• 제목/요약/키워드: Reperfusion Injury

검색결과 329건 처리시간 0.025초

황기와 원지분획의 뇌허혈에 관한 약효연구 (Effects of Astragali Radix and Polygalae Radix on Cerebral Ischemic and Reperfused Injury)

  • 한석희;박진혁;김진숙;이선미
    • 약학회지
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    • 제44권4호
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    • pp.371-377
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    • 2000
  • In order to investigate the pharmacological properties of fractions of Astragali Radix and Polygalae Radix, the effects of the fractions on cerebral ischemia and subsequent reperfusion were studied. Brain ischemia was induced by bilateral common carotid artery occlusion in mongolian gerbil. Brains were recirculated for 30 mins after the 20 min occlusion. Methanol and butanol fractions of Astragali Radix and Polygalae Radix were administered orally 2 hrs before common carotid artery occlusion. Histological observations showed that brain ischemia induced severe brain damage evidenced by the presence of necrotic foci, edema and hemorrhage. This injury was prevented by the methanol fraction and butanol fraction of Polygalae Radix. The level of ATP in brain tissue significantly decreased in ischemic gerbils. This decrease was prevented by the pretreatment with butanol fraction of Polygalae Radix. In contrast, the levels of lactate and lipid peroxide were both elevated in ischemic gerbils. This elevation was inhibited by the pretreatments with methanol fraction and butanol fraction of Polygalae Radix. Our findings suggest that the Polygalae Radix improves ischemia-induced brain damage.

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항산화력이 우수한 Fructose 1,6-diphosphate(FDP)를 피부적용제로 응용하기 위한 안전성 평가 (The Safety Evaluation of a Potent Antioxidant, Fructose 1,6-diphosphate(FDP), for the Skin Application)

  • 김배환;이병석;정경미;안수미;안수선;심영철
    • Toxicological Research
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    • 제18권3호
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    • pp.267-273
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    • 2002
  • Fructose 1,6-diphosphate(FDP), a glycolytic metabolite, is reported to ameliorate inflammation and inhibit the nitric oxide production in murine macrophages stimulated with endotoxin. It is also reported that FDP has cytoprotective effects against hypoxia or ischemia/reperfusion injury in brain and heart, and may play a protective role in ultraviolet B (UVB, 280~320 nm)-injured keratinocyte by attenuating prostaglandin (PG)-E$_2$production and cyclooxygenase (COX)-2 expression, which are possibly through blocking the intracellular reactive oxygen species (ROS) accumulation. Therefore FDP is considered to act as a potent antioxidant especially in the skin. We conducted the several safety tests (single-dose toxicity, primary skin irritation test, eye irritation test, skin sensitization test, phototoxicity test, photosenitization test and human patch test) to see if FDP is safe in case used for the skin application. Our data obtained hitherto suggest that FDP is very safe if applied to the skin.

이식을 위한 심장의 장시간 보존에 관한 실험 (Experimental Studies on the Cold Storage of the Rabbit Heart for Transplantation)

  • 노중기;이철세;이길노
    • Journal of Chest Surgery
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    • 제22권6호
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    • pp.887-893
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    • 1989
  • Donor availability is a major limiting factor in heart transplantation. Prolonging donor heart preservation would facilitate distant heart procurement. The setup used was the isolated retrograde perfused nonworking rabbit heart model and 4 hours of preservation at 2oC. And the electron microscopic findings of the myocardium were evaluated after reperfusion for 5 minutes. The following three groups [each group, n=4] were prepared: Group I: the heart was arrested with the St. Thomas Hospital solution [STH] and stored in Ringers lactate solution [RLS]; Group II: the heart was arrested with STH and stored in Modified Collins-Sachs solution [MCS]; Group g: the heart was arrested with and stored in MCS. The result was the most severe myocardial injury in the Group III on electron microscopic study.

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Synthesis and Biological Evaluation of 4-Heteroaryl-2-amino-5-methylimidazole Analogs as NHE-1 Inhibitors

  • Lee, Sun-Kyung;Yi, Kyu-Yang;Lee, Byung-Ho;Yoon, Boo-Soon
    • Bulletin of the Korean Chemical Society
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    • 제30권11호
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    • pp.2621-2625
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    • 2009
  • To identify a non-acylguanidine NHE-1 inhibitor, an acylguanidne group was replaced with an imidazole group in the potent NHE-1 inhibitors with furan or benzothiphene core template, found from our previous studies. We synthesized and biologically evaluated 4-heteroaryl-2-amino-5-methylimidazole derivatives. All those imidazole compounds (16-18) represented the potent NHE-1 inhibitory activities, similar to the corresponding acylguanidine compounds.

Critical Care after Lung Transplantation

  • Kim, Song Yee;Jeong, Su Jin;Lee, Jin Gu;Park, Moo Suk;Paik, Hyo Chae;Na, Sungwon;Kim, Jeongmin
    • Acute and Critical Care
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    • 제33권4호
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    • pp.206-215
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    • 2018
  • Since the first successful lung transplantation in 1983, there have been many advances in the field. Nevertheless, the latest data from the International Society for Heart and Lung Transplantation revealed that the risk of death from transplantation is 9%. Various aspects of postoperative management, including mechanical ventilation, could affect intensive care unit stay, hospital stay, and immediate postoperative morbidity and mortality. Complications such as reperfusion injury, graft rejection, infection, and dehiscence of anastomosis increase fatal adverse side effects immediately after surgery. In this article, we review the possible immediate complications after lung transplantation and summarize current knowledge on prevention and treatment.

Neuroprotective Effect of Polygae Radix on the Brain Ischemia Induced by Four- Vessel Occlusion in Rats

  • Kim, Young-Ock;Lee, Hyun-Sun;Lee, Young-Ah;Shin, Joon-Shik;An, Deuk-Kyun;Kim, Ho-Chol
    • 대한약학회:학술대회논문집
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    • 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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    • pp.148.1-148.1
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    • 2003
  • The effects of methanolic extracts of Polygalae Radix (PR 100mg/kg) was tested to evaluate on the neuroprotective activity (92% p<0.001) on global cerebral schemia. Based on bioassays guided fractionation, butanol soluble fraction (BtOH 25mg/kg) had the neuroprotive effect (87% p<0.001) of global cerebral ischemia in rat. Oxygen free radical injury plays an important role in neuronal damage induced by brain ischemia and reperfusion. (omitted)

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Whole body hypoxic preconditioning-mediated multiorgan protection in db/db mice via nitric oxide-BDNF-GSK-3β-Nrf2 signaling pathway

  • Li, Yuefang;Huang, Yan;Cheng, Xi;He, Youjun;Hu, Xin
    • The Korean Journal of Physiology and Pharmacology
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    • 제25권4호
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    • pp.281-296
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    • 2021
  • The beneficial effects of hypoxic preconditioning are abolished in the diabetes. The present study was designed to investigate the protective effects and mechanisms of repeated episodes of whole body hypoxic preconditioning (WBHP) in db/db mice. The protective effects of preconditioning were explored on diabetes-induced vascular dysfunction, cognitive impairment and ischemia-reperfusion (IR)-induced increase in myocardial injury. Sixteen-week old db/db (diabetic) and C57BL/6 (non-diabetic) mice were employed. There was a significant impairment in cognitive function (Morris Water Maze test), endothelial function (acetylcholine-induced relaxation in aortic rings) and a significant increase in IR-induced heart injury (Langendorff apparatus) in db/db mice. WBHP stimulus was given by exposing mice to four alternate cycles of low (8%) and normal air O2 for 10 min each. A single episode of WBHP failed to produce protection; however, two and three episodes of WBHP significantly produced beneficial effects on the heart, brain and blood vessels. There was a significant increase in the levels of brain-derived neurotrophic factor (BDNF) and nitric oxide (NO) in response to 3 episodes of WBHP. Moreover, pretreatment with the BDNF receptor, TrkB antagonist (ANA-12) and NO synthase inhibitor (L-NAME) attenuated the protective effects imparted by three episodes of WBHP. These pharmacological agents abolished WBHP-induced restoration of p-GSK-3β/GSK-3β ratio and Nrf2 levels in IR-subjected hearts. It is concluded that repeated episodes of WHBP attenuate cognitive impairment, vascular dysfunction and enhancement in IR-induced myocardial injury in diabetic mice be due to increase in NO and BDNF levels that may eventually activate GSK-3β and Nrf2 signaling pathway to confer protection.

Effect of Ischemic Preconditioning on the Oxygen Free Radical Production in the Post-ischemic Reperfused Heart

  • 박종완;김영훈;엄창섭;배재문;박찬웅;김명석
    • 대한약리학회지
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    • 제30권3호
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    • pp.321-330
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    • 1994
  • 허혈전처치(ischemic preconditioning)의 재관류심근손상 보호작용과 그 기전을 규명하기 위한 연구의 일환으로 허혈전처치가 심근세포의 산소라디칼 생성능력에 미치는 영향을 검토하였다. 흰쥐 적출심장의 Langendorff 관류표본에서 실험적인 허혈(30분)-재관류(20분)손상을 유도하였고, 허혈전처치는 재관류손상 유도전에 5분 허혈-5분 재관류를 3회 반복하여 시행하였다. 허혈심근 재관류손상의 지표로 심수축기능, 세포질효소 유출, 칼슘 유입 및 미세형태학적 변화를, 그리고 심근세포의 산소라디칼 생성기전으로 xanthine oxidase system의 변동을 허혈전처치와 비전처치 재관류 심장들에서 비교검토하였다. 연구 성적은 다음과 같다. 1. 허혈전처치는 허혈-재관류 심장의 관상혈류량, 심박수, 좌심실압 등 심기능의 저하를 현저히 회복시켰다(회복률; 91%) 2. 허혈-재관류 심장에서 lactate dehydrogenase 유출증가는 허혈전처치에 의해 현저히 저하되었다. 3. 허혈-재관류 심근세포의 전자현미경상 미세구조는 허혈전처치시 비교적 잘 보존되었으며, 특히 myofibril 구조의 보존이 매우 뚜렷하였다. 4. 허혈-재관류시 산화성 조직손상 척도의 하나인 malondialdehyde 생성이 허혈전처치에 의하여 현저히 감소되었다. 5. 허혈전처치 심장에서 xanthine oxidase(D,O 및 D/O형)활성은 변화되지 않았으나 그 기질인 hypoxanthine의 조직함량은 현저히 감소되었다. 이상의 결과들로 부터 허혈전처치는 세포수준에서 허혈심근의 재관류손상을 방지하며, 허혈전처치에 따른 산소라디칼 생성 감소가 재관류손상 방지에 일부 기여할 수 있으리라 사료된다.an을 2주간 처치한 경우에도 영향을 받지 않았다. 이상의 결과로 미루어 아마도 losartan의 내피세포에 대한 작용은 constitutive NO 생성을 증가시키나 inducible NO 생성에는 영향을 미치지 않을 것으로 여겨진다.cium ion이 상당히 중요한 역할을 하는데, 특히 소뇌에서의 NO생성의 감소는 이들 약물들의 치명적 부작용인 tardive dyskinesia와 매우 깊은 관련을 추측할 수 있다. 그러나, 더 많은 약물들의 검색으로 일관적인 기본 결과가 필요 되고 또 각개 약물의 특정적 기전이 연구되기 위하여 현재 실험중이다.(신칭(新稱), Cystostereum subabruptum), 털융단버섯(신칭(新稱), Tomentella pilosa), 노란소나무무늬버섯(신칭(新稱), Asterostroma laxum), 붉은소나무비늘버섯(신칭(新稱), Hymenochaete cruenta), 가루소나무비늘버섯(신칭(新稱), Hymenochaete fuliginosa), 소나무비늘버섯(신칭(新稱), Hymenochaete tabacina), 갈색시루삔버섯(신칭(新稱), Inonotus radiatus), 벚나무진흙버섯(신칭(新稱), Phellinus pomaceus), 회주름구멍버섯(신칭(新稱), Antrodia crassa), 층주름구멍버섯(신칭(新稱), Antrodia serialis), 흰그물구멍버섯(신칭(新稱), Ceriporia reticulata), 겹친손등버섯(신칭(新稱), Oligoporus balsameus), 점박이손등버섯(신칭(新稱), Oligoporus guttulatus), 무른흰살버섯(신칭(新稱), Oxyporus cuneatus), 각목버섯(신칭(新稱),

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Involvement of Adenosine in Cardioprotective Effect of Catecholamine Preconditioning in Ischemia-Reperfused Heart of Rat

  • Kim, Young-Hoon;Kim, Chan-Hyung;Kim, Gi-Tae;Kim, In-Kyu;Park, Jong-Wan;Kim, Myung-Suk
    • The Korean Journal of Physiology and Pharmacology
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    • 제2권6호
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    • pp.753-761
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    • 1998
  • Preconditioning of a heart with small doses of catecholamines induces a tolerance against the subsequent lethal ischemia. The present study was performed to find a specific receptor pathway involved with the catecholamine preconditioning and to test if adenosine plays a role in this cardioprotective effect. Isolated rat hearts, pretreated with small doses of ${\alpha}-\;or\;{\beta}-adrenergic$ agonists/antagonists, were subjected to 20 minutes ischemia and 20 minutes reperfusion by Langendorff perfusion method. Cardiac mechanical functions, lactate dehydrogenase and adenosine release from the hearts were measured before and after the drug treatments and ischemia. In another series of experiments, adenosine $A_1\;or\;A_2$ receptor blockers were treated prior to administration of adrenergic agonists. Pretreatments of a ${\beta}-agonist,\;isoproterenol(10^{-9}{\sim}10^{-7}\;M)$ markedly improved the post-ischemic mechanical function and reduced the lactate dehydrogenase release. Similar cardioprotective effect was observed with an ?-agonist, phenylephrine pretreatment, but much higher $concentration(10^{-4}\;M)$ was needed to achieve the same degree of cardioprotection. The cardioprotective effects of isoproterenol and phenylephrine pretreatments were blocked by a ${\beta}_1-adrenergic$ receptor antagonist, atenolol, but not by an ${\alpha}_1-antagonist,$ prazosin. Adenosine release from the heart was increased by isoproterenol, and the increase was also blocked by atenolol, but not by prazosin. A selective $A_1-adenosine$ receptor antagonist, 1,3-dipropyl-8-cyclopentyl xanthine (DPCPX) blocked the cardioprotection by isoproterenol pretreatment. These results suggest that catecholamine pretreatment protects rat myocardium against ischemia and reperfusion injury by mediation of ${\beta}_1-adrenergic$ receptor pathway, and that adenosine is involved in this cardioprotective effect.

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