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F Kashiwagi

Publications and source records attributed to F Kashiwagi.

25 records · Page 2Linked to original sources

Role of arachidonic acid metabolism on ischemic brain edema and metabolism.

Arachidonic acid is liberated from damaged cell membranes during ischemia and is the source of vasoactive prostanoids. In this study, specific drugs that influence AA metabolism were investigated for their effects on brain edema and energy metabolites during ischemia. The agents tested were: methylprednisolone (phospholipase A2 inhibition), indomethacin (cyclooxygenase inhibitor), trapidil (TXA2 synthetase inhibitor), and OP-41483 (prostacyclin derivative). Cerebral ischemia was produced using bilateral common carotid artery occlusion in spontaneously hypertensive rats. Brain water content and concentrations of ATP, pyruvate, and lactate were determined 3 hr after occlusion. Compared with its vehicle, methylprednisolone significantly reduced water content and lactate concentration and maintained high levels of ATP. Indomethacin had no effect on brain water content nor metabolite levels. Trapidil decreased water content and lactate levels and increased levels of ATP and pyruvate. OP-41483 had no effect on water content and lactate, but maintained ATP and pyruvate at high levels. These results indicate that some of the AA metabolites may play an important role in the development of brain edema and in the impairment of energy metabolism.

Animals↗

Effects of fluosol-DA on brain edema, energy metabolites, and tissue oxygen content in acute cerebral ischemia.

Perfluorochemicals were developed as a blood substitute and were reported to have an advantage in oxygen transport compared with blood. The present study was undertaken to investigate the therapeutic effects of a perfluorochemical, FDA, on brain edema and metabolites in acute cerebral ischemia. Cerebral ischemia was induced in SHR by BLCO followed by recirculation. The FDA administration resulted in (a) the significant inhibition of brain edema as shown by brain water content in the treated group, and (b) significant amelioration of metabolic impairments as shown by lesser degree of ATP and pyruvate decrease and lactate accumulation. The TpO2 was compared between FDA-infused and nontreated group during ischemia. The FDA-infused group had significantly higher TpO2 than nontreated group. These results indicate that the improvement of brain edema and metabolite levels were due to alleviation of ischemic hypoxia by FDA under the same ischemic insult.

Animals↗

[Effect of glycerol administration on experimental cerebral ischemia--Part 1. Studies on lipid peroxides, prostaglandins, brain edema and brain metabolites].

Using two different models of non ischemic and transient cerebral ischemia in SHR, the effect of hyperosmolar solution with intravenous 10% glycerol on serum lipid peroxides, plasma prostaglandins (TXA2, PGI2), brain water content and brain metabolites were studied. Glycerol did not influence the levels of lipid peroxides, plasma prostaglandins and brain water content in the non ischemic rats. In the transient ischemia group, on the other hand, serum lipid peroxides were significantly reduced in the glycerol administrated group. On the study of plasma prostaglandins, there was no difference of TXA2 levels between two groups, but PGI2 levels were significantly increased in the glycerol administrated group. Brain water content was significantly decreased. And on the study of brain metabolites, ATP concentrations remained higher and lactate concentrations were lower in the glycerol administrated group compared with those in the control group. But there was no difference with pyruvate concentrations between two groups, furthermore L/P ratio improved in the glycerol administrated group. Besides the effect on reduction of brain edema as for hyperosmolar solution, glycerol may indicate improvement of ischemic impediments on brain by the action of antioxidation and reinforcement of PGI2.

Animals↗

Systemic circulatory parameters. comparison between patients with normal tension glaucoma and normal subjects using ambulatory monitoring.

PURPOSE: To compare circadian changes of systemic circulation in patients with normal tension glaucoma (NTG) and normal subjects. METHODS: Forty-three patients with NTG and 226 normal subjects were enrolled in this study. Circulatory parameters, including blood pressure (BP) and pulse rate (PR), were measured in all subjects for 49 hours using an ambulatory monitoring system. In addition to a comparison between NTG patients and normal controls, the same parameters were compared between NTG patients who had progressive field defects and NTG patients who had stable field defects. RESULTS: The BP in NTG patients was significantly higher than in normal subjects. The nocturnal dip of BP in NTG patients was similar to the dip in normal subjects. However, the BP dip in NTG patients showing progressive visual field defects was significantly smaller than in patients with NTG showing stable visual field defects. Blood pressure fluctuation in sleep in the "progressive" patients was significantly greater than in the "stable" patients. Patients with NTG whose random BP was in a normal range showed a higher BP than normal subjects. The dip in PR in NTG patients was significantly lower than in normal subjects. CONCLUSIONS: An insufficient physiological nocturnal BP dip or a greater nocturnal fluctuation in BP may disturb the microcirculation of, and/or may directly damage, the optic nerve, resulting in increasing field loss in NTG.

Adult↗