No abstract available.
Methicillin Resistance* ; Methicillin-Resistant Staphylococcus aureus*

BACKGROUND: Intracellular calcium overload is a common final feature of the ischemic-reperfused heart and mediates the genesis of irreversible cell damage. Reactive oxygen medabolites have been known to play and important role as toxic mediators in myocardial injuries resulting from ischemia and reperfusion. In order to investigate the mechanism of intracellular calcium accumulation in the ischemic-reperfused myocardium, the present study observed the possible contribution of the reactive oxygen metabolite to the calcium transport of cardiac mitochondria. METHODS: Mitochondrial were isolated from rabbit hearts. The effects of a reactive oxygen metabolite, H2O2 on calcium uptake and release, redox states of endogenous pyridine nucleotides and glutathiones of mitochondria respiring with succinate were observed. Calcium uptake and release were monitored by dual-wave length spectrophotometer using a calcium indicator, arsenaze III. Contents and redox states of pyridine nucleotides and glutathiones were measured by enzymatic methods using spectrofluorometer and HPLC. RESULTS: Hydrogen peroxide(10-500microM) promoted calcium release dose-dependently from CA++-preloaded mitochondria, but did not affect the mitochondrial calcium uptake. The H2O2-induced calcium release was accompanied by simultaneous oxidation of the pyridine nucleotides and decrease in the content of the reduced form of glutathione(GSH). When mitochondria were treated with BCNU(N,N=bis(2-chloroethyl)-N-nitrosourea) to inhibit glutathione reductase and so as to reduce the GSH content, there were no increase in calcium release from the mitochondria. These results may indicate that H2O2 increases the permeability of cardiac mitochondrial membrane to calcium in association with the changes in redox state of endogenous pyridine nucleotides, but not with that of glutathiones. CONCLUSION: It is suggested that the reactive oxygen metabolites induce the release of calcium from mitochondria by altering the redox state of pyridine nucleotides, and it may partly be involved in the elevation of cytosolic calcium concentration in the ischemic-reperfused myocardial cells.
Calcium* ; Chromatography, High Pressure Liquid ; Cytosol ; Glutathione Reductase ; Heart ; Hydrogen ; Ischemia ; Mitochondria* ; Mitochondrial Membranes ; Myocardium ; Nucleotides ; Oxidation-Reduction ; Oxygen* ; Permeability ; Reperfusion ; Succinic Acid

No abstract available.

No abstract available.
Emphysema* ; Fistula* ; Pneumonectomy*

No abstract available.
Thoracic Wall* ; Thorax*

BACKGROUND: Oxygen free radicals have been implicated as a cause of deleterious effects in the setting of coronary reperfusion, and they are believed to be generated by the xanthine oxidase system, from activated neutrophiles and from mitochondria. We evaluate the contribution of mitochondria to the production of oxygen free radicals and clarify the mechanism of cellular damage in ischemic reperfused hearts. METHODS: Mitochondria isolated from the ischemic rabbit hearts were incubated in the reaction conditions with different oxygen tensions. Generation of superoxide anion and activities of defensive enzymes aginst oxidative stress were mesured. RESULTS: Superoxide anion genertion by mitochondria incubated in 21% oxygen condition were 0.54+/-0.09 and 0.27+/-0.04(O2./min/mg protein) in ischemic mitochondria and in control respectively(P<0.05). Activites of defensive enzymes against oxidative stress, superoxide dismutase and glutathione peroxidase, were significantly reduced in mitochondria isolated from either ischemic or reperfused hearts. With the lapse of respiration in 21% oxygen condition, ADP-stimulated state 3 oxygen consumption(306.4+/-31.5 vs 214.4+/-11.4n atoms O/min/mg protein) at 30 minutes, P : O ratio and phosphorylation rate were significantly decreased in ischemic mitochondria. CONCLUSION: Elevation of oxygen free radical generation as well as the reduction of defensive enzyme activities in ischemic reperfused mitochondria are injurious to mitochondrial respiratory function. It may contribute to the mechanism of cellular damage in ischemic reperfused hearts.
Free Radicals ; Glutathione Peroxidase ; Heart* ; Mitochondria* ; Myocardial Reperfusion ; Neutrophils ; Oxidative Stress ; Oxygen ; Phosphorylation ; Respiration ; Superoxide Dismutase ; Superoxides* ; Xanthine Oxidase

No abstract available.
Drug Therapy* ; Lung*

No abstract available.
Biopsy* ; Lung Diseases* ; Lung*

No abstract available.
Thoracic Outlet Syndrome*

No abstract available.
Acetazolamide* ; Aneurysm* ; Brain* ; Humans ; Perfusion* ; Subarachnoid Hemorrhage* ; Tomography, Emission-Computed, Single-Photon*