• The Journal of Internal Korean Medicine
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• v.20 no.1
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• pp.111-121
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• 1999

Cervus elaphus (CE), being known to reinforce Kidney, have tested to study the effects concerning damages of renal tissue induced by oxygen free radicals. I had observed the effects of CE extract on damages of rat's kidney following ischemia and reflow. Before ischemia was caused, CE extract was applied $0.2m{\ell}$ per 250g through femoral vein in ischemia and reflow group and normal sailine was applied in normal group, Ischemia was caused by renal artery's clamp for 60 min and reflowed by clamp remove after 30 min. It was increased on the content of lipid peroxidation, activies and type conversion ratio of xanthine oxidase following ischemia and reflow. by clamp remove after 30 min. It was increased on the content of lipid peroxidation, activies and type conversion ratio of xanthine oxidase following ischemia and reflow. However, they were decreased when CE extract was pre-applied. Glutathione level was decreased in ischemia and reflow group, and increased in CE extract's pre-applied group. However, it could not seen special changes on aldehyde oxidase activities, either. In conclusion, CE extract recovers the damage of kidney due to ischemia and reflow by decreasing the lipid peroxidation.

• The Journal of Internal Korean Medicine
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• v.20 no.1
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• pp.167-180
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• 1999

Cervus elaphus, being known to reinforce Kidney, have tested to study the effects concerning damages of brain tissue induced by lipid peroxidation. In vitro, the level of lipid peroxide in brain tissue was decreased proportinally according to dose by Cervus elaphus extract solution for aqua-acupuncture (CESAA). It was much more decreased, when lipid peroxidation was induced with Fe(II). And, it was seen proportinally decrease according to the dose of CESAA on xanthine oxidase activities and type conversion ratio. However, I can not find special changes about aldehyde oxidase activities. And, I had observed the effects of CESAA on damages of rat's brain following ischemia and reflow. Before ischemia was caused, CESAA was applied 0.2 ml per 250 g through femoral vein in ischemia and reflow group and normal sailine was applied in normal group. Ischemia was caused by cervical artery's clamp for 30 min and reflowed by clamp remove after 15 min. It was increased on the content of lipid peroxidation, activies and type conversion ratio of xanthine oxidase following ischemia and reflow. However, they were decreased when CESAA was pre-appllied. However, it could not seen special changes on aldehyde oxidase activities, either. In conclusion. CESAA recovers the damage of brain due to ischemia and reflow by decreasing the lipid peroxidation through decreasing of xanthine oxidase activies and type conversion ratio.

• Korean Journal of Veterinary Research
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• v.37 no.1
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• pp.111-117
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• 1997

This study was carried out determine the effect of renal ischemia on amino acid transport in rabbit renal cortical slices. The animal models of renal ischemia induced experimentally by clamping the renal artery. These results were summarized as follows: 1. The uptake of amino acids lysine and ${\alpha}$-aminobutyrate(AIB), dicarboxylate succinate and organic anion PAH in cortical slices was normal or increased after 30 or 60 min of ischemia in vivo. 2. In a 30 min ischemic kidney, the slice uptake of amino acids was returned to the control level by 30 min of reflow. In a 60 or 90 min ischemic kidney, the lysine uptake was returned to the control level after of reflow, but the uptake of AIB and succinate was significantly reduced during reflow period of 30-120 min. 3. Oxygen consumption in cortical slices was increased after 30 min of ischemia but was not altered by 60 min of ischemia. This results indicat that transient ischemia caused increasing of amino acid uptake in renal cortical slices without metabolic disorder of renal proximal tubule.

• Archives of Reconstructive Microsurgery
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• v.3 no.1
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• pp.40-44
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• 1994

Microsurgery has advanced beyond its nascent stages reaching success rates of 90% to 95%. However, this means that even in the best circumstances, 5% to 10% of free flaps and replants fail. Almost all failures are due to vessel thrombosis, resulting in ischemia of the transplanted tissue. Many attemps have been undertaken to treat and reverse its effects. Zdeblick and colleagues noted an improvement in the viability of amputated limbs replanted after an extended period of ischemia following intraarterial infusion of urokinase. Subsequent studies have investigated many modalities of urokinase administration in various animal models by differing ischemic periods. These studies, however, have failed to establish a definitive, generally accepted protocol for administration of urokinase in the salvage of tissue subjected to prolonged ischemia. Our clinical observations suggest that a bolus of urokinase delivered under pressure may increase the thromoblytic effect of the drug, probably by means of increased delivery to microvasculature. We intend to investigate the role of selective pressure perfusion of ischemic flaps as a new means for increasing the effectiveness of urokinase in the treatment of the "no-reflow" phenomenon. A total of 32 male New Zealand rabbits were used and divided into the four groups according to the method of infusion. After 12 hours of ischemia the flaps were injected with Hartmann's solution or with urokinase and the percent survival of the flap was determined at 7 days following flap reperfusion. As the result, the flap survival rate was highest in the pressure injection of urokinase group.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1997.04a
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• pp.97-97
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• 1997

It was reported that ATP depletion occurs and accelerates cell damage during ischemia and reperfusion. To determine the mechanism of cell damage, the change of energy metabolism in liver was studied during ischemia/reperfusion. The groups were divided into four categories : sham-operated group, ischemia/reperfusion group, and two types of ATP-MgCl$_2$ treatment groups(one was treated during ischemia and the another during reperfusion). Rats were administered intravenously saline or ATP-MgCl$_2$. Rats were anesthetized and blood vessels in the left and median lobes of the liver were occluded. After 60min of ischemia, the clamp at those vessels were removed. After ischemia, one and five hours after reflow, energy metabolites(ATP, ADP, AMP, inosine, adenosine, hypoxanthine, xanthine) in liver were measured with HPLC. To observe mitochondrial function, aterial keton body ratio in blood and mitochondrial glutamate dehydrogenase activity in liver were measured. And lipid peroxidation was measured to evalutate the involvement of free radicals. In this study, ATP and ADP were catabolized to their metabolites(AMP, inosine, adenosine, hypoxanthine, xanthine) during ischemia and they resynthesized ATP and ADP during reperfusion. But total purine base were not restored to level of normal rat. The main source of resynthesizing ATP and ADP was AMP. In both ATP-MgCl$_2$ treated groups, mitochondrial function was protected and lipid peroxidation was significantly reduced. Our findings suggest that ischemia/reperfusion impairs hepatic energy metabolism.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1994.04a
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• pp.340-340
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• 1994

Since total hepatic ischemia(IS) occurs with transplantation, there has been interest in evaluating hepatic function after ischemia and subsequent reflow of blood. Four groups of animals were studied: group 1 (sham), group 2 (30mins IS), group 3 (60mins IS), and g.cup 4 (90mins IS). Serum transaminase(STA), wet weight-to-dry weight ratio(W/D), lipid peroxides(LPO), glucose-6-phosphatase(G-6-Pase) activity, Na$\^$+//K$\^$+/-ATPase(ATPase) activity were measured at 1, 5 and 24hrs after hepatic ischemia. Significant changes occurred between 1 and 5hrs of reperfusion. STA was 3579${\pm}$401, 4593${\pm}$675 and 6348${\pm}$808 U/L in group 2, 3 and 4 respectively. These changes were ischemic time-dependent manner. W/D in group 3 and 4 were significantly increased than that in sham group at all time points measured. In sham group, the level of LPO in the liver microsome remained constant at approximately 0. 5nmole MDA formed/mg protein througllout the experiment, In all ischemic groups on the other hand, the level of LPO started to increase at ischemia and markedly increased at all reperfusion period. Similar to STA, these changes were also dependent on duration of ischemia. Although G-6-Pase activity remained unchanged in both group 2 and group 3 until 5hrs of reperfusion, marked decrease in G-6-Pase activity was observed at grcup 4. ATPase activity was significantly decreased at 1, 5 and 24 hrs of reperfusion in group 3, whereas it was not changed in group 2. Furthermore, ATPase activity in group 4 started to decrease at ischemia and markedly decreased for entire reperfusion period. These data suggest that severity of hepatocellular injury is associated with period of ischemia as well as period of reperfusion.