• 한국임상약학회지
• /
• 제2권1호
• /
• pp.1-9
• /
• 1992

Protective effect of urokinase on reperfusion were studied followed by global ischemia in the isolated perfused rat heart. Separately, anti-platelet aggregation effect of urokinase also investigated. Urokinase exhibited positive effect for the protection of rat heart function by increasing the LV dp/dt, coronary flow(CF) and the Tate pressure product(RPP), and by decreasing the LVEDP on reperfusion. Urokinase also decreased arrhythmia by $74.7\%(P<0.05) induced by global ischemia in the rat heart. In the platelet aggregation study, urokinase did not show the inhibitory effect of ADP or collagen induced platelet aggregation inviuo and exvivo.

• Journal of Chest Surgery
• /
• 제17권4호
• /
• pp.565-573
• /
• 1984

The increasing use of cardioplegic solution for the reduction of ischemic tissue injury requires that all cardioplegic solution be carefully assessed for any protective or damaging properties. This study describes functional assessment of the efficiency of steroid in cardioplegic solution by using a Langendorffs perfusion model. Isolated rat heart were subject to a 2 minute period of coronary infusion with the steroid mixed cold cardioplegic solution immediately before and also at the midpoint of a 60 minutes period of hypothermic [10\ulcorner\ulcorner] ischemic arrest. The result of this study were as follows: 1.Spontaneous heart beat after ischemic arrest occurred 14 second later Langendorffs reperfusion in the steroid mixed Young & GIK group and 16 second later in the control group. [Young & GIK without steroid] A good recovery state of spontaneous heart beat was shown in both groups. 2.The percentage of recoveries of heart rate during the 30 minute after postischemic Langendorffs reperfusion was; at first 5 minute 106.3\ulcorner.7% [P<0.05] in the steroid mixed Young & GIK group. This percentage of recovery of steroid mixed Young & GIK group was significantly greater than the control group during the first 5 minute course. 3.The percentage of recovery of coronary flow during the 30 minute after postischemic Langendorffs reperfusion was; at first 5 minute 101\ulcorner.2% in the steroid mixed Young & GI K group. This percentage of recovery of the steroid mixed Young & GIK group was not significantly than the control group during the first 5 minute.

• The Korean Journal of Physiology and Pharmacology
• /
• 제13권3호
• /
• pp.181-187
• /
• 2009

Intestinal ischemia/reperfusion (I/R) is one of common causes of acute lung injury (ALI). Early and accurate diagnosis of patients who are like to develop serious acute respiratory distress syndrome (ARDS) would give a therapeutic advantage. Ferritin and heme oxygenase-1 (HO-1) are increased by oxidative stress and are potential candidates as a predictive biomarker of ARDS. However, the mechanisms responsible for the increases of ferritin and HO-1, and their relationship to ALI, are unclear. In order to elucidate the interactions between ferritin and HO-1, we studied the changes in ferritin and HO-1 levels in serum and bronchoalveolar lavage (BAL) fluid after intestinal I/R injury in rats. Leukocyte number and protein contents in BAL fluid were elevated following I/R, and the increases were attenuated by mepacrine pretreatment. Both serum ferritin and HO-1 concentrations were progressively elevated throughout the 3 h observation period. Mepacrine pretreatment attenuated the increase of serum and BAL fluid ferritin concentrations, but did not suppress the increase of serum HO-1. Moreover, BAL fluid HO-1 levels did not change after I/R or after mepacrine pretreated I/R compared with sham rats. Unlike ferritin, HO-1 levels are not exactly matched with the ALI. Therefore, there might be a different mechanism between the changes of ferritin and HO-1 in intestinal I/R-induced ALI model.

• The Korean Journal of Physiology and Pharmacology
• /
• 제10권4호
• /
• pp.187-191
• /
• 2006

Serum ferritin levels are increased in subjects at-risk for or with acute lung injury (ALI), and there are observations to suggest that increases in serum ferritin levels may help predict the development of ALI in at-risk individuals. To deepen our understanding of increases of serum ferritin and their relationship to the development of ALI, we measured serum ferritin levels before and after intestinal ischemia/reperfusion (I/R) injury in rats, and found that serum ferritin levels increased significantly following I/R. Increases in serum and lavage ferritin levels paralleled increases in lung inflammation (lavage leukocyte numbers and tissue myeloperoxidase activities) and lung leak (lavage protein levels). In contrast, pre-treatment of rats with mepacrine (60 mg/kg, i.p.), a phospholipase $A_2$ inhibitor, attenuated not only I/R-induced serum and lavage ferritin increases, but also the development of ALI. These findings indicate that, besides of human subjects with ALI, serum ferritin levels increase early on also in an animal model of ALI. Therefore, serum and lavage ferritin can be a candidate for early biomarker of ALI.

• 대한의생명과학회지
• /
• 제16권4호
• /
• pp.359-363
• /
• 2010

The miniature pig is a very suitable donor species in xenotransplantation of human organs. Intestine ischemia/reperfusion (I/R) is associated with high morbidity and mortality. Endoplasmic reticulum (ER) stress and apoptosis has been associated with the onset of diverse diseases. Thus, we examined the effect of intestine I/R on the expression of ER stress and apotptosis related molecules. In the present study, I/R induced phosphorylation of protein kinase-like endoplasmic reticulum kinase (PERK), IRE, and ATF-4. I/R also increased the expression of the proapoptotic transcription factor CAAT/enhancer-binding protein homologous protein (CHOP). In addition, I/R decreased the expression of Bcl-2, but increased the expression of Bax, cleaved PARP, and cleaved caspase-3. Moreover, I/R increased splicing form of XBP-1 mRNA and the expression of caspase-6 and caspase-3 mRNA. In conclusion, intestine I/R induced ER stress and apoptosis in miniature pig.

• Toxicological Research
• /
• 제32권1호
• /
• pp.35-46
• /
• 2016

No-flow ischemia occurs during cardiac arrest, hemorrhagic shock, liver resection and transplantation. Recovery of blood flow and normal physiological pH, however, irreversibly injures the liver and other tissues. Although the liver has the powerful machinery for mitochondrial quality control, a process called mitophagy, mitochondrial dysfunction and subsequent cell death occur after reperfusion. Growing evidence indicates that reperfusion impairs mitophagy, leading to mitochondrial dysfunction, defective oxidative phosphorylation, accumulation of toxic metabolites, energy loss and ultimately cell death. The importance of acetylation/deacetylation cycle in the mitochondria and mitophagy has recently gained attention. Emerging data suggest that sirtuins, enzymes deacetylating a variety of target proteins in cellular metabolism, survival and longevity, may also act as an autophagy modulator. This review highlights recent advances of our understanding of a mechanistic correlation between sirtuin 1, mitophagy and ischemic liver injury.

• 대한본초학회지
• /
• 제20권3호
• /
• pp.75-81
• /
• 2005

Objectives : In brain disorders such as ischemic stroke, the final outcome depends largely on the duration and the degree of the ischemia as well as the susceptibility of various cell types in the affected brain region. In the present study, the effects of Nodus Nelumbinis Rhizomatis Extract(NNRe) were tested for the anti-oxidative action of rCBF. Methods : Regional cerebral blood flow(rCBF) were determined by LDF methods. LDF allows for real time, noninvasive, continuous recordings of local CBF. The LDF method has been widely used to trace hemodynamic changes in the superficial or the deep brain structures in experimental stroke research. Results : NNRe treatment showed no change on rCBF in methylene blue, ODQ and L-NNA pretreated rats. 120 minutes of MCAO and followed reperfusion, 0.1% concentration of NNR treatment improved the altered cerebral hemodynamics of cerebral ischemic by increasing rCBF. Conclusions : The ischemia/reperfusion induced oxidative stress may have contributed to cerebral damage in rats, and the present study provides clear evidences for the beneficial effect of NNR on ischemia/reperfusion induced brain injury.

• The Korean Journal of Physiology and Pharmacology
• /
• 제23권5호
• /
• pp.329-334
• /
• 2019

Diabetes is associated with an increased risk of cardiovascular complications. Dipeptidyl peptidase-4 (DPP-IV) inhibitors are used clinically to reduce high blood glucose levels as an antidiabetic agent. However, the effect of the DPP-IV inhibitor gemigliptin on ischemia/reperfusion (I/R)-induced myocardial injury and hypertension is unknown. In this study, we assessed the effects and mechanisms of gemigliptin in rat models of myocardial I/R injury and spontaneous hypertension. Gemigliptin (20 and 100 mg/kg/d) or vehicle was administered intragastrically to Sprague-Dawley rats for 4 weeks before induction of I/R injury. Gemigliptin exerted a preventive effect on I/R injury by improving hemodynamic function and reducing infarct size compared to the vehicle control group. Moreover, administration of gemigliptin (0.03% and 0.15%) powder in food for 4 weeks reversed hypertrophy and improved diastolic function in spontaneously hypertensive rats. We report here a novel effect of the gemigliptin on I/R injury and hypertension.

• 대한중풍순환신경학회지
• /
• 제10권1호
• /
• pp.8-19
• /
• 2009

Scutellaria Radix, originated from Scutellaria baicalensis Georgi, is one of the most important medicine in traditional Oriental medicine, and possesses anti-bacterial activity and sedative effects, can be applied in the treatment of a range of conditions including diarrhea and hepatitis. It is reported that chronic global ischemia induces neuronal damage in selective, vulnerable regions of the brain, especially the hippocampus and cerebral cortex. In the present study, to investigate the effect of Scutellaria Radix extract on cerebral disease, the changes of regional cerebral blood flow and pial arterial diameter on ischemia/reperfusion state was determinated by Laser-Doppler Flowmetry and some parameters concerned with oxidative stress also measured. When SRe were administered for five days with the concentration of 100 mg/kg, GSH activity significantly increased. But SRe administeration showed no significant change in lipid peroxidation. When the activities of CAT, Cu, Zn-SOD and GSH were measured, CAT and GSH were activated by SRe administration. When 1 and 3 ㎍/㎖ SRe was applied to the neuronal cell cultures, the quantities of LDH was significantly reduced when compared with cultures treated only with NMDA. Through this study, it can be concluded that the ischemia/reperfusion induced brain stress may have contributed to cerebral damage in rats, and the present study provides clear evidence for the beneficial effect of SRe on ischemia induced brain injury.

• Journal of Yeungnam Medical Science
• /
• 제41권2호
• /
• pp.61-73
• /
• 2024

Acute kidney ischemia-reperfusion (IR) injury is a life-threatening condition that predisposes individuals to chronic kidney disease. Since the kidney is one of the most energy-demanding organs in the human body and mitochondria are the powerhouse of cells, mitochondrial dysfunction plays a central role in the pathogenesis of IR-induced acute kidney injury. Mitochondrial dysfunction causes a reduction in adenosine triphosphate production, loss of mitochondrial dynamics (represented by persistent fragmentation), and impaired mitophagy. Furthermore, the pathological accumulation of succinate resulting from fumarate reduction under oxygen deprivation (ischemia) in the reverse flux of the Krebs cycle can eventually lead to a burst of reactive oxygen species driven by reverse electron transfer during the reperfusion phase. Accumulating evidence indicates that improving mitochondrial function, biogenesis, and dynamics, and normalizing metabolic reprogramming within the mitochondria have the potential to preserve kidney function during IR injury and prevent progression to chronic kidney disease. In this review, we summarize recent advances in understanding the detrimental role of metabolic reprogramming and mitochondrial dysfunction in IR injury and explore potential therapeutic strategies for treating kidney IR injury.