BACKGROUND: Echocardiography gives a window to mediastinal or paracardiac structures. When mediastinal or paracardiac masses are detected by a routine chest X-ray and thoracic CT, the difference between vascular and nonvascular lesions may be difficult to diagnose. In these situations, echocardiography has been successfully used recently. CT can be easily standardized and allows visualization of the whole chest, but it is less precise in defining highly mobile structures, more expensive and difficult to perform in patients with orthopnea. But echocardiography is easy to perform, gives real time images. We performed this study to evaluate the usefulness of echocardiography in the identification and investigation of the structural and functional effects of paracardiac masses. METHODS: Twenty patients with paracardiac masses detected by chest X-ray and thoracic CT were examined by transthoracic and/or transesophageal echocardiography. We studied the characteristics of masses and compression site by 2-D echocardiographic techniques and also evaluation of functional effects of a paracardiac masses on heart and great vessels by color pulsed waved Doppler echocardiographic techniques. RESULTS: Nine patients(45.0%) had cystic masses, eleven patients(55.0%) had solid masses. All cystic masses revealed benign, and all solid masses revealed malignant. Among metastatic paracardiac tumors, the most frequent primary site were lung. heart chambers were compressed by paracardiac masses in five cases(26.7%) and great vessel compressed in thirteen cases(76.4%). Turbulent flow and peak velocity documented by color and PW dopple suggested that it is hemodynamically significant compression states of the great vessels by masses. CONCLUSIONS: We consider that echocardiography is as useful as other noninvasive radiographic techniques in the evaluation of paracardiac masses and their mechanical effect upon the function of the heart and great vessels.
Echocardiography* ; Echocardiography, Doppler ; Echocardiography, Transesophageal ; Heart ; Humans ; Lung ; Thorax

BACKGROUND: In hypertensive patients, the left ventricular hypertrophy(LVH) is very important as an independent risk factor along with developing complications. The present study was attempted to assess whether LVE assessed by echocardiography is related to diurnal variations of blood pressure in patiens with essential hypertension. METHOD: After 24hr ambulatory blood pressure monitoring, echocardiographic parameters were investigated in 30 healthy normotensive subjects and 17 patients with diurnal variation of blood pressure and 19 patients without diurnal variation respectively. RESULTS: Left ventricular mass index was higher in essential hypertensive patients than normotensive subjects. In patients without nocturnal fall in systolic blood pressure, left ventricular mass tended to be higher than in patients with a nocturnal fall without statistic significance. In the hypertensive patients with nocturnal fall, there was a correlationship between LVMI and changes in systolic blood pressure, but no correlation between left ventricular mass index and changes in diastolic blood pressure. In the hypertensive patients without nocturnal fall, changes of both systolic and diastolic pressure did not affect LVMI. CONCLUSION: It is suggested strongly that left ventricular hypertrophy may occur highly in the hypertensive patients without nocturnal(diurnal) variation in blood pressure and may be associated with changes in diastolic and systolic blood pressure. But in hypertensive patient with nocurnal fall, left ventricular hypertrophy may be associated with changes in systolic blood pressure.
Blood Pressure Monitoring, Ambulatory ; Blood Pressure* ; Echocardiography ; Humans ; Hypertension* ; Hypertrophy, Left Ventricular ; Risk Factors

Aspergillus funigatus and other pathogenic fungi synthesize a toxic epidithi- odiopiperzine (ETP) metabolite called gliotoxin. Gliotoxin is an epidithiodiopiperzine compound which can both react with sulfhydryl groups and form hydrogen peroxide. The fungal toxin gliotoxin induces apoptotic cell death in a variety of cells. Apoptosis induced by gliotoxin need calcium but effect of calcium preconditioning is unknown by gliotoxin. We studied the effect of protein kinase C and calcium preconditioning on gliotoxin-induced apoptosis in H9c2 cell. PKC and calcium preconditiong inhibited DNA fragmentation by gliotoxin. From this above results suggest that gliotoxin induce apoptosis via caspase-3 activation, because caspase-3 inhibitor (DEVD-CHO) didn't induce apoptosis in gliotoxin treated H9c2 clls. Calcium and PKC preconditioning inhibit caspase-3 activation by gliotoxin. These data means that PKC preconditioning is related with caspase-3 regulate in gliotoxin-induced apoptosis.
Apoptosis* ; Aspergillus ; Calcium ; Caspase 3 ; Cell Death ; DNA Fragmentation ; Fungi ; Gliotoxin* ; Hydrogen Peroxide ; Protein Kinase C* ; Protein Kinases*

Nitric oxide (NO) is mainly involved in brain ischemic damage to elucidate the protective mechanism of NO pretreatment on ischemic-induced cytotoxicity. This study was investigated whether NO pretreatment inhibits the increase of iNOS expression by lipopolysaccharide (LPS) combined phorbol 12-myristate 13-acetate (PMA) via regulating NF-kB activation in C6 glial cells. C6 glial cells with LPS and PMA for 72 hours markedly induced NO, but sodium nitroprusside (SNP) (100 nM) pretreatment before exposure of LPS and PMA significantly supressed NO production, iNOS expression and NF-kB activation by LPS and PMA. In addition, LPS and PMA treatment for 72 hours induced severely cell death and LDH release from cell into media in C6 glial cells. However SNP pretreatment before treatment of LPS and PMA significantly protected LPS and PMA induced cytotoxicity. Treatment with LPS and PMA induced caspase 3 activation follewed by chromosomal condensation, and fragmentation of nuclei in C6 glial cells. SNP pretreatment before exposure to LPS and PMA supressed caspase 3 activation and inhibited chromosomal condensation and fragmentation of nuclei. From these above results, it is suggest that the protective effects of SNP pretreatment against LPS and PMA induced cytotoxicity may be mediated by inhibiting the expression of iNOS via regulating NF-kB activation.
Brain ; Caspase 3 ; Cell Death ; Neuroglia ; NF-kappa B ; Nitric Oxide* ; Nitroprusside