• Journal of Chest Surgery
• /
• v.26 no.6
• /
• pp.441-451
• /
• 1993

Protective effect of superoxide dismutase[SOD] and substrates on acute ischemic and reperfused myocardium was assessed by cardiac microdialysis. 30 Rabbits were divided into 4 groups; normal control group [group I, n=5], ischemic group [group II, n=5], SOD treated group [group III, n=10], and substrates treated group [group IV, n=10]. After a microdialysis apparatus was implanted in rabbit myocardium, coronary artery was occuluded for 5 minutes and reperfusion was performed for 30 minutes. Hemodynamic changes, CK-MB isoenzyme level and adenine ring compound level in effluent dialysates [equilibrated with interstitial fluid], and ultrastructural changes of myocardial cell were analysed. Systolic blood pressure at 10 and 30 minutes after reperfusion was higher in group III and IV than in group II [p<.05]. Also percent recovery of systolic blood pressure in group III [p<.01] and IV [p<.02] was higher than in group II. CK-MB isoenzyme level in effluent dialysates was peaked at 10 minutes after reperfusion, thereafter decreased in group II, III and IV. At 30 minutes after reperfusion, its level was lower in group III and IV than in group II[p<.05]. Adenine ring compound level in effluent dialysates increased till 10 minutes after reperfusion and progressively decreased. At 10 and 30 minutes after reperfusion, its level was lower in group III and IV than in group II without significance. Degree of myocardial damage was estimated by scoring of mitochondrial injury. Group I was within normal range and most severe injury was seen in group II. And the score of mitochondrial injury in group III and IV was lower than in group II. In conclusion, SOD and substrates[KMP solution] had protective effect on stunned myocardium. The microdialysis appratus was a good device for studying stunned myocardium, and cardiac microdialysis might be a unique technique for analysis of regional intramyocardial interstitial fluid.

• Journal of Ginseng Research
• /
• v.46 no.2
• /
• pp.275-282
• /
• 2022

Background: Stroke is a neurological disorder characterized by brain tissue damage following a decrease in oxygen supply to brain due to blocked blood vessels. Reportedly, 80% of all stroke cases are classified as cerebral infarction, and the incidence rate of this condition increases with age. Herein, we compared the efficacies of Korean White ginseng (WG) and Korean Red Ginseng (RG) extracts (WGex and RGex, respectively) in an ischemic stroke mouse model and confirmed the underlying mechanisms of action. Methods: Mice were orally administered WGex or RGex 1 h before middle cerebral artery occlusion (MCAO), for 2 h; the size of the infarct area was measured 24 h after MCAO induction. Then, the neurological deficit score was evaluated and the efficacies of the two extracts were compared. Finally, their mechanisms of action were confirmed with tissue staining and protein quantification. Results: In the MCAO-induced ischemic stroke mouse model, WGex and RGex showed neuroprotective effects in the cortical region, with RGex demonstrating superior efficacy than WGex. Ginsenoside Rg1, a representative indicator substance, was not involved in mediating the effects of WGex and RGex. Conclusion: WGex and RGex could alleviate the brain injury caused by ischemia/reperfusion, with RGex showing a more potent effect. At 1,000 mg/kg body weight, only RGex reduced cerebral infarction and edema, and both anti-inflammatory and anti-apoptotic pathways were involved in mediating these effects.

• The Korean Journal of Physiology and Pharmacology
• /
• v.1 no.6
• /
• pp.665-672
• /
• 1997

This study aimed to investigate the mechanism of cerebroprotection of platelet-activating factor(PAF) antagonists in transient cerebral ischemia of rat. Right middle cerebral artery(MCA) of Sprague-Dawley rat was occluded for 2 hours using an intraluminal filament technique. After 22 hours of reperfusion, morphometrically detectable infarct was developed in the cortex and striatum identical to the territory of MCA. The infarct size was significantly reduced by PAF antagonists, BN 52021 and CV-6209, as well as an inducible nitric oxide synthase(iNOS) inhibitor aminoguanidine(1 mg/kg, i.p., respectively) administered 5 min after MCA occlusion. PAF antagonists significantly inhibited the enzymatic activities of both myeloperoxidase and iNOS in the cerebral hemisphere ipsilateral to ischemia, whereas aminoguanidine did not inhibit myeloperoxidase activity but significantly inhibited the iNOS activity. These results suggest that PAF antagonists exert a cerebroprotective effect against ischemic brain damage through inhibition of leukocyte infiltration and iNOS activity in the postischemic brain.

• Biomolecules & Therapeutics
• /
• v.7 no.4
• /
• pp.354-361
• /
• 1999

In this study, the effects of tauroursodeoxycholic acid (TUDCA) on ischemia/ reperfusion injury were investigated on isolated heart perfusion models. Hezrts were perfused with oxygenated Krebs-henseleit solution (pH 7.4, $37^{\cire}C$) on a Langendorff apparatus. After equilibration, isolated hearts were treated with TUDCA 100 and 200 $\mu\textrm{M}$ or vehicle (0.02% DMSO) for 10 min before the onset of ischemia in single treatment group. In 7 day pretreatment group. TUDCA 50, 100 and 200 mg/kg body weight were given orally for 7 days before operation. After global ischemia (30 min), ischemic hearts were reperfused for 30 min. The physiological (i.e. heart rate, left ventricdular developed pressure, coronary flow, double product, time to contracture formation) and biochemical (lactate dehydrogenase; LDH) parameters were evaluated. In vehicle-treated group, time to contracture formation was 810 sec during ischemia, LVDP was 34.0 mmHg at the endpoint of reperfusion and LDH activity in total reperfusion effluent was 34.3 U/L. Single treatment with TUDCA did not change the postischemic recovery of cardiac function, LDH and time to contractur compared with ischemic control group. TUDCA pretreatment showed the tendency to decrease LDH release and to increase time to contracture and coronary flow. Our findings suggest that TUDCA does not ameliorate ischemia/reperfusion-reduced myocardial damage.

• Biomolecules & Therapeutics
• /
• v.5 no.3
• /
• pp.306-315
• /
• 1997

In order to investigate pharmacological properties of ι -muscone, effects of ι-muscone and musk on cerebral ischemia and central nervous system were compared. Cerebral ischemia insult was performed using unilateral carotid artery occlusion in Mongolian gerbils. The histological observations showed a preventive effect of the ι-muscone treatment with ischemia-induced brain damage. The ATP in brain tissue was decreased in vehicle-treated ischemic gerbils. This decrease was prevented by the ι-muscone treatment. In contrast to what was seen with ATP, the lactate and lipid peroxide were both elevated in vehicle-treated ischemic gerbils.˙ This elevation was prevented by the ι-muscone treatment. While ι-muscone had no effects on the hexobarbital-induced sleeping time and the convulsions induced by electric shock, pentetrazol and strychnine, it had effect on rotarod test and spontaneous activity test. Respiration rate and depth were increased by the ι-muscone treatment. Furthermore, ι-muscone showed anti-stress effect. Our findings suggest that the pharmacological profile of ι-muscone on cerebral ischemia and central nervous system are similar to that of musk.

• Journal of Chest Surgery
• /
• v.32 no.5
• /
• pp.480-483
• /
• 1999

The widely accepted method for coronary artery bypass grafting(CABG) is performing the distal coronary artery anastomoses on the flaccid and nonbeating heart with the aid of cardiopulmonary bypass(CPB) and cardioplegic arrest. However, current cardioplegic techniques are not consistent in avoiding myocardial ischemic damages especially in high risk patients undergoing CABG. In this regard, "Off-Pump" seems to be an ideal method for preventing myocardial ischemic damage and adverse effects during CPB. However, "Off-pump" CABG is not always technically feasible. We report 2 cases of "On-pump" CABG performed on the beating heart in high risk patients; The first patient had left ventricular dysfunction(Ejection Fraction=25%), and the second patient had cardiogenic shock after percutaneous transluminal coronary angioplasty.

• The Korean Journal of Physiology and Pharmacology
• /
• v.8 no.4
• /
• pp.187-194
• /
• 2004

Middle cerebral artery occlusion (MCAO) results in cell death by activation of complex signal pathways for cell death and survival. Hypothermia is a robust neuroprotectant, and its effect has often been attributed to various mechanisms, but it is not yet clear. Upstream from the cell death promoters and executioners are several enzymes that may activate several transcription factors involved in cell death and survival. In this study, we immunohistochemically examined the phosphorylation of mitogen-activated protein kinase, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 kinase during early period of the ischemic injury, following 2 hours (h) of transient MCAO. Increased phosphorylation of ERK and p38 was observed in the vessels at 3 h, neuron-like cells at 6 and 12 h and glia-like cells at 12 h. Activation of JNK was not remarkable, and a few cells showed active JNK following ischemia. Phosphorylation of Elk-1, a transcription factor, was reduced by ischemic insult. Hypothermia attenuated the activation of ERK, p38 and JNK, and inhibited reduction of Elk-1. These data suggest that signals via different MAPK family members converge on the cell damage process and hypothermia protects the brain by interfering with these pathways.

• 한국생물공학회:학술대회논문집
• /
• 2005.10a
• /
• pp.205-205
• /
• 2005

• The Journal of Korean Medicine
• /
• v.24 no.2
• /
• pp.204-212
• /
• 2003

Current therapy for acute ischemic stroke is highly focused on neuroprotective agents, and many herbal medicines have been challenged for experimental models. The aim of this study is to investigate whether Angelicae gigantis Radix can protect nerve cells against ischemic neural damage of middle cerebral artery occlusion (MCAO) in rats' brains. Rats were treated with Angelicae gigantis Radix immediately after 2 hours of MCAO for 7 days. On the 7th day, the brains of the rats were sliced through the hippocampus and dyedby c-Fos immunohistochemistry stain and cresyl violet stain for microscopic examination. The number of viable neurons and c-Fos immunoreactive cells in CA1 regions was counted. MCAO caused significant decrease in density of neurons and c-Fos immunoreactive cells compared to those of sham-operated rats. Administration of Angelicae gigantis Radix significantly elevated MCAO-induced decrease in density of neurons and c-Fos immunoreactive cells. These results suggest that the neuroprotective effect of Angelicae gigantis Radix against focal cerebral ischemia is related to c-Fos gene expression. Thus, these findings indicate that Angelicae gigantis Radix can be used for treatment and prevention of cerebral ischemia.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.19 no.6
• /
• pp.1546-1551
• /
• 2005

This Study was designed to investigate the effects of Nelumbinis Rhizomatis Nodus (NRN) on the change of cerebral hemodynamics [regional cerebral blood flow (rCBF), pial arterial diameter (PAD) and mean arterial blood pressure (MABP)] in normal and cerebral ischemic rats. And, this study was designed to investigate the inhibition of lactate dehydrogenase activity in neuronal cells The results were as follows NRN significantly increased rCBF and PAD in a dose-dependent manner, and NRN increased MABP in a dose-dependent manner. This results suggested that NRN significantly increased rCBF by dilating PAD. Both rCBF and PAD were significantly and stably increased by NRN (10 mg/kg, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in control group. NRN significantly inhibited lactate dehydrogenase activity in neuronal cells. This results suggested that NRN prevented the neuronal death. It is suggested that NRN had an anti-ischemic effect through the improvement of cerebral hemodynamics and inhibitive effect on the brain damage.