BACKGROUND: Recently involvenment of apoptosis, or programmed cell death, has been suggested in myocardial reperfusion injury. Free radicals are one of the inducers of apoptosis, and superoxide dismutase(SOD), a oxygen free radical scavenger, inhibits apoptotic cell death of neurons. Reperfusion of ischemic myocardium results in a burst of oxygen free radical production, however, it has not been defined that oxygen free radicals mediate apoptosis in myocardial reperfusion injury. This study was undertaken to investigate the role of oxygen free radicals by examining the inhibition of apoptosis by SOD. METHOD: New Zealand white rabbits (n=16) weighing 1.8-20kg underwent 30 minutes of left anterior descending coronary artery occlusion followed by reperfusion for 1 or 4 hours. In control group, bovine serum albumin(5mg/kg) was administered continuously via the left atrial appendage starting 10 minutes before reperfusion and ending simultaneously with reperfusion for 1 hour(n=4) or 4 hours(n=4). In SOD group, bovine erythrocyte SOD(15,000u/kg) was administered starting 10 minutes before reprefusion and ending simultaneously with reperfusion for 1 hour(n=5) or 4 hours(n=3). Ventricles were excised immediately after intervention. Tissues were fixed in 10% buffered formalin and 2.5% glutaraldehyde. Apoptosis was examined by hematoxylin and eosin(H&E) staining, in situ nick end labeling, and transmission electron microscopy. Number of apoptotic cells was evaluated semi-quantitatively on H&E stained section. RESULTS: Evidence of apoptosis was detected in every ischmia-reperfused myocardium, and apoptotic cells were found in the non-necrotic myocardium near areas of contraction band necrosis. In control group, the average number of apoptotic cells was 1.7(range 1.5-2.0)for 1 hour reperfused myocardium and 1.4(range 0.3-2.5) for 4 hours reperfused myocardium per high power field(x400). In SOD group, the average number of apoptotic cells was 0.2(range 0.2 -0.3) for 1 hour reperfused myocardium and 0.3(range 0.2-0.4) for 4 hours reperfused myocardium. There was a significant difference in the number of apoptotic cells between conrol and SOD groups (as a whole group 1.5 +/- 0.2 vs 0.3 +/- 0.1,p<0.01). CONCLUSION: SOD partially, however, singificantly inhibits apoptosis, which suggests that oxygen free radicals may induce apoptosis in ischemia-reperfused myocardium of rabbit.
Apoptosis* ; Atrial Appendage ; Cell Death ; Coronary Vessels ; Erythrocytes ; Formaldehyde ; Free Radicals ; Glutaral ; Hematoxylin ; In Situ Nick-End Labeling ; Microscopy, Electron, Transmission ; Myocardial Reperfusion Injury ; Myocardium* ; Necrosis ; Neurons ; Oxygen ; Rabbits ; Reperfusion ; Superoxide Dismutase* ; Superoxides*

No abstract available.
Pneumothorax* ; Risk Factors*

No abstract available.
Anemia* ; Humans ; Spinal Cord*

Between April, 1984 and September 1988, 459 patients underwent cardiovascular surgery at the Yeungnam University Hospital. Of these, 355 cases were open heart surgeries and 104 cases were non-open heart surgeries. There were 237 patients of acyanotic congenital cardiac anomalies, 40 patients of cyanotic congenital cardiac anomalies, and 85 patients of acquired heart diseases. The sex ratio of cardiovascular diseases was represented as 1:1.3 in male and female. The age distribution was ranged from 1 day to 65 years old. The common congenital cardiovascular anomalies were ventricular septal defect (38.7%), patent ductus arteriosus (25.5%), atrial septal defect (20.7%), Tetralogy of Fallot (8.3%), and pulmonary stenosis (2.4%) in order of frequency. Among 87 acquired cardiovascular diseases, 81 patients underwent operation for cardiac valvular lesions, 51 patients had mitral valve replacement and 13 patients had aortic valve replacement and 17 patients had double valve replacement. The overall mortality of cardiovascular surgery was 3.3% and mortality of open heart surgery was 3.9%.
Age Distribution ; Aortic Valve ; Cardiovascular Diseases ; Clinical Study* ; Ductus Arteriosus, Patent ; Female ; Heart ; Heart Diseases ; Heart Septal Defects, Atrial ; Heart Septal Defects, Ventricular ; Humans ; Male ; Mitral Valve ; Mortality ; Pulmonary Valve Stenosis ; Sex Ratio ; Tetralogy of Fallot ; Thoracic Surgery

To examine the usefulness of cardiac MRI in assessing patients (pt) with congenital heart diseases(CHD), informations obtained from MRI and echocardiogrphy (echo) were compared in 91 consecutive pt with CHD and was correlated with findigs at cardiac catheterization (53pt) and at surgery (71pt). Pt were studied with 1.5 Tesla MRI unit and multiplanar images of the heart and great vessels were obtained using ECG-gated multislice spin-echo technique. Age ranged from newborn to 22 years. We obtained the following results. MRI was vary useful in providing important diagnostic informations in 19pt, provided informations which was not crucial to the clinical decision in 28pt, and did not provide additional informations in 44pt. MRI was very useful in assessing complex lesions, particularly in identifying atrial situs, rudimentary ventricular chamber, criss-cross atrioventricular connection, total anomalous pulmonary venous connection, anatomy of ventricular septal defect in double outlet right ventricle, anomalous ventricular muscles, aortopulmonary collateral artery and distal pulmonary artery anatomy. En face view of the ventricular septum was very useful in clearly outlining the ventricular septal defect. MRI gave false information in 17pt. Diagnostic accuracy of MRI was poor for coarctation of the aorta in neonates and small infants, patent ductus arteriosus and pulmonary stenosis. Cardiac MRI is recommended for preoperative planning in selected pt with CHD, particularly with complex lesions.
Aortic Coarctation ; Arteries ; Cardiac Catheterization ; Cardiac Catheters ; Double Outlet Right Ventricle ; Ductus Arteriosus, Patent ; Echocardiography* ; Heart Septal Defects, Ventricular ; Heart* ; Humans ; Infant ; Infant, Newborn ; Magnetic Resonance Imaging* ; Muscles ; Pulmonary Artery ; Pulmonary Valve Stenosis ; Ventricular Septum

No abstract available.
Empyema*

To elucidate the effects of dimethyl sulfoxide on of myocardial and endothelial cells in culture, the cells were exposed to 10% dimethyl sulfoxide in culture medium for 1 hour at 48 hours after cell isolation. The general morphology and the cytochemical reaction of marker enzymes for mitochondria and Golgi complexes were investigated. The results were summarized as follows 1. DMSO induced elongation and narrowing of the cells and increase of mitochondrial reaction in myocardial cells. 2. DMSO induced destruction and disruption of myofibrils in myocardial cells resulting in increase of contractile activities. 3. In the endothelial cells, DMSO suppressed proliferative activities but thiamine pyrophosphatase reactions were enhanced indicating increase of Golgi complex activity. 4. DMSO seemed to hamper with the adhesiveness and motility of the endothelial cells causing the decrease of the number of cells in vitro.
Adhesiveness ; Cell Separation ; Dimethyl Sulfoxide* ; Endothelial Cells* ; Golgi Apparatus ; In Vitro Techniques ; Mitochondria ; Myofibrils ; Thiamine Pyrophosphatase

BACKGROUND: Cardiac hypertrophy is an adaptive mechanisms in response to an increased cardiac work load. Alterations in gene expression play an important role in this adaptive process. Recent investigations have indicated that the alpha-1 adrenergic stimulation in vitro induces hypertrophic change of neonatal cardiomyocytes. The signalling mechanisms of this alpha-1 agonist induced cardiomyocyte hypertrophy are largely unknown. however, recent evidence favors an effector pathway that involves phospholipase C(PLC) mediated hydrolysis of phosphatidylinositol 4,50 bisphosphate. It should be recognized that the demonstration of enhanced phosphoinositol turnover in the presence of alpha-1 adrenergic agonist in vitro does not necessarily imply that a similar response is operative in vivo. Furthermore, the role of subtypes of phospholipase C in this system should be determined. In this context, we produced in vivo cardiac hypertrophy by repeated injection of alpha-1 adrenergic agonist, phenylephrine, and tried to evaluate any change of phospholipase C subtypes by immunohistochemistry and immunoblotting technique and also measured the phosphatidylinositol hydrolyzing activity of the enzyme. METHOD: To produce cardiac hypertrophy, we injected phenylephrine 12mg/kg i.p. to the 28 female S-D rats weighing 150-250g daily for 5 days. This measures produced 22% increase of heart weight/body weight ratio. After 5 days. rats were sacrificed and hearts were rapid excised and freezed for next procedure. The immunohistochemical stainings of myocardium were carried out using monoclonal antibodies against PLC-beta1,-gamma1,-delta1 with Avidine-Biotin Complex method. Immunoblotting was done with monoclonal anti-PLC-gamma1 antibody after immnoprecipitation. The activity of PLC-gamma1 was determined in the assay mixture containing [3H] phosphatidylinositol of 20,000 cpm. The reaction was performed by incubating with resuspended immunoprecipttol of 20,000 cpm. The reaction was performed by incubating with resuspended immunoprecipitate for 10 min and supernatant was collected for -scintillation counting. RESULTS: Immunohistochemical staining demonstrated increased staining of PLC-gamma1 in the phenylephrine induced hypertrophied heart as compared with normal control heart. PLC-beta1 and-o1 did not showed any change. Elghteen out of 20 hypertrophied cardiac tissue(90%) demonstrated increased expression of the PLC-gamma1 compared with control heart tissue in immunoblotting. [3H] PI hydrolyzing activity of PLC-gamma1 in the immunoprecipitates of the hypertrophied hearts(4650+/-614 cpm) were increased consistently in 6 samples as compared with control normal hearts (2387+/-651 cpm). CONCLUSION: In the present experiments we demonstrated that Phospholipase C-gamma1 was overexpressed compared with control normal heart of rat by immunohistochemistry and immunoblotting technique and showed that the activity of this isoenzyme was elevated. Our findings of increased PLC-gamma1 expression in the alpha1-adrenergic agonist induced cardiac hypertrophy tissue suggest that the phosphatidylinositol signalling pathway is important in the genesis of cardiac hypertrophy and the isoenzyme of PLC-gamma1 may play a central role in this mechanism.
Adrenergic Agonists ; Animals ; Antibodies, Monoclonal ; Cardiomegaly* ; Female ; Gene Expression ; Heart ; Humans ; Hydrolysis ; Hypertrophy ; Immunoblotting ; Immunohistochemistry ; Myocardium ; Myocytes, Cardiac ; Phenylephrine* ; Phosphatidylinositols ; Phospholipases* ; Rats* ; Signal Transduction ; Type C Phospholipases

No abstract available.

The Marfan syndrome is a generalized connective tissue disease involving eye, musculoskeletal system, cardiovascular system, and inherited autosomal dominant with various expression type. The cardiovascular complications such as aortic aneurysm, aortic dissection, aortic regurgitation, mitral regurgitation and aortic dissection which usually occurs in previously normal sized aorta are poor prognostic factors. However, the aortic dissection which developed in patient with Marfan syndrome and aortic aneurysm was rare. We experienced one case of dissecting aneurysm in patient diagnosed as previous aortic aneurysm, aortic regurgitation, and Marfan syndrome, receiving successful operation.
Aneurysm, Dissecting ; Aorta ; Aortic Aneurysm* ; Aortic Valve Insufficiency ; Cardiovascular System ; Connective Tissue Diseases ; Humans ; Marfan Syndrome* ; Mitral Valve Insufficiency ; Musculoskeletal System