• Toxicological Research
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• v.4 no.1
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• pp.23-35
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• 1988

The role of calcium in the production of oxygen radical which causes reperfusion damage of ischemic heart has been examined. The reperfusion damage was indrced in isolated Langendorff perfused rat hearts by aortic clamping for 60 min followed by reperfusion with oxygenated Krebs-Henseleit solution with or without 1.25 mM $CaCl_2.$ On reperfusion of the ischemic hearts with the calcium containing solution, the release of cytosolic enzymes (LDH and CPK) increased abruptly. These increased release of enzymes were significantly inhibited by additions of oxygen radical scavengers (SOD, 5,000 U; catalase, 12,500 U) into the reperfusion solution. In the hearts isolated from rats pretreated with allopurinol(20 mg/kg orally, 24 hr and 2 hr prior to the experiments), the levels of enzymes being released during reperfusion were significantly lower than that of the control. However, in the hearts perfused with the calcium-free but oxygenated solution, the increase in the release of cytosolic enzymes during reperfusion was neither inhibited by oxygen radical scavengers nor by allopurinol pretreatment. For providing the evidence of oxygen radical generation during the reperfusion of ischemic hearts in situ, the SOD-inhibitable reduction of exogenously administered ferricytochrome C was measured. In the hearts perfused with the calcium containing solution, the SOD-inhibitable ferricytochrome C reduction increased within the first minute of reperfusion, and was almost completely inhibited by allopurinol pretreatment. When the heart was perfused with the calcium free solution, however, the reduction of ferricytochrome C was not only less than that in the calcium containing condition, but also was not so completely inhibited by allopurinol pretreatment. By ischemia, xanthine oxidase (XOD) in the ventricular tissue was changed qualitatively, but not quantitatively. In the heart made ischemic with the calcium containing condition, the oxygen radical producing O-form of XOD increased, while the D- and D/O-form decreased. However, in the ischemic heart reperfused with the calcium free condition, the D/O-form of XOD was elevated without significant increase in O-form of the enzyme. It is suggested from these results that the calclum may play a contributing role in the genesis of reperfusion damage by promoting the conversion of xanthine oxidase from the D/O-form to the oxygen radical producing O-form in the ischemic myocardium.

• The Journal of Korean Physical Therapy
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• v.20 no.1
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• pp.57-65
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• 2008

Purpose: Heat shock proteins (HSPs) are a group of proteins that are activated when cells are exposed to a variety of environmental stresses, such as infection, inflammation, exposure to toxins, starvation, hypoxia, brain injury, or water deprivation. The activation of HSPs by environmental stress plays a key role in signal transduction, including cytoprotection, molecular chaperone, anti-apoptotic effect, and anti-aging effects. However, the precise mechanism for the action of small HSPs, such as HSP27 and mitogen-activated protein kinases (MAPKs: extracellular-regulated protein kinase 1/2 (ERK1/2), p38MAPK, stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), is not completely understood, particularly in application of cell stimulators including platelet-derived growth factor (PDGF), angiotensin II (AngII), tumor necrosis factor $\alpha$ (TNF$\alpha$), and $H_2O_2$. This study examined the relationship between stimulators-induced enzymatic activity of HSP27 and MAPKs from rat smooth and skeletal muscles. Methods: 2-dimensional electrophoresis (2DE) and matrix assisted laser desorption ionizationtime-of-flight/time-of-flight (MALDI-TOF/TOF) analysis were used to identify HSP27 from the intact vascular smooth and skeletal muscles. Three isoforms of HSP27 were detected on silver-stained gels of the whole protein extracts from the rat aortic smooth and skeletal muscle strips. Results: The expression of PDGF, AngII, TNF$\alpha$, and $H_2O_2$-induced activation of HSP27, p38MAPK, ERK1/2, and SAPK/JNK was higher in the smooth muscle cells than the control. SB203580 (30${\mu}$M), a p38MAPK inhibitor, increased the level of HSP27 phosphorylation induced by stimulators in smooth muscle cells. Furthermore, the age-related and starvation-induced activation of HSP27 was higher in skeletal muscle cells (L6 myoblast cell lines) and muscle strips than the control. Conclusion: These results suggest, in part, that the activity of HSP27 and MAPKs affect stressors, such as PDGF, AngII, TNF$\alpha$, $H_2O_2$, and starvation in rat smooth and skeletal muscles. However, more systemic research will be needed into physical therapy, including thermotherapy, electrotherapy, radiotherapy and others.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.20 no.1
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• pp.371-375
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• 2019

The role of resuscitative endovascular balloon occlusion of the aorta (REBOA) in hemodynamically unstable pancreatic trauma is unclear. We report here a case of traumatic pancreatic bleeding controlled with REBOA and angioembolization of the splenic artery before surgery. A 65-year old man experienced blunt trauma upon falling from a height of 20 m. Computed tomography (CT) revealed distal pancreatic trauma (grade III) and contrast extravasation around the splenic artery. Shortly after CT, his systolic blood pressure was 60 mmHg and REBOA was performed for hemodynamic stability. His systolic pressure increased to 130 mmHg after balloon inflation and angioembolization of the splenic artery was performed. On angiography, no further arterial bleeding was identified and the balloon was removed. Subsequently, the patient underwent emergent laparotomy with distal pancreatectomy. There was no active bleeding during surgery and distal main pancreatic duct injury was identified. After surgery, the patient recovered without complication. In this case, hemodynamically unstable hemorrhagic pancreatic trauma was treated effectively and safely with distal pancreatectomy after REBOA with angioembolization.

• Korean Journal of Radiology
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• v.21 no.11
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• pp.1230-1238
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• 2020

Objective: We aimed to assess the effects of remote ischemic pre-conditioning (RIPC) on the incidence of contrast-induced nephropathy (CIN) after an intravenous (IV) or intra-arterial injection of contrast medium (CM) in patient and control groups. Materials and Methods: This prospective, randomized, single-blinded, controlled trial included 26 patients who were hospitalized for the evaluation of the feasibility of transcatheter aortic valve implantation and underwent investigations including contrast-enhanced computed tomography (CT), with Mehran risk scores greater than or equal to six. All the patients underwent four cycles of five minute-blood pressure cuff inflation followed by five minutes of total deflation. In the RIPC group (n = 13), the cuff was inflated to 50 mm Hg above the patient's systolic blood pressure (SBP); in the control group (n = 13), it was inflated to 10 mm Hg below the patient's SBP. The primary endpoint was the occurrence of CIN. Additionally, variation in the serum levels of cystatin C was assessed. Results: One case of CIN was observed in the control group, whereas no cases were detected in the RIPC group (p = 0.48, analysis of 25 patients). Mean creatinine values at the baseline, 24 hours after injection of CM, and 48 hours after injection of CM were 88 ± 32 μmol/L, 91 ± 28 μmol/L and 82 ± 29 μmol/L, respectively (p = 0.73) in the RIPC group, whereas in the control group, they were 100 ± 36 μmol/L, 110 ± 36 μmol/L, and 105 ± 34 μmol/L, respectively (p = 0.78). Cystatin C values (median [Q1, Q3]) at the baseline, 24 hours after injection of CM, and 48 hours after injection of CM were 1.10 [1.08, 1.18] mg/L, 1.17 [0.97, 1.35] mg/L, and 1.12 [0.99, 1.24] mg/L, respectively (p = 0.88) in the RIPC group, whereas they were 1.11 [0.97, 1.28] mg/L, 1.13 [1.08, 1.25] mg/L, and 1.16 [1.03, 1.31] mg/L, respectively (p = 0.93), in the control group. Conclusion: The risk of CIN after an IV injection of CM is very low in patients with Mehran risk score greater than or equal to six and even in the patients who are unable to receive preventive hyperhydration. Hence, the Mehran risk score may not be an appropriate method for the estimation of the risk of CIN after IV CM injection.

• Journal of Chest Surgery
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• v.34 no.9
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• pp.653-661
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• 2001

Background: Retrograde cerebral perfusion(RCP) is one of the methods used for brain protection during aortic arch surgery. The author previously published the data, however, for the safety of it, there still remains many controversies. The author performed RCP and checked various parameters to clarify the possibility of early detection of cerebral injury. Material and Method: The author used pigs(Landrace species) weighing 25 to 30kg and performed RCP for 120 minutes. After weaning of cardiopulmonary bypass, we observed pigs for another 120 minutes. Rectal temperature, jugular venous oxygen saturation, central venous pressure were continuously monitored, and the hemodynamic values, histological changes, and serum levels of neuron-specific enolose(NSE) and S100$\beta$ protein were checked. Central venous pressure during RCP was maintained in the range of 20 to 25 mmHg. Result: Flow rates(ml/min) during RCP were 224.3$\pm$87.5(20min), 227.1$\pm$111.0(40min), 221.4$\pm$119.5(60min), 230.0$\pm$136.5(80min), 234.3$\pm$146.1(100min), and 184.3$\pm$50.5(120min). Serum levels of NSE did not increase after retrograde cerebral perfusion. Serum levels of S100$\beta$ protein(ng/ml) were 0.12$\pm$0.07(induction of anesthesia), 0.12$\pm$0.07(soon after CPB), 0.19$\pm$0.12(20min after CPB), 0.25$\pm$0.06(RCP 20min), 0.29$\pm$0.08(RCP 40min), 0.41$\pm$0.05(60min), 0.49$\pm$0.03(RCP 80min), 0.51$\pm$0.10(RCP 100min), 0.46$\pm$0.11(RCP 120min), 0.52$\pm$0.15(CPBoff 60min), 0.62$\pm$0.15(60min after rewarming), 0.76$\pm$0.17(CPBoff 30min), 0.81$\pm$0.20(CPBoff 60min), 0.84$\pm$0.23(CPBoff 90min) and 0.94$\pm$0.33(CPBoff 120min). The levels of S100$\beta$ after RCP were significantly higher than thosebefore RCP(p<0.05). The author could observe the mitochondrial swellings using transmission electron microscopy in neocortex, basal ganglia and hippocampus(CA1 region). Conclusion: The author observed the increase of serum S100$\beta$ after 120 minutes of RCP. The correlation between its level and brain injury is still unclear. The results should be reevaluated with longterm survival model also considering the confounding factors like cardiopulmonary bypass.

• Journal of Chest Surgery
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• v.37 no.1
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• pp.27-34
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• 2004

Background: Infective endocarditis shows higher operative morbidity and mortality rates than other cardiac diseases. The vast majority of studies on infective endocarditis have been made on aortic endocarditis, with little attention having been paid to infective endocarditis on the mitral valve. This study attempts to investigate the clinical aspects and operative results of infective endocarditis on the mitral valve. Meterial and Method: The subjects of this study consist of 23 patients who underwent operations for infective endocariditis on the mitral valve from June 1995 to May 2003. Among them, 2 patients suffered from prosthetic valvular endocarditis and the other 21 from native valvular endocarditis. The subjects were evenly distributed age-wise with an average age of 44.8$\pm$15.7 (11∼66) years. Emergency operations were performed on seventeen patients (73.9%) due to large vegetation or instable hemodynamic status. In preoperative examinations, twelve patients exhibited congestive heart failure, four patients renal failure, two patients spleen and renal infarction, and two patients temporary neurological defects, while one patient had a brain abscess. Based on the NYHA functional classification, seven patients were determined to be at Grade II, 9 patients at Grade III, and 6 patients at Grade IV. Vegetations were detected in 20 patients while mitral regurgitation was dominant in 19 patients with 4 patients showing up as mitral stenosis dominant on the preoperative echocardiogram. Blood cultures for causative organisms were performed on all patients, and positive results were obtained from ten patients, with five cases of Streptococcus viridance, two cases of methicillin-sensitive Staphylococcus aureus, and one case each of Corynebacteriurn, Haemophillis, and Gernella. Operations were decided according to the AA/AHA guidelines (1988). The mean follow-up period was 27.6 $\pm$23.3 (1 ∼ 97) months. Result: Mitral valve replacements were performed on 43 patients, with mechanical valves being used on 9 patients and tissue valves on the other 4. Several kinds of mitral valve repair or mitral valvuloplasty were carried out on the remaining 10 patients. Associated procedures included six aortic valve replacements, two tricuspid annuloplasty, one modified Maze operation, and one direct closure of a ventricular septal defect. Postoperative complications included two cases of bleeding and one case each of mediastinitis, low cardiac output syndrome, and pneumonia. There were no cases of early deaths, or death within 30 days following the operation. No patient died in the hospital or experienced valve related complications. One patient, however, underwent mitral valvuloplasty 3 months after the operation. Another patient died from intra-cranial hemorrhage in the 31st month after the operation. Therefore, the valve-related death rate was 4.3%, and the valve-related complication rate 8.6% on mid-term follow-up. 1, 3-, and 5-year valve- related event free rates were 90.8%, 79.5%, and 79.5%, respectively, while 1, follow-up. 1, 3-, and 5-year valve- related event free rates were 90.8%, 79.5%, and 79.5%, respectively, while 1, 3-, and 5-year survival rates were 100%, 88.8%, and 88.8%, respectively. Conclusion: The findings suggest that a complete removal of infected tissues is essential in the operative treatment of infectious endocarditis of the mitral valve. It is also suggested that when infected tissues are completely removed, neither type of material nor method of operation has a significant effect on the operation result. The postoperative results also suggest the need for a close follow-up observation of the patients suspected of having brain damage, which is caused by preoperative blood contamination or emboli from vegetation, for a possible cerebral vascular injury such as mycotic aneurysm.

• Journal of Chest Surgery
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• v.36 no.9
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• pp.638-645
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• 2003

The purposes of this study were to evaluate the effect of myocardial protection with our cold blood cardioplegic solution and to observe the relationship between ultrastructural study and other evaluation methods and its effectiveness. Material and Method: We evaluated the changes of myocardial ultrastructure using semi-quantitative scoring system, CK-MB fraction, SGOT and LDH1/LDH2, and EKG in 18 patients undergoing valvular heart surgery and coronary artery bypass grafting (CABG). Right atrial auricular biopsies were taken before the cardiopulmonary bypass (CPB) and shortly after the end of CPB. Myocardium-related serum enzymes ＆ EKG were checked for 3 days of postoperative period and their postoperative peak enzyme value and observed new Q wave ＆ ST segment elevation in EKG were choosen. Result: There were 8 males and 10 females, and their mean age was 55.6$\pm$13. Eight patients underwent valvular heart surgery and ten coronary artery bypass grafting, The mean CPB time was 119$\pm$29 minutes and the mean aortic cross-clamp (ACC) time was 75.4$\pm$24 minutes. Before the start of CPB, the mean mitochondrial score was 4.28$\pm$0.53 and after the end of CPB, it significantly increased to 2.35$\pm$0.79. There was no evidence of perioperative myocardial infarction in terms of myocardiumrelated serum enzyme value and Q wave and ST change in EKG. There was no significant relationship between pre-CPB and post-CPB mitochondrial score and the mean time of CPB and ACC, and the mean value of postoperative peak CK-MB, SGOT and LDH1/LDH2, but there was relatively positive correlation of CPB time with peak LDH1/LDH2. Conclusion: Despite the apparent satisfactory results in myocardium-related serum enzymes ＆ EKG, with this study using the cold blood cardioplegic solution, there were many changes in myocardial ultrastructures, and more studies are needed to obtain further information.

• Journal of Chest Surgery
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• v.42 no.2
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• pp.135-140
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• 2009

Background: Chronic rejection after a cardiac allograft usually occurs about six months after the operation. Vasculopathy due to chronic rejection causes atherosclerosis in the coronary artery of the transplanted heart and then this causes myocardial injury. We intended to discover and document those findings that occur in a transplanted ascending aorta. Material and Method: In rats weighting $200{\sim}300gm$ (Spraque-Dawley rat), we carried out heterotopic heart allo-transplantation with the modified Ono-Lindsey method and then the rats were administrated cyclosporine (10mg/kg/day). After three months survival, we acquired biopsy materials from the native ascending aorta and the allo-transplanted ascending aorta and we compared them. We classified each severity of 1) intimal thickening, 2) medial hyperplasia, 3) medial calcification, 4) medial inflammation and 5) chondroid metaplasia, which are specific biopsy findings for chronic rejection after a cardiac allograft. Each severity was classified, according to the opinion of one pathologist, in the native ascending aorta biopsies (n=9) and the allo-transplanted ascending aorta biopsies (n=13). The data of the control group and the study group were statistically analyzed with using the Mann-Whitney test (SPSS version 12.0 window). Result: The important changes of the allo-transplanted aorta were intimal thickening (p<0.0001), medial calcification (p=0.045), medial inflammation (p<0.0001) and chondroid metaplasia (p=0.045), but not medial hyperplasia (p=0.36). Conclusion: Cardiac allograft vasculopathy was seen in the transplanted ascending aorta, the same as was seen in the coronary artery, after allograft cardiac transplantation. We have reached the conclusion that chronic rejection also progresses in the aorta.

• Journal of Chest Surgery
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• v.32 no.2
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• pp.130-137
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• 1999

Background: In cardiac surgery, hypothermia is associated with a number of major disadvantage, including its detrimental effects on enzymatic function, energy generation and cellular integrity. Warm cardioplegia with normothermic cardiopulmonary bypass cause three times more incidence of permanent neurologic deficits than the cold crystalloid cardioplegia with hypothermic cardiopulmonary bypass. Interruptions or inadequate distribution of warm cardioplegia may induce anaerobic metabolism and warm ischemic injury. To avoid these problems, tepid blood cardioplegia was recently introduced. Material and Method: To evaluate whether continuous tepid blood cardioplegia is beneficial in clinical practice during valvular surgery, we studied two groups of patients matched by numbers and clinical characteristics. Warm group(37$^{\circ}C$) consisted of 18 patients who underwent valvular surgery with continuous warm blood cardioplegia. Tepid group(32$^{\circ}C$) consisted of 17 patients who underwent valvular surgery with continuous tepid blood cardioplegia. Result: Heartbeat in 100% of the patients receiving continuous warm blood cardioplegia and 88.2% of the patients receiving continuous tepid blood cardioplegia converted to normal sinus rhythm spontaneously after removal of the aortic cross clamp. There were no differences between these two groups in CPB time, ACC time, the amount of crystalloid cardioplegia used and peak level of potassium. During the operation, the total amount of urine output was more in the warm group than the tepid group(2372${\pm}$243 ml versus 1535${\pm}$130 ml, p<0.01). There were no differences between the two groups in troponin T level measured 1hr and 12hrs after the operation. Conclusion: Continuous tepid blood cardioplegia is as safe and effective as continuous warm blood cardioplegia undergoing cardiac valve surgery in myocardial protection.

• Journal of Chest Surgery
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• v.29 no.2
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• pp.199-207
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• 1996

Ischemic myocardial damage is inevitable to cardiac surgery. Myocardial damage after initiation of reperfusion through the coronary arteries is one of the most important determinants of a successful surgery. Adenosine is a potent vasodilator, and is also known to induce rapid cardioplegic arrest by its property of antagonizing cardiac calcium channels and activating the potassium channel. Thus, we initiated this study with adenosine to improve postischemic recovery in the isolated rat heart. We tested the hypothesis that adenosine could be more effective than potassium in inducing rapid cardiac arrest and enhancing postischemlc hemodynamic recovery. Isolated rat hearts, connected to the Langendorff appratus, were perfused with Krebs-Henseleit buffer and all hearts were subjected to arrest for 60 minutes. Three groups of hearts were studied according to the composition of cardioplegic solutions : Group A (n=10), adenosine 10mmo1/L+potassium free modified St. Thomas cardioplegia : Group B (n=10), adenosine 400mo1/L+S1. Thomas cardioplegia:Group C(control, n=10), St. Thomas cardioplegia. Adenosine-treated groups (group A & B) resulted in more rapid cardiac arrest than control group (C) (p< 0.01). There was greater improvement in recovery of coronary blood flow at 20 and 30 minutes of reperfusion in group A and at 20 minutes in group B when compared with control group(p<0.01). Recovery of systolic blood pressure at 10 minutes after reperfusion in group A and B was significantly superior to that in group C (p<0.01). Recovery of dp/dt at 10 minute after reperfusion in group A was also significantly superior to group C (p<0.05). Group A and B showed better recovery rates than control group in aortic blood flow, cardiac output, and heart rate, but there were no statistical differences. CPK levels of coronary flow in group A were significantly low (p< 0.01). We concluded that adenosine-enriched cardioplegic solutions have better effects on rapid cardiac arrest and postischemic recovery when compared with potassium cardioplegia.