Treatment with the nitric oxide-(NO)-generating compound S-nitroso-N-acetylpenicillamine protected cul-tured L929 cells from apoptosis induced by tumor necrosis factor-alpha (TNF-alpha) plus actinomycin D, as determined by the detection of DNA fragmentation and morphological changes. NO also prevented an enhancement of the production of reactive oxygen intermediates by TNF-alpha plus actinomycin D, as assessed by the oxidation of dihydrorhodamine 123 and hydroethidine. Because the inhibition of mitochondrial respiration by rotenone or antimycin A suppressed the increased oxidation of both dihydrorhodamine 123 and hydroethidine, it was suggested that TNF-alpha accelerated the leakage of reactive oxygen intermediates from the mitochondrial electron transport system. Polarography showed that NO reversibly inhibited mitochondrial respiration at either complexes I-III, II-III, or IV, thus suggesting the inhibition of cytochrome oxidase. Taken together, these findings indicate that the decreased mitochondrial formation of reactive oxygen intermediates in the presence of NO might have a protective effect against TNF-alpha plus actinomycin D-induced apoptosis.
Early diagnosis of phlebothrombosis of the superior mesenteric vein is difficult, and in most cases this condition must be treated by enterectomy. The patient, a 56-year-old male with no past history of phlebothrombosis, was brought to the hospital with a chief complaint of abdominal pain. Angiography led to a diagnosis of phlebothrombosis of the superior mesenteric vein, and fibrinolytic agents were therefore administered via a catheter placed in the superior mesenteric artery. Following partial enterectomy on the 10th day, a catheter was inserted into the superior mesenteric vein. Continuous fibrinolytic therapy was effective in preventing postoperative recurrence; dissolution of the phlebothrombosis in the portal vein was also observed.
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