• Journal of Korean Neurosurgical Society
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• 제51권2호
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• pp.117-119
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• 2012

The sinking skin flap syndrome is a rare complication after a large craniectomy. It consists of a sunken skin above the bone defect with neurological symptoms such as severe headache, mental changes, focal deficits, or seizures. In patient with sinking skin flap syndrome, cerebral blood flow and cerebral metabolism are decreased by sinking skin flap syndrome, and it may cause the deterioration of autoregulation of brain. We report a case of a patient with sinking skin flap syndrome who suffered from reperfusion injury after cranioplasty with review of pertinent literature.

• The Korean Journal of Nuclear Medicine
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• 제35권6호
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• pp.343-351
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• 2001

Cerebral post-ischemic hyperperfusion has been observed at the acute and subacute periods of ischemic stroke. In the animal stroke model, early post-ischemic hyperperfusion is the mark of recanalization of the occluded artery with reperfusion. In the PET studios of both humans and experimental animals, early post-ischemic hyperperfusion is not a key factor in the development of tissue infarction and indicates the spontaneous reperfusion of the ischemic brain tissue without late infarction or with small infarction. But late post-ischemic hyperperfusion shows the worse prognosis with reperfusion injury associated with brain tissue necrosis. Early post-ischemic hyperperfusion defined by PET and SPECT may be useful in predicting the prognosis of ischemic stroke and the effect of thrombolytic therapy.

• Korean Journal of Oriental Medicine
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• 제7권1호
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• pp.115-124
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• 2001

Yukmijihwangwon (YM) has been known to reinforce the vital essence and have antioxidant activities. This study was designed to examine the inhibitory effects of YM against in vitro hypoxia/reperfusion-induced inflammatory response. We have characterized the production of prostaglandin $E_2$ and arachidonic acid during hypoxia/reperfusion in the human neuroblastoma SK-N-MC and human monocytic macrophage U937 cells and the ingibitory effect of YM on these inflammation-related substance formation has been found out in this study. To investigate inhibition of COX expression by YM during hypoxia in vitro. This result suggested that YM used in this experiment reinforced antiinflammatory potentials and protected cells against hypoxia/reperfusion induced inflammatory response.

• Journal of Chest Surgery
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• 제32권7호
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• pp.637-647
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• 1999

Background: Ischemia-reperfusion injury is one of the major contributing causes of early graft failure in lung transplantation. It has been suggested that triiodothyronine (T3) may ameliorate ischemia-reperfusion injury to various organs in vivo and in vitro. Predicting its beneficial effect for ischemic lung injury, we set out to demonstrate it by administering T3 into the in situ canine ischemia-reperfusion model. Material and Method: Sixteen adult mongrel dogs were randomly allocated into group A and B. T3 $(3.6\mug/kg)$ was administered before the initiation of single lung ischemia in group B, whereas the same amount of saline was administered in group A. Ischemia was induced in the left lung by clamping the left hilum for 100 minutes. After reperfusion, various hemodynamic parameters and blood gases were analyzed for 4 hours while intermittently clamping the right hilum in order to allow observation of the injured left lung function. Result: Arterial oxygen partial pressure $(PaO_2)$ decreased 30 minutes after reperfusion and recovered gradually thereafter in both groups. In group B the decrease of $PaO_2$ was less marked than in group A. The recovery of $PaO_2$ was faster in group B than in group A. The differences between the two groups were statistically significant from 30 minutes after reperfusion $(125\pm34$ mmHg and $252\pm44$ mmHg, p<0.05) until the end of the experiment $(178\pm42$mmHg and $330\pm37$ mmHg, p<0.05). The differences in the arterial carbon dioxide pressure, airway pressure and lung compliance showed no statistical significance. The malondialdehyde (MDA) level, measured from the tissue obtained 240 minutes after reperfusion, was lower in group B $(0.40\pm0.04\mu$M) than in group A $(0.53\pm0.05\mu$M, p<0.05). The ATP level of group B $(0.69\pm0.07\mu$M/g) was significantly higher than that of group A $(0.48\pm0.07\mu$M/g, p<0.05). The microscopic exami nation revealed varying degrees of injury such as perivascular neutrophil infiltration, capillary hemorrhage and interstitial congestion. There were no differences in the microscopic findings between the two groups. CONCLUSION T3 has beneficial effects on the ischemic canine lung injury including preservation of oxygenation capacity, less production of lipid peroxidation products and a higher level of tissue ATP. These results suggest that T3 is effective in pulmonary allograft preservation.

• Korean Journal of Veterinary Research
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• 제39권5호
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• pp.878-895
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• 1999

Ischemic preconditioing (IPC), i.e., a preliminary brief episode of ischemia and reperfusion, has been shown to reduce the cell damage induced by long ischemia and reperfusion. Superoxide radical which is produced during reperfusion after ischemia was recognized as a factor of the ischemic injury and it is dismutated into $H_2O_2$ and $O_2$ by two types of intracellular superoxide dismutase (SOD), Cu,Zn-SOD in cytoplasm and Mn-SOD in mitochondria. Recently oxygen free radicals are suggested to induce the apoptosis, however mechanism of the reduced apoptosis by ischemic preconditioing was unknown, while many studies performed in mammalian heart indicated that ATP-sensitive $K^+$ ($K_{APT}$) channel activation related with the protective effects. The aim of present study is to investigate 1) whether IP upregulate the Cu,Zn-SOD and Mn-SOD activities, and 2) whether ischemic preconditioning decreases apoptosis via $K_{APT}$ channel activation in timely reperfused skeletal muscle after long ishemia. The experimental animals, Sprague-Dawley rats weighing 250~300g, were divided into 8 groups; 1) control group, 2) ischemic preconditioning only groups, 3) pinacidil, a $K_{APT}$ channel opener, treatment only groups, 4) glibenclamide, a $K_{APT}$ channel blocker, treatment only groups, 5) ischemia groups, 6) ischemia after IPC groups, 7) ischemia and pinacidil treatment groups, and 8) IP and ischemia after glibenclamide pretreatment groups. Animals of the control group were administered with the vehicle (DMSO) alone. Pinacidil (1mg/kg) was administered intravenously 5 minutes after initiation of ischemia, and glibenclamide (0.5mg/kg) was injected intravenously 20 minutes before IPC. In rats that were ischemic preconditioned, the left common iliac artery was occluded for 5 minutes followed by 5 minutes of reperfusion by three times using vascular clamp. Ischemia was done by occlusion of the same artery for 4 hours. The specimens of left rectus femoris muscle were obtained immediately (0 hour), 12 hours, 24 hours after drug administrations, IP or ischemia and reperfusion. The immunoreactivities of SOD and its alterations were observed by use of sheep antihuman Cu,Zn-SOD and Mn-SOD antibodies on the $10{\mu}m$ cryosections. The incidencies of apoptosis were observed by TUNEL methods with in situ apoptosis detection kit on $6{\mu}m$ paraffine section. The results obtained were as follows : 1. After IPC, immunoreactivities of Cu,Zn-SOD mainly in the small-sized fibers were increased by 24 hours, that of Mn-SOD at 0 hour and 24 hours. 2. No significant changes in immunoreactivities of SOD was observed in the pinacidil and in the glibenclamide treatment only groups, and in the ischemia only groups. 3. The immunoreactivities of the Cu,Zn-SOD were increased in the ischemia after IPC groups and the ischemia and pinacidil treatment groups. 4. The immunoreactivities of the Cu,Zn-SOD in the IPC and ischemia after glibenclamide pretreatment groups were not increased except for the 12 hours reperfusion group. But, Mn-SOD immunoreactivities were increased in the 0 hours, 12 hours and 24 hours after reperfusion. 5. In the control group, the IPC only groups, and the pinacidil treatment only groups, negative or trace apoptotic reactions were observed, but the positive apoptotic reaction occured in the glibenclamide treatment groups. 6. Moderate or many number of apoptosis were revealed in the ischemia groups, and also the IPC and ischemia after glibenclamide pretreatment group except for 12 hours and 24 hours after reperfusion. However, the incidence of apoptosis was decreased in the ischemia after IPC groups and in the ischemia and pinacidil treatment groups. 7. There is a coincidence between the increase of Cu,Zn-SOD immunoreactivities and the decrease of apoptosis in the presence of ischemia and reperfusion. These results suggest that the protective effects of ishemic preconditioing may related to the SOD activation, and the ischemic preconditioning decreases the apoptosis partially via $K_{APT}$ channel activation in timely reperfused rat skeletal muscle. It is also suggested that inhibition of apoptosis by IPC may related with the SOD activation.

• Journal of Veterinary Clinics
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• 제27권5호
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• pp.553-558
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• 2010

The purpose of this study was to investigate the effects of premedicated ascorbic acid and hepa-saline irrigation/aspiration on attenuation of ischemia-reperfusion (I/R) injury and recovery of renal function in canine nephrotomy model. In the canine model, nine mixed dogs were subjected to renal nephrotomy with premedicated ascorbic acid and hepa-saline irrigation-aspiration (treatment group 2), and only hepa-saline irrigation-aspiration (treatment group 1). The level of renal function and antioxidant enzymes after nephrotomy were measured. And the expression pattern of TNF-${\alpha}$ and INF-${\gamma}$ was examined in the renal tissue at $7^{th}$ day after nephrotomy. BUN and creatinine levels significantly decreased in the treatment group 1 and 2 compared to that of control group at the $3^{rd}$, 5th and $7^{th}$ day after reperfusion (p < 0.05). And, there was significant difference between treatment group 1 and 2 at the $3^{rd}$ day after reperfusion (p < 0.05). The activities of antioxidant enzymes in plasma was significantly increased in the treatment group 1 and 2 compared to that of control group at the $3^{rd}$, $5^{th}$ and $7^{th}$ day after reperfusion (p < 0.05). And, there was significant difference between treatment group 1 and 2 at the $3^{rd}$ day after reperfusion (p < 0.05). TNF-${\alpha}$ was decreased and INF-${\gamma}$ was increased in treatment groups. The result of this study suggested that irrigation-aspiration has effects on attenuation of renal ischemia-reperfusion injury, and the exogenous ascorbic acid has a role in the attenuation of renal ischemia-reperfusion injury and recovery of renal function in canine nephrotomy model.

• Applied Microscopy
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• 제19권1호
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• pp.1-18
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• 1989

It has been debated whether postischemic reperfusion is necessarily beneficial to salvage the myocardium after ischemic insult or not. Therefore, this study was undertaken to compare the ultrastructural changes as well as the distribution of $Ca^{2+}$ in the ventricular myocardial cells after transient ischemia and after postischemic reperfusion, and to suspect to what extent the postischemic reperfusion is beneficial. After 10 minutes of ischemia, the heart developed wide I bands, glycogen depletion, intramyofibrillar edema, mitochondrial swelling, clumping and migration of chromatin, ghosts of lipid droplets, disintegration of cell junctions, sarcolemmal disruption, and loss of $Ca^{2+}$ binding capacity of the sarcolemma and the mitochondria. In spite of reperfusion, in a large number of cells, the ultrastructure was more severely damaged, however, $Ca^{2+}$ binding capacity of the sarcolemma and the mitochondria restored. These results suggest that postischemic reperfusion may help the myocardial cells to restore their function to control $Ca^{2+}$ to a certain extent, but that it could aggravate the ischemic insult.

• Journal of Chest Surgery
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• 제29권8호
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• pp.807-815
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• 1996

The protective effect of'ischemic preconditioning'on ischemid-reperfusion injury of heart has been reported in various animal species. but without known mechAnism in detail, In An attempt to investigate the cardioprotective mechanism of ischemic preconditioning, we examined the effects of nitric oxide(UO) synthesis in preconditioned heart of rat The isolated hearts perfused by Langendorfr's method were ex- posed to 30min global ischemia followed by 30min reperfusion with oxygenated Krebs-Henseleit(K-H) sol- ution. Ischemic preconditioning was performed with three episodes of Sm n ischemia and Smin repeyfusion before the induction of prolong ischemia(30min)-reperfusion(30min). Ischemic preconditioning prevented the depression of cardiac function(left ventricular pressure .K heart rate) observed in the ischemia- reperfusion hearts and reduced the release of lactate dehydrogenase during the reperfusion period. On electromicroscopic pictures, myocardial ultrastructures wore relatively well preserved in isthemic preconditioned hearts. N6_nitro-L-arginine methyl ester(L-NAME) an inhibitor of L-arginine citric oxide pathway, was infused at a rate O.Smllmin In a dose of 10mg kg-1 before the initial ischemic preconditioning. neither the protection of cardiac function nor the reduction of LDH releAse in ischemic preconditioning hearts was altered in the presence of added L-NAME On ultrastructural finding, the preservation of morphology in ischemic preconditioning heart was not change by the pretreatment of L-UAME. The failure of the WO synthesis inhibitor to reduce t e effect of ischemic preconditioning may be related to be species specific in that NO may allot be the trigger for ischemic preconditioning in rats.

• Journal of Chest Surgery
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• 제31권10호
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• pp.924-927
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• 1998

Background: Myocardial cell death after myocardial infarction or reperfusion is classified into necrosis and apoptosis. Bcl-2 protein is a cytoplasmic protein, which inhibits apoptosis and is expressed in acute stage of myocardial infarction but not in normal heart. This study was performed to investigate whether Bcl-2 protein was expressed respectively to the reperfusion time. Materials and methods: Thirty nine New Zealand white rabbits weighing 1.5-4.8 kg (mean, 2.9kg) were alloted into 7 groups (n=5 in each group) which underwent left anterior descending coronary artery(LAD) occlusion for 30 minutes, followed by reperfusion. The animals were sacrificed at 1, 4, 8, 12, 24 hours, and 3, 7 days after occlusion. Ventricle was excised immediately after intervention. Tissues were fixed in 10% buffured formalin and embedded in paraffin. Bcl-2 protein was detected by immunohistochemical stain with using monoclonal antibody against Bcl-2 protein. Results: The positive immunohistochemical reactivity for Bcl-2 protein was observed in 12, 24 hours, and 3 days reperfusion groups. Bcl-2 protein was detected in salvaged myocytes surrounding the infarcted area. Conclusions: Bcl-2 protein is expressed at the late acute stage of infarct. Therefore, the expression of Bcl-2 protein may not protect acute cell death, but may play a role in the prevention of late cell death after myocardial is chemia-reperfusion.

• Archives of Plastic Surgery
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• 제32권4호
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• pp.503-510
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• 2005

If we could predict the necrosis of the flap caused by reperfusion injury, we can minimize the necrosis of the flap by taking appropriate action before necrosis begins. In this study, we examined whether we can predict the survival of flap under reperfusion injury or not, by measuring laser doppler flow meter values. We divided the group into the control and experimental groups corresponding to 6, 8, 9, 10, and 12hours after reperfusion(hours after ligation of auricular central artery). In each group, we examined necrotic change, perfusion unit (PU), serum superoxide dismutase (SOD), glutathione peroxidase, angiography and pathologic findings. No necrosis was observed in the 6 and 8 hours group but 8, 18, 20 hours after ligation, necrosis was observed, Also in each of 9, 10 and 12 hours group (each group consisted of 20 flaps), necrosis were noted. According to the above data, the critical time of necrosis in the auricular skin flap model lies between about 8 to 9 hours. Comparing the PU between the necrosis and non-necrosis groups, the former group showed a mean 39.57 PU increase after 60 min of reperfusion, and the latter group showed a mean increase of 21.21 PU. We can conclude that better flow can dilute oxygen free radical into systemic circulation, and this means less injuries are caused on vessels. Our study implies that if blood flow increase is less than 30 PU, intensive care is needed to save the flap. Additionally, we found significant decrease of serum SOD and glutathione peroxidase in the necrotic group. Therefore, monitoring these serum markers will be helpful in predicting reperfusion injury and supplementing these enzymes could be helpful to save the flap. The laser doppler flow meter is thought to be helpful in clinical circumstances for evaluating the circulation of the flap after the operation. However, more accumulation of clinical studies should be necessary establishing useful clinical data.