• YAKHAK HOEJI
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• v.43 no.6
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• pp.756-761
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• 1999

Lipid peroxidation mediated by hydroxyl radicals which are generated during myocardial ischermia has suggested as a possible mechanism of ischemic myocardial damage. Recently, it has been reported that anti-arrhythmic action of lidocaine, a local anesthetic, is attributed to its "membrane-stabilizing" properties through scavenging free radicals, thus, inhibiting lipid peroxidation. Aldehyde oxidase and xanthine oxidase which catalyze the oxidation of many purine, pyrimidine and pteridine derivatives are known as free radical generating systems. In this experiment, we studied the effect of lidocaine and procainamide on the hepatic aldehyde and xanthine oxidase activity and antioxidative activities. It was found that lidocaine and procainamide inhibited both NADPH-dependent and independent lipid peroxidation. Both of tested compounds were found to be ineffective in inhibiting xanthine oxidase. Lidocaine and procainamide, however, inhibited aldehyde oxidase activity in vitro as well as in vivo. Based on the above results, lidocaine and procainamide could be employed as a therapeutic agent for aldehyde oxidaserelated disease.d disease.

• Journal of Yeungnam Medical Science
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• v.23 no.1
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• pp.113-117
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• 2006

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that may affect many organ systems including the nervous system. The immune response in patients with SLE can cause inflammation and other damage that can cause significant injury to the arteries and tissues. A 48-year-old woman was admitted to the hospital because of transient monocular blindness. Magnetic resonance imaging and conventional angiography showed severe stenosis of the distal intracranial internal carotid artery. The patient was diagnosed as having SLE but the antiphospholipid antibodies were negative. Amaurosis fugax has not been previously reported as an initial manifestation of SLE in Korea. We report a patient with a retinal transient ischemic attack as the first manifestation of SLE.

• Korean Journal of Clinical Pharmacy
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• v.29 no.2
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• pp.109-114
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• 2019

Background: Rheumatoid arthritis (RA) is a systemic inflammatory disease that manifests as joint damage or athletic disability via sustained inflammation of the synovial membrane. The risk of cardiovascular disease (CVD) is higher in RA patients. This study aimed at evaluating the association between CVD comorbidities and RA by comparing a pharmacotherapy group with a non-pharmacotherapy group. Methods: Patient sample data from the Health Insurance Review and Assessment Service (HIRA-NPS-2016) were used. Inverse probability of treatment weighting (IPTW) using the propensity score was used to minimize the differences in patient characteristics. Logistic regression analysis was used to evaluate the risk of CVD comorbidities. Results: The analyses included 1,207,213 patients, of which 33,122 (2.8%) had RA. The odds ratios (OR) of CVD comorbidities were increased in RA patients; ischemic heart disease (IHD: OR 1.75; 95% CI 1.73, 1.77), cerebral infarction (CERI: OR 1.28; 95% CI 1.26, 1.30), hypertension (HTN: OR 1.44; 95% CI 1.43, 1.45), diabetes mellitus (DM: OR 2.04; 95% CI 2.03, 2.06), and dyslipidemia (DL: OR 3.49; 95% CI 3.47, 3.51). The ORs of IHD, CERI, HTN, and DM in the traditional DMARD and biologic treatment groups were decreased, compared with those in the non-pharmacotherapy group. Conclusions: Thus, CVD risk was higher in RA patients, considering age, sex, and socioeconomic status. Appropriate pharmacotherapy could decrease the risk of CVD comorbidities in RA patients.

• The Korean Journal of Emergency Medical Services
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• v.25 no.1
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• pp.243-249
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• 2021

A decrease in coronary blood flow leads to an imbalance between the supply of oxygen to the myocardium and its demand, and reversible or irreversible damage to the myocardium could occur depending on the severity of the resultant ischemia and the duration of the imbalance. This imbalance results in a cascade of ischemic reactions in the following order: metabolic abnormalities, diastolic dysfunction, systolic dysfunction, and electrocardiogram changes. Variant angina is caused by the closure of the coronary artery due to reversible coronary artery spasm, resulting in myocardial ischemia and subsequent chest pain as a clinical symptom. Variant angina may be observed as ST segment elevation in electrocardiogram measured when present in chest pain. However, 12-lead electrocardiogram performed after the patient's chest pain resolves does not help in the diagnosis. Since the duration of chest pain appears to be <15 minutes, it is important to perform the 12-lead electrocardiogram when clinical symptoms are present. If nitroglycerin is administered without performing 12-lead electrocardiogram by 119 pre-hospital paramedics, the chest pain would be resolved, making it impossible to identify changes in the ST segment. Before administration of nitroglycerin, changes in the ST segment must be recorded by performing 12-lead electrocardiogram.

• BMB Reports
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• v.55 no.7
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• pp.336-341
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• 2022

Narrowing of arteries supplying blood to the limbs provokes critical hindlimb ischemia (CLI). Although CLI results in irreversible sequelae, such as amputation, few therapeutic options induce the formation of new functional blood vessels. Based on the proangiogenic potentials of stem cells, in this study, it was examined whether a combination of dental pulp stem cells (DPSCs) and human umbilical vein endothelial cells (HUVECs) could result in enhanced therapeutic effects of stem cells for CLI compared with those of DPSCs or HUVECs alone. The DPSCs+ HUVECs combination therapy resulted in significantly higher blood flow and lower ischemia damage than DPSCs or HUVECs alone. The improved therapeutic effects in the DPSCs+ HUVECs group were accompanied by a significantly higher number of microvessels in the ischemic tissue than in the other groups. In vitro proliferation and tube formation assay showed that VEGF in the conditioned media of DPSCs induced proliferation and vessel-like tube formation of HUVECs. Altogether, our results demonstrated that the combination of DPSCs and HUVECs had significantly better therapeutic effects on CLI via VEGF-mediated crosstalk. This combinational strategy could be used to develop novel clinical protocols for CLI proangiogenic regenerative treatments.

• International Journal of Computer Science & Network Security
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• v.23 no.11
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• pp.183-189
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• 2023

A stroke is a medical disease where a blood vessel in the brain ruptures, causes damage to the brain. If the flow of blood and different nutrients to the brain is intermittent, symptoms may occur. Stroke is other reason for loss of life and widespread disorder. The prevalence of stroke is high in growing countries, with ischemic stroke being the high usual category. Many of the forewarning signs of stroke can be recognized the seriousness of a stroke can be reduced. Most of the earlier stroke detections and prediction models uses image examination tools like CT (Computed Tomography) scan or MRI (Magnetic Resonance Imaging) which are costly and difficult to use for actual-time recognition. Machine learning (ML) is a part of artificial intelligence (AI) that makes software applications to gain the exact accuracy to predict the end results not having to be directly involved to get the work done. In recent times ML algorithms have gained lot of attention due to their accurate results in medical fields. Hence in this work, Stroke disease identification system by using Machine Learning algorithm is presented. The ML algorithm used in this work is Artificial Neural Network (ANN). The result analysis of presented ML algorithm is compared with different ML algorithms. The performance of the presented approach is compared to find the better algorithm for stroke identification.

• The Journal of Internal Korean Medicine
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• v.22 no.4
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• pp.503-512
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• 2001

Objective : This study was carried out to investigate the effects of DDT on the brain damage and hypertension. Methods : We observed the effect of Dodamtang(DDT) extract on KCN-induced coma, focal brain ischemia by MCA occlusion, cytotoxicity and protection of PC12 cells and B103 cells induced by amyloid ${\beta}$ protein(25-35). To prove the effect of DDT as a blood pressure depressant, we measured aldosterone, renin activity, catecholamine, sodium and NO density using the seperated blood plasma. Results : DDT showed a protective effect on cytotoxicity of PC12 cells and B103 cells induced by amyloid ${\beta}$ protein(25-35) in a dose dependent manner and proved the significant abridgement of brain ischemic area and edema induced by MCA occlusion, a critical decrease of neurologic deficitic grade in the fore-limbs. DDT didn't reduce the duration of KCN(1.87mg/kg iv.)-induced coma and prolonged the survival rate in the case of KCN(3.0mg/kg iv.)-induced coma by the ratio of 20%. While DDT increased the value of NO in SHR, it significantly decreased the blood pressure of SHR and the value of aldosterone& epinephrine in SHR. Conclusions : These results suggested that DDT might be usefully applied for treatment of hypertension, cerebral infarction, and brain damage.

• Journal of Chest Surgery
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• v.31 no.8
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• pp.739-748
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• 1998

Background: It has been well documented that transient occlusion of the coronary artery causes myocardial ischemia and finally cell death when ischemia is sustained for more than 20 minutes. Extensive studies have revealed that ischemic myocardium cannot recover without reperfusion by adequate restoration of blood flow, however, reperfusion can cause long-lasting cardiac dysfunction and aggravation of structural damage. The author therefore attempted to examine the effect of postischemic reperfusion on myocardial ultrastructure and to determine the rationales for recanalization therapy to salvage ischemic myocardium. Materials and methods: Young Holstein-Friesian cows(130∼140 Kg body weight; n=40) of both sexes, maintained with nutritionally balanced diet and under constant conditions, were used. The left anterior descending coronary artery(LAD) was occluded by ligation with 4-0 silk snare for 20 minutes and recanalized by release of the ligation under continuous intravenous drip anesthesia with sodium pentobarbital(0.15 mg/Kg/min). Drill biopsies of the risk area (antero-lateral wall) were performed at just on reperfusion(5 minutes), 1-, 2-, 3-, 6-, 12-hours after recanalization, and at 1-hour assist(only with mechanical respiration and fluid replacement) after 12-hour recanalization. The materials were subdivided into subepicardial and subendocardial tissues. Tissue samples were examined with a transmission electron microscope (Philips EM 300) at the accelerating voltage of 60 KeV. Results: After a 20-minute ligation of the LAD, myocytes showed slight to moderate degree of ultrastructural changes including subsarcolemmal bleb formation, loss of nuclear matrix, clumping of chromatin and margination, mitochondrial destruction, and contracture of sarcomeres. However, microvascular structures were relatively well preserved. After 1-hour reperfusion, nuclear and mitochondrial matrices reappeared and intravascular plugging by polymorphonuclear leukocytes or platelets was observed. However, nucleoli and intramitochondrial granules reappeared within 3 hours of reperfusion and a large number of myocytes were recovered progressively within 6 hours of reperfusion. Recovery was apparent in the subepicardial myocytes and there were no distinct changes in the ultrastructure except narrowed lumen of the microvessels in the later period of reperfusion. Conclusions: It is likely that the ischemic myocardium could not be salvaged without adequate restoration of coronary flow and that the microvasculature is more resistant to reversible period of ischemia than subendocardium and subepicardium. Therefore, thrombolysis and/or angioplasty may be a rational method of therapy for coronarogenic myocardial ischemia. However, it may take a relatively longer period of time to recover from ischemic insult and reperfusion injury should be considered.

• Journal of Chest Surgery
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• v.31 no.1
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• pp.20-27
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• 1998

It is well known that troponin T(below TnT) is present in the myocardial cells and released during myocardial damage, so it`s very specific enzyme to myocardium. Availability of cardiac specific TnT in assessing perioperatively myocardial damage was evaluated from 34 open heart surgery patients. They consisted of 11 ischemic heart, 13 acquired valvular heart and 10 congenital heart cases. Patients were divided into two groups, group A(patients with myocardial damage) and group B(patients without myocardial damage), according to the symptom of chest pain suspecting angina and the ECG findings of ST segment and T wave changes which show myocardial ischemia and injury. Serum TnT levels were measured by enzyme immunoassay method preoperatively, immediately postoperatively, postoperative day 1, day 2, day 3, and day 7. We observed and analyzed the changes of serum TnT levels in two groups and compared the serum TnT levels with CK-MB levels measured at the same time. In group A, serum TnT levels showed 1.37$\pm$0.26$\mu$g/L, 3.16$\pm$0.66$\mu$g/L, 2.39$\pm$0.74$\mu$g/L, 2.49$\pm$0.76$\mu$g/L, and 1.23$\pm$0.60$\mu$g/L, immediate postoperatively, postoperatively day1, day2, day3, and day7, respectively. It was observed there were significant differences compared with those of group B(0.38$\pm$0.04$\mu$g/L, 0.34$\pm$0.05$\mu$g/L, 0.25$\pm$0.03$\mu$g/L, 0.24$\pm$0.04$\mu$g/L, and 0.11$\pm$0.03$\mu$g/L) during identical periods(P<0.01). Serum CK-MB level in group A significantly elevated to 145.04$\pm$35.08 IU/L on the postoperative day 1 compared to group B(31.28$\pm$5.87 IU/L, P<0.05), However, it stiffly decreased from day 2 and returned to preoperative level at day 3. When serum TnT level more than 1.0$\mu$g/L is thought to reflect myocardial damage, serum TnT had 100% of sensitivity and 87% of specificity in diagnosing the postoperative myocardial damage(p<0.01). I conclusion, serum TnT levels increased significantly at very early stage of myocardial damage and persisted much longer period than CK-MB. This suggests that serum TnT has more advantage and availability in assessing the perioperatively myocardial damage than any other tests.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.6
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• pp.681-690
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• 1997

Loss of synaptic transmission and accumulation of extracellular $K^+([K^+]_O)$ are the key features in ischemic brain damage. Here, we examined the effects of several $K^+$channel modulators on the early ischemic changes in population spike (PS) and $[K^+]_o$ in the CA1 pyramidal layer of the rat hippocampal slice using electrophysiological techniques. After onset of anoxic aglycemia (AA), orthodromic field potentials decreased and disappeared in $3.3{\pm}0.22\;min$ $(mean{\pm}SEM,\;n=40)$. The hypoxic injury potential (HIP), a transient recovery of PS appeared at $6.0{\pm}0.25\;min$ (n=40) in most slices during AA and lasted for $3.3{\pm}0.43\;min$. $[K^+]_o$ increased initially at a rate of 0.43 mM/min (Phase 1) and later at a much faster rate (12.45 mM/min, Phase 2). The beginning of Phase 2 was invariably coincided with the disappearance of HIP. Among $K^+$ channel modulators tested such as 4-aminopyridine (0.03, 0.3 mM), tetraethylammonium (0.1 mM), NS1619 $(0.3{\sim}10\;{\mu}M)$, niflumic acid (0.1 mM), glibenclamide $(40\;{\mu}M)$, tolbutamide $(300\;{\mu}M)$ and pinacidil $(100\;{\mu}M)$, only 4-aminopyridine (0.3 mM) induced slight increase of $[K^+]_o$ during Phase 1. However, none of the above agents modulated the pattern of Phase 2 in $[K^+]_o$ in response to AA. Taken together, the experimental data suggest that 4-aminopyridine-sensitive $K^+$channels, large conductance $Ca^{2+}-activated$ $K^+$ channels and ATP-sensitive $K^+$ channels may not be the major contributors to the sudden increase of $[K^+]_o$ during the early stage of brain ischemia, suggesting the presence of other routes of $K^+$ efflux during brain ischemia.