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Biomedical subjects

T Kawase

Publications and source records attributed to T Kawase.

At least 307 records · Page 17Linked to original sources
PubMed1979

[Arterial occlusion following cerebral vasospasm (author's transl)].

1. The present study analysed the clinical course, the serial angiograms and the CT scans of the patients with angiographic arterial occlusion following vasospasm after subarachnoid hemorrhage. The occlusion was observed in 6 out of 84 patients with vasospasm. 2. The angiograms which showed this phenomenon were obtained between the 11th and the 30th day of the illness. The affected vessels were the branches of middle cerebral artery. 3. Thrombus formed on the intima which had been injured by vasospasm is suspected to be a genesis of this arterial occlusion. The pathological findings of a case in this series support this concept. 4. The surgical procedure during the direct aneurysmal operation performed in the period of "smooth narrowing" seems to be a contributing factor to the arterial occlusion. There was no correlation between antifibrinolytic therapy and this phenomenon except in one case. 5. Fibrinolytic therapy after clipping of aneurysm may be a treatment of choice for this arterial occlusion following vasospasm.

Cerebral Angiography↗
PubMedDate not supplied

Modulation of hepatotoxicity by macrophages in the liver.

In an attempt to elucidate the role of hepatic macrophages in liver injury, we investigated galactosamine-treated rats (500 mg per kg body weight). The rats received an i.v. injection of latex particles (2 x 10(9) particles per animal) prior to (latex-galactosamine) or 12 to 16 hr subsequent to the galactosamine treatment (galactosamine-latex). Effect of superoxide dismutase on hepatic injury induced by galactosamine or galactosamine-latex treatment was also examined. Oxygen-derived free radical-generating capacity of isolated hepatic macrophages was measured as chemiluminescence with the stimulation of phorbol myristate acetate or latex particles. As compared with normal rats, chemiluminescence of hepatic macrophages from galactosamine-treated rats was 5- to 10-fold enhanced 12 hr following galactosamine treatment and remained elevated for 48 hr. Chemiluminescence of the latex particle-pretreated macrophages in the liver was markedly suppressed even following the galactosamine treatment (p less than 0.01). Compared to galactosamine-treated rats, both lipid peroxide level in the liver tissue and AST and ALT concentration in serum were significantly decreased in the latex-galactosamine-treated rats (p less than 0.01) and increased in the galactosamine-latex-treated rats (p less than 0.01). Furthermore, superoxide dismutase supplementation protected against liver injury induced by the galactosamine-latex treatment. From these results, pretreatment with latex particles suppressed the free radical-generating capacity of hepatic macrophages and protected against hepatic injury induced by galactosamine. In contrast, injection of latex particles after galactosamine treatment aggravated hepatic injury, which was prevented by superoxide dismutase. These data suggest that liver injury induced by galactosamine is modulated by oxygen-derived free radicals from hepatic macrophages.

Alanine Transaminase↗