demonstrate the difference between normoxemic and hypoxemic group. But hypoxemic group showed significantly increased shunt fraction of $11.4{\pm}4.1%$ than normoxemic group of $4.1{\pm}2.0%$ (p<0.05). Conclusions: Hypoxemia is not infrequently observed complication in liver cirrhosis and intrapulmonary shunting is suggested to p1ay a major ro1e in the development of hypxemia. But there was no great likelihood of clinically significant hypoxemia in our domestic cirrhotic patients predominantly composed of postnecrotic type.

• The Korea Swine Journal
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• v.30 no.2 s.342
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• pp.217-221
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• 2008