• 대한약침학회지
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• 제21권3호
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• pp.159-167
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• 2018

Objectives: Myocardial reperfusion is the only logical cure for ischemic heart disease. However, ischemic-reperfusion (I/R) injury is one of the underlying factors facilitating and accelerating the apoptosis in the myocardium. This study set to investigate the impact of Teucrium polium (TP) hydro-alcoholic extract on I/R induced apoptosis in the isolated rat heart. Methods: Isolated rat hearts were classified into six groups. The control samples were subjected to 80 min of perfusion with Krebs-Henseleit bicarbonate (KHB) buffer; in control-ischemia group, after primary perfusion (20 min) the hearts were exposed to global ischemia (20 min) and reperfusion (40 min). Pretreated groups were perfused with $500{\mu}M$ of vitamin C and various TP concentrations (0.5, 1, 2 mg/ml) for 20 min, and then the hearts were exposed to ischemia and reperfusion for 20 min and 40 min, respectively. Cardiodynamic parameters including rate pressure product (RPP), heart rate (HR), the maximum up/down rate of left ventricular pressure (${\pm}dp/dt$), left ventricular developed pressure (LVDP), and coronary artery flow (CF) were achieved from Lab Chart software data. The Bax and BCl-2 gene expressions were measured in heart samples. Results: Hearts treated with TP extract and vit C represented a meaningful improvement in cardiac contractile function and CF. The overexpression of Bcl-2, downregulation of Bax, and improvement of apoptotic index (Bax/Bcl-2) were observed in pretreated TP extract and vit C hearts. Conclusion: The TP extract was found to ameliorate the cardiac function in the reperfused myocardium. Also, it can hinder apoptotic pathways causing cardioprotection.

• Journal of Chest Surgery
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• 제17권2호
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• pp.280-285
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• 1984

Although it is suspected that the foreign body sensation on the pharyngoesophageal region is caused by motility disturbance of upper esophageal sphincter, its pathophysiology is not yet clear. Esophageal manometry has become an important diagnostic tool in the evaluation of esophageal motor disorders such as dysfunction of upper esophageal sphincter. Intraluminal esophageal pressures were measured by perfusion manometry in fifteen patients with foreign body sensation on the pharyngoesophageal region and in twenty six controls. In upper esophageal sphincter, mean value of resting pressure of the patients by rapid pull-through technique was 45,9\ulcorner 15.6mmHg and 80.9\ulcorner9.7mmHg in the controls. The difference between the two groups was statistically significant. The distance from nostril to sphincter, length of sphincter, and resting pressure by station pull-through technique were not significantly different. The amplitude of esophageal peristalsis in the patients was reduced significantly at the level of the upper, mid and lower esophagus. The wave duration of the patients was reduced significantly at the level the upper and mid esophagus. The speed showed no difference between two groups. Length and resting pressure of lower esophageal sphincter revealed almost same values in two groups.

• Journal of Chest Surgery
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• 제33권8호
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• pp.605-612
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• 2000

Background: Ischemic preconditioning enhances the tolerance of myocardium against ischemia/reperfusion injury, with the enhancement of the recovery of post-ischemic myocardial function. This study was disigned to assess whether the protective effect of ischemic preconditioning could provide one additional hour of myocardial preservation in four hour myocardial ischemia in a rate heart. Material and method: Fourty four Spargue-Dawley rats, weighing 300~450gm, were divided into four groups. Group 1(n=7) and group 3(n=12) were subjected to 30 minutes of aerobic Langendorff perfusion without ischemic preconditioning and then preserved in saline solution at 2~4$^{\circ}C$ for 4 hours and 5 respectively. Group 2(n=7) and group 4(n=18) were perfused in the same way for 20 minutes, followed by 3 minutes of global mormothermic ischemia and 10 minutes of perfusion and then preserved in the same cold saline solution for 4 hours and 5 hours respectively. Heart rate, left ventricular developed pressure(LVDP), and coronary flow were measured at 15 minutes during perfusion as baseline. Spontaneous defibrillation time was measured after reperfusion. Heart rate, LVDP, and coronary flow were also recorded at 15 minutes, 30 minutes, and 45 minutes during reperfusion. Samples of the apical left ventricular wall were studied using a transmission electron microscope. Result: Time of spontaneous defibrillation(TSD) was significantly longer in group 4 than in group 1(p<0.001), and TSD in group 1 was significantly longer in comparision to that of group 2(p<0.05). Heart rate at 45 minutes was significantly higher in group 1 than in group 4(p<0.05). Heart rate at 15 min was significantly higher in group 2 than in group 1(p<0.001) and in group 4 than in group 3(p<0.05). Left ventricular developed pressure(LVDP) at 30 minutes and 45 minutes was higher in group 1 than in group 4(p<0.01), LVDP at 45 minutes was higher in group 4 than in group 3(p<0.05). Rate-pressure product(RPP) at 30 minutes and 45 minutes was higher in group 1 than in group 4(p<0.05). RPP at 15 minutes was higher in group 2 than in group 1(p<0.01). RPP at 30 minutes and 45 minutes was higher in group 4 than in group 3(p<0.05). Group 2 showed relatively less sarcoplasmic edema and less nuclear chromatin clearance than group 1. Group 4 showed less myocardial cell damage than group 3, group 4 showed less myocardial cell damage than group 3, group 4 showed more myocardial cell edema than group 1. Conclusion: Ischemic preconditioning enhanced the recovery of postischemic myocardial function after 4 hours and 5 hours preservation. However, it was not demonstrated that ischemic preconditioning could definitely provide one additional hour of myocardial preservation in four hour myocardial ischemia in a rat heart.

• 대한핵의학회:학술대회논문집
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• 대한핵의학회 2001년도 제40차 추계학술대회 및 총회
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• pp.41.2-41.2
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• 2001

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1995년도 제3회 추계심포지움
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• pp.115-124
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• 1995

The purpose of the present study was to address whether the in vivo noradrenergic neural activities in the locus coeruleus are involved in the regulation of blood pressure. Two groups of the animals were prepared, 1) SHR and 2) age-matched normotensive control, WKY. At the age of 6 and 16 weeks, blood pressure and the releases of NE from the locus coeruleus in SHR and KWY were measured by in vivo microdialysis at three different conditions: 1) normal, 2) elevated state of blood pressure by systemic injected phenylephrine and 3) increased state of neural activity by perfused phenylephrine into the locus coeruleus. The basal release of NE of SHR were significantly higher than that of WKY, Phenylephrine treatment caused elevation of blood pressure in both SHR and WKY in dose-dependent manner. Following phenylephrine injection, the releases of NE from the locus coeruleus of SHR were significantly decreased, whereas the significant change of NE in WKY was observed in the highest dose of phenylephrine. Phenylephrine perfusion into the locus coeruleus through microdialysis probe caused pressor responses and the pressor response in SHR was greater compared with that in WKY. The results from the present study suggests that the noradrenergic nervous system in the locus coeruleus may contribute as one of the development and maintenance factors for hypertension in SHR.

• Archives of Reconstructive Microsurgery
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• 제3권1호
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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.

• Journal of Chest Surgery
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• 제17권4호
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• pp.574-586
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• 1984

Although corticosteroid have been shown to stabilize lysosomal membranes and prevent release of hydrolytic enzymes, the mechanism of membrane stabilization remains obscure. This study described functional assessment of efficiency of methylprednisolone in GIK solution by using a isolated Rat Heart Model. Isolated rat heart were subjected to a 2-minute period of coronary infusion with a cold GIK or methylprednisolone mixed cold GIK solution immediately before and also at the midpoint of a 60-minute period of hypothermic [$10{\pm}1^{\circ}C$] ischemic arrest. The result of this were as follow: 1.Spontaneous heart beat after ischemic arrest occurred 11 second later after Langendorffs reperfusion in the methylprednisolone mixed GIK group and 14 second later in the control group. 2.The percentage of recoveries of heart rate at 30 minute after postischemic working heart perfusion was 88.6\ulcorner.6% in the methylprednisolone mixed GIK group. This percentage of recovery was not significantly greater than the control group. 3.The percentage of heart function at 30 minute after postischemic working heart perfusion were; peak aortic pressure $90.8{\pm}4.5%$ coronary flow $87.5{\pm}1.45$ and aortic flow $74.9{\pm}11.8%$ in the methylprednisolone mixed GIK group. This percentage of recovery was significantly greater than the control group. [p<0.05]

• International Journal of Vascular Biomedical Engineering
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• 제4권1호
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• pp.9-16
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• 2006

In this article we introduce computer models that have been developed in the past to determine the concentration of metabolic gases, the oxygen and carbon dioxide, along the pulmonary circulation. The terminal concentration of these gases in the arterial blood is related with the total change of the partial pressure of the same gases in the alveoli for the time beginning with inspiration and ending with expiration. It is affected not only by the ventilation-perfusion ratio and the gas diffusion capacity of the lung membrane but also by the pulmonary defect such as shunt, dead space, diffusion impairment and ventilation-perfusion mismatch. Some pathological pulmonary symptoms such as ARDS and CDPD can be understood through the mathematical models of these pulmonary dysfunctions. Quantitative study on the blood oxygenation process using various computer models is therefore of foremost importance in order to monitor not only the pulmonary health but also the cardiac output and cell metabolism. Reviewed in this paper include the basic and advanced methods that enable numerical study on the gas exchange and on the arterial oxygenation process, which might depend on the various heart and lung physiological conditions listed above.

• The Korean Journal of Physiology
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• 제9권1호
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• pp.69-76
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• 1975

Cardiac performances were analyzed in intact turtle heart(Amyda japonica), perfusing with turtle Ringer-Locke's solution containing various hydrogen ion concentration, at several levels of arterial and venous pressure. 1. Ventricular work increased when venous pressure, or venous filling pressure increased, and also increased when arterial pressure increased. 2. The higher the arterial pressure, the lower the cardiac to output, for arterial pressure is the resistance to the ventricular blood flow. On the other hand, in specific arterial pressure, cardiac output was proportional to the venous filling pressure. 3. Heart rates did not change significantly during the perfusion with Ringel· solution of various pH. 4. In the heart Perfused with Ringer solution of various pH, ventricular work was the highest at PH 7.6 (at 6 $cmH_2O$ arterial pressure and 8 $cmH_2O$ venous pressure, the ventricular work was 63.09m$\cdot$cm). However, within the range of pH $7.1{\sim}7.6$, there were no significant changes in cardiac output and ventricular work. Below the level of pH 7.0, ventricular work decreased to less than 56% of maximium value (at $6cmH_2O$ arterial pressure and $8cmH_2O$ venous Pressure, ventricular work was 36.0$gm{\cdot}$ at pH 7.0). At pH 7.7 ventricular work decreased to less than 48% of maximum value (ventricular work: 30.0 $gm{\cdot}$). The nature of the cardiac performance at the various arterial and venous pressures was similar to that of normal heart. 5. Turtle heart seemed to be relatively insensitive to acid-base disturbances. The mechanism of negative inotropic effect of hydrogen ion was discussed.

• Annals of Clinical Neurophysiology
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• 제1권1호
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• pp.60-63
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• 1999

Transcranial Doppler(TCD) is an important diagnostic tool for evaluating the patients with stroke. It has some advantages and unique role when compared with other neuroimaging modalities. Recent development of transcranial color-coded Doppler(TCD) improves the limitation and pitfalls of TCD. The current indications of TCD are as follows: 1. Screening and evaluation of the intracranial major vessels 2. early detection and follow-up of vasospasm due to SAH 3. emboli detection (high-imtensity transient signals, HITs) 4. dignosis and follow-up of subclavian steal 5. evaluation of intracranial collaterals when the extracranial ICA has severe stenosis or occlusion 6. evaluation of cerebral perfusion pressure (intracranial pressure) 7. evaluation of arteriovenous malformation 8. diagnosis and follow-up of arterial dissenction 9. diagnosis and follow-up of venous sinus thrombosis (experimental).