• Title, Summary, Keyword: ischemia-reperfusion

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Effect of Preconditioning Ischemia on Endothelial Dysfunction Produced by Ischemia-Reperfusion in Rabbit Coronary Artery

  • Suh, Suk-Hyo;Park, Yee-Tae;Kim, Woong-Heum;Kim, Ki-Whan
    • The Korean journal of physiology & pharmacology
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    • v.29 no.1
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    • pp.51-59
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    • 1995
  • This study was designed to test whether or not 1) ischemia-reperfusion attenuates endothelium-dependent relaxation of coronary arteries and 2) preconditioning protects the arterial endothelium from ischemia-reperfusion injury. In anesthetized open chest rabbits, branches of the left circumflex artery were exposed to different combinations of the experimental conditions; ischemia (15 minutes), ischemia (15 minutes)-reperfusion (10 minutes), preconditioning ischemia, and pre-conditioning fellowed by ischemia-reperfusion. Preconditioning consisted of 3 occlusions of 2-min duration, each followed by n 5-min reperfusion. Rings of the artery exposed to the experimental condition and of normal left anterior descending coronary artery were prepared and suspended for isometric force measurement in organ chambers containing Krebs Ringer bicarbonate solution. The rings were contracted with 29.6 mM KCI. Ischemia alone did not attenuate endothelium-dependent relaxation by acetylcholine. However, ischemia-reperfusion significantly impaired endothelium-dependent relaxation. Endothelium-independent relaxation by sodium nitroprusside was not impaired by ischemia-reperfusion and the constrictive response to acetylcholine was not altered in reperfused rings without endothelium, compared with control rings. Arterial rings exposed to preconditioning followed by ischemia-reperfusion exhibited impaired endothelium-dependent relaxation by acetyl-choline. However, although preconditioning not fellowed by ischemia-reperfusion, attenuated endothelium-dependent relaxation at low concentrations of acetylcholine, the magnitude of the impairment by preconditioning followed by ischemia-reperfusion was significantly less than that of the impairment by ischemia-reperfusion alone. These data demonstrate that ischemia-reperfusion significantly attenuates endothelium-dependent relaxation by producing endothelial dysfunction and preconditioning Protects the endothelium of coronary arteries from ischemia-reperfusion injury.

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The Effect of Melatonin on Biochemical Changes after Ischemia-Reperfusion Injury of Rat Skeletal Muscle (흰쥐 골격근의 허혈-재관류 손상후 생화학적 변화에 미치는 Melatonin의 효과)

  • Park, Hye June;Burm, Jin Sik
    • Archives of Plastic Surgery
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    • v.32 no.6
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    • pp.683-688
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    • 2005
  • The ischemia-reperfusion injury of the skeletal muscles is caused by generation of reactive oxygen during ischemia and reperfusion. Melatonin or N-Acetyl-5-methoxy- tryptamine is suggested to have antioxidant effects in several tissues. In present study, we examined the protective effect of melatonin in a rat hind limb ischemia-reperfusion injury. Dimethyl-sulfoxide(DMSO) was also tested for comparison. Ischemia was induced for 4 hours by vascular clamping and followed by 1 hour or 24 hours of reperfusion. Muscle injury was evaluated in 4 groups such as single laparotomy group(control), ischemia-reperfusion group, DMSO group, melatonin group. Eedema ratio and malondialdehyde(MDA) of muscle tissue and serum level of creatine kinase(CK), were measeured at the end of reperfusion. DMSO and melatonin group showed significant amelioration of edema and serum CK compared with ischemia-reperfusion group. The decreasing effect was more prominent in melatonin group. The muscle tissue MDA concentration is significantly lower in melatonin group than in ischemia-reperfusion group. The results show that melatonin prevents and improves ischemia-reperfusion injury more effectively in a rat hind limb than DMSO dose. Thus, clinically the melatonin may be used for a beneficial treatment of such injuries

Hesperidin improves warm ischemia/reperfusion-induced oxidative renal injury in rats

  • Gandhi, Chintan;Zalawadia, Rishit;Balaraman, R.
    • Oriental Pharmacy and Experimental Medicine
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    • v.9 no.4
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    • pp.292-302
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    • 2009
  • Ischemia/reperfusion injury, which is commonly seen in the field of renal surgery or transplantation, is a major cause of acute renal failure. Previous studies showed that antioxidant treatments attenuated renal ischemia/reperfusion injury. The objective of this study was to examine the role of hesperidin in modulating reactive oxygen species induced inflammation and apoptosis after renal ischemia/reperfusion injury. Rats were subjected to right nephrectomy, 15 days later 45 min of renal ischemia and 24 h reperfusion with or without treatment with hesperidin. Renal function, inflammation and apoptosis were compared at 24 h after reperfusion injury. Hesperidin improved the renal dysfunction and reduced inflammation and apoptosis after ischemia/reperfusion injury. In conclusion, hesperidin shows potent anti-apoptotic and antiinflammatory properties due to antioxidant property. These findings may have major implications in the treatment of human ischemic acute renal failure.

The Role of Oxygen Free Radicals and Phospholipase $A_2$ in Ischemia-reperfusion Injury to the Liver

  • Park, Mee-Jung;Cho, Tai-Soon;Lee, Sun-Mee
    • Archives of Pharmacal Research
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    • v.18 no.3
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    • pp.189-194
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    • 1995
  • The focus of this study was to investigate the influences of enzymatic scavengers of active oxygen metabolites and phospholipase $A_2$ inhibitor on hepatic secretory and microsomal function during hepatic ischemia/reperfusion. Rats were pretreated with free radical scavengers such as superoxide dismutase (SOD), catalase, deferoxamine and phospholipase $A_2$ inhibitor such as quinacrine and then subjected to 60 min. no-flow hepatic ischemia in vivo. After 1, 5 hr of reperfusion, bile was collected, blood was obtained from the abdominal aorta, and liver microsomes were isolated. Serum aminotransferase (ALT) level was increased at 1 hr and peaked at 5 hr. The increase in ALT was significantly attenuated by SOD plus catalase, deferoxamine and quinacrine especially at 5 hr of reperfusion. The wet weight-to-dry weight ratio of the liver was significantly increased by ischemia/reperfusion. SOD and catalase treatment minimized the increase in this ratio. Hepatic lipid peroxidiltion was elevated by ischemia/reperfusion, and this elevation was inhibited by free radical scavengers and quina crine. Bile flow and cholate output, but not bilirubin output, were markedly decreased by ischemia/reperfusion and quinacrine restored the secretion. Cytochrome $P_{450}$ content was decreased by ischemia/reperfusion and restored by free radical scavengers and quinacrine to the level of that of the sham operated group. Aminopyrine N-demethylase activity was decreased and aniline p-hydroxylase was increased by ischemia/reperfusion. The changes in the activities of the two enzymes were prevented by free radical scavengers and quinacrine. Our findings suggest that ischemia/reperfusion diminishes hepatic secretory functions as well as microsomal drug metabolizing systems by increasing lipid peroxidation, and in addition to free radicals, other factors such as phospholipase $A_2$ are involved in pathogenes of hepatic dysfunction after ischemia/reperfusion.

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The Expression of CD 18 on Ischemia- Reperfusion Injury of TRAM Flap of Rats (흰쥐의 복직근피부피판에 일으킨 허혈-재관류 손상에서 CD18의 발현)

  • Yoon, Sang Yup;Lee, Taik Jong;Hong, Joon Pio
    • Archives of Plastic Surgery
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    • v.33 no.6
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    • pp.737-741
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    • 2006
  • Purpose: This study was to evaluate the expression pattern of CD 18(leukocyte adhesion glycoprotein) in ischemia-reperfusion injury of TRAM flap of rats. Through this study, we can obtain more information about ischemia-reperfusion injury. We want to develop specific medicine to improve the survival rate of TRAM flap in the future. Methods: A TRAM flap supplied by a single pedicle superior epigastric artery and vein was elevated on 60 Sprauge-Dawley rats. The rats were divide into 6 groups (each group n=10); Group O: sham, no ischemia-reperfusion injury, Group I: 2 hour reperfusion after 4 hour ischemia, Group II: 4 hour reperfusion after 4 hour ischemia, Group III: 8 hour reperfusion after 4 hour ischemia, Group IV: 12 hour reperfusion after 4 hour ischemia, and Group V: 24 hour reperfusion after 4 hour ischemia. This study consisted of gross examination for flap survival and flow cytometry study of CD18 on neutrophils. Results: The gross measurement of the flap showed different survival rate in group I(71%), II(68%), III(37%), IV(34%) and V(34%). All experimental groups showed an increase in the expression of CD18 compared to group O. The expression of CD18 was rapidly increased in ascending order in group I, II and III. But, the expression of CD18 was maintained in group IV and V. Conclusion: The results can be implemented in the study to develop drugs which are capable of reducing ischemia-reperfusion injury in microsurgical breast reconstruction.

Protective Mechanism of Nitric Oxide and Mucus against Ischemia/Reperfusion-Induced Gastric Mucosal Injury

  • Kim, Hye-Young;Nam, Kwang-Soo;Kim, Kyung-Hwan
    • The Korean Journal of Physiology and Pharmacology
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    • v.2 no.4
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    • pp.511-519
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    • 1998
  • This study investigated the role of nitric oxide on the oxidative damage in gastric mucosa of rats which received ischemia/reperfusion and its relation to mucus. Nitric oxide synthesis modulators such as L-arginine and $N^G-nitro-L-arginine$ methyl ester, and sodium nitroprusside, a nitric oxide donor, were injected intraperitoneally to the rats 30 min prior to ischemia/reperfusion which was induced by clamping the celiac artery and the superior mesenteric artery for 30 min and reperfusion for 1 h. Lipid peroxide production, the contents of glutathione and mucus, and glutathione peroxidase activities of gastric mucosa were determined. Histological observation of gastric mucosa was performed by using hematoxylin-eosin staining and scanning electron microscopy. The result showed that ischemia/reperfusion increased lipid peroxide production and decreased the contents of glutathione and mucus as well as glutathione peroxidase activities of gastric mucosa. Ischemia/reperfusion induced gastric erosion and gross epithelial disruption of gastric mucosa. Pretreatment of L-arginine, a substrate for nitric oxide synthase, and sodium nitroprusside prevented ischemia/reperfusion-induced alterations of gastric mucosa. However, $N^G-nitro-$ L- arginine methyl ester, a nitric oxide synthase inhibitor, deteriorated oxidative damage induced by ischemia/reperfusion. In conclusion, nitric oxide has an antioxidant defensive role on gastric mucosa by maintaining mucus, glutathione, and glutathione peroxidase of gastric mucosa.

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Involvement of Cortical Damage in the Ischemia/Reperfusion-Induced Memory Impairment of Wistar Rats

  • Hong, Jin-Tae;Ryu, Seung-Rel;Kim, Hye-Jin;Lee, Sun-Hee;Lee, Byung-Moo;Kim, Pu-Young
    • Archives of Pharmacal Research
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    • v.23 no.4
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    • pp.413-417
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    • 2000
  • The effect of ischemia/reperfusion-induced neuronal damage on the memory impairment were investigated using active avoidance and Morris water maze tasks in Wistar rats. Focal ischemia was induced by 1 h occlusion of the right middle cerebral artery (MCA) of Wistar male rats. Reperfusion was induced by releasing the occlusion and restoring the blood circulation for 24 h. The acquisition and preservation memory tested by active avoidance showed a significant difference between the sham and ischemia/reperfusion group. The water maze acquisition performance was also significant difference between sham and ischemia/repefusion groups in both latency and moving distance. The infarction volume was increased by the ischemia/reperfusion. Furthermore, the cresyl violet staining of the ischemia/reperfusion brain showed severe neuronal damage (pyramidal cell loss) in the cortex in addition to the striatum lesion of brain. This study shows that pyramidal cell damage in the cortex lesion may be partially related to memorial disturbance in the ischemia/reperfusion brain injury.

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The Effect of Indomethacin on the Production of Eicosanoids and Edema during Ischemia-Reperfusion Injury in Skeletal Muscle

  • Chung, Yoon-Jae;Sohn, Byung-Kyu;Hyun, Kwang-Soon;Yoo, Sang-Hee;Ryu, Hyong-Kyun;Kim, Hyung-Gun
    • The Korean Journal of Physiology and Pharmacology
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    • v.4 no.6
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    • pp.525-530
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    • 2000
  • During reperfusion of skeletal muscle after ischemia, lipid mediators, mainly eicosanoids, are released and may have a role in the pathogenesis of reperfusion injury. To validate the role of eicosanoids in the ischemia-reperfusion induced functional deficits in skeletal muscle, we compared muscle edema and the changes of eicosanoid concentration in the rat hind limb after ischemia-reperfusion injury by application of tourniquet. After 4 hours of ischemia, reperfusion was established for 4 hours by releasing tourniquet. To assess tissue damage, edema, and wet/dry weight ratios were determined and the eicosanoid concnentrations were measured by the HPLC. The muscle edema and the release of cyclooxygenase metabolites were not induced by the ischemia itself rather they were significantly increased by reperfusion. Indomethacin treatment ameliorated limb edema and decreased the release of $6-keto-PGF_{1{\alpha}},$ thromboxane $B_2,$ and $PGE_2$ inducedby reperfusion. But the inhibitory effect of indomethacin on edema (35%) was relatively low than the inhibitory effect on release of cyclooxygenase metabolites (up to 69%) by reperfusion. These results support the view that cyclooxygenase products may play a significant role in the formation of muscle injury by ischemia-reperfusion and suggest that nonsteroidal antiinflammatory agents might be partially beneficial to the management of acute limb ischemia-reperfusion injury.

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Vitamins E and C: Are They Synergistic in Protecting Liver Cells against Hepatic Ischimia and Reperfusion Injury\ulcorner (간장내 허혈 및 재관류시 Vitamin E와 C의 간세포 보호작용)

  • 이선미;김순애;조태순
    • Biomolecules & Therapeutics
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    • v.5 no.1
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    • pp.59-66
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    • 1997
  • This study was done to determine that vitamins I and C are synergistic in protecting liver cells during hepatic ischemia and repefusion. Rats treated with vitamins I and C were subjected to 60 min of hepatic ischemia and to 1 and 5 hr of reperfusion thereafter. Serum aminotransferase level and microsomal lipid peroxidation were markedly increased by ischemia/reperfusion. These increases were significantly attenuated by vitamins E, C or its combination. Hepatic wet weight-to-dry weight ratio was increased in ischemic group, but this increase was prevented by combination of vitamin I and C. Bile flow and cholate output were markedly decreased by ischemia/reperfusion and vitamin C alone and combination of vitamin I and C restored their secretion. Cytochrome P-450 content and aminopyrine N-demethylase activity were decreased by ischemia/ reperfusion and restored by vitamin C and combination of vitamin I and C to the level of sham-operated rat. Aniline p-hydroxylase activity was increased by ischemia/reperfusion and this increase was prevented by vitamin E. Our findings suggest that ischemia/reperfusion diminishes hepatic secretory and microsomal functions by increasing lipid peroxidation and vitamins I and C synergistically ameliorates these changes.

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Effect of Ursodeoxycholic Acid on Ischemia/Reperfusion Injury in Isolated Rat Heart

  • Lee, Woo-Yong;Han, Suk-Hee;Cho, Tai-Soon;Yoo, Young-Hyo;Lee, Sun-Mee
    • Archives of Pharmacal Research
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    • v.22 no.5
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    • pp.479-484
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    • 1999
  • In this study, the effects of ursodeoxycholic acid (UDCA) on ischemia/reperfusion injury were investigated on isolated heart perfusion model. Hearts were perfused with oxygenated Krebs-Henseleit solution (pH 7.4, $37^{\circ}C$) on a Langendroff apparatus. After equilibration, isolated hearts were treated with UDCA 20 to 160 $\mu$M or vehicle (0.04% DMSO) for 10 min before the onset of ischemia. After global ischemia (30 min), ischemic hearts were reperfused and allowed to recover for 30 min. The physiological (i.e. heart rate, left ventricular developed pressure, coronary flow, double product and time to contracture formation) and biochemical (lactate dehydrogenase; LDH) parameters were evaluated. In vehicle-treated group, time to contracture formation was 21.4 min during ischemia, LVDP was 18.5 mmHg at the endpoint or reperfusion and LDH activity in total reperfusion effluent was 54.0 U/L. Cardioprotective effects of UDCA against ischemia/reperfusion consisted of a reduced TTC $(EC_{25}=97.3{\mu}M)$, reduced LDH release and enhanced recovery of cardiac contractile function during reperfusion. Especially, the treatments of UDCA 80 and $160 {\mu}M $ significantly increased LVDP and reduced LDH release. Our findings suggest that UDCA ameliorates ischemia/reperfusion-induced myocardial damage.

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