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E Aoki

Publications and source records attributed to E Aoki.

At least 73 records · Page 4Linked to original sources
PubMed1986

New candidates for GABAergic neurons in the rat cerebellum: an immunocytochemical study with anti-GABA antibody.

Cerebellar cortical neurons immunoreactive to anti-gamma-aminobutyric acid (GABA) antibody were examined in the rat. In addition to the Purkinje, Golgi, basket and stellate cells, spindle-shaped cells lying just below the Purkinje cell layer were found to be strongly immunoreactive to the antibody. By the combination of immunofluorescence and hematoxylin stainings, these GABA-positive cells were shown to be the Lugaro cells. Unlike the immunopositive small Golgi cell, the pale cell was not immunoreactive to the antibody.

Animals↗
PubMed1986

Postnatal changes of the number and lobular distribution of acid phosphatase positive and lipid granule-containing cells in the cerebellum of hyperbilirubinemic Gunn rats.

Developing homozygous (jj) and heterozygous (j+) Gunn rat cerebella were examined histologically from postnatal days 5 to 60. Sagittal sections of the cerebellar vermis of jj rats revealed that the anterior and medial lobes were significantly smaller in area than in j+ rats on and after postnatal day 10. However, the nodulus did not display significant differences in jj rats. Two classes of acid phosphatase (ACPase)-positive cells (L cells and S cells), and lipid granule-containing S cells were recognized exclusively in the jj rat cerebellum during the postnatal period studied. S cells, which are probably microglia, had an oval dark nucleus and contained many lysosomes, some of which contained lipid droplets. They appeared in all the lobules except the nodulus on day 5 and reached maximum in incidence by day 15. They were distributed all over the cerebellar layers including the white matter. Lipid granule-containing S cells appeared on postnatal day 10 and were most abundant in severely affected lobules, such as the declive and tuber, on day 30. Purkinje cells of jj rats showed vacuolation in their cytoplasm on and after postnatal day 5. After 20 days of life, the number of Purkinje cells in anterior- and medius-lobus were markedly decreased. Some severely damaged Purkinje cells became L cells with an extremely high ACPase activity. They appeared initially on postnatal day 15 and increased in number until day 30. No L cells were observed in the nodulus. These show that the severely damaged Purkinje cells and ACPase-positive and lipid granule-containing microglia cells are most abundant in the late- and intermediate-maturing regions of the vermis. Since they are either rare or absent in any earlier-maturing region, the nodulus, these data suggest toxic effects of bilirubin in the cerebellum are closely related to the ontogenic development of the individual cerebellar lobules.

Acid Phosphatase↗
PubMed1984

Histochemical observations of lipids in the cerebellum of young Gunn rats.

Cerebella of 20-day-old homozygous (jj) and heterozygous (j+) Gunn rats were examined histochemically for the presence of lipids. The j+ rat cerebellum showed no lipid granules, whereas many granules were recognized in the hypoplastic jj rat cerebellum. The degree of appearance of lipid granules differed considerably among the lobes--a high content in the declive and tuber but none in the nodulus. Two kinds of cells showed a strong acid phosphatase activity and contained many lipid granules. It is suggested that the accumulation of lipids, probably cholesteryl esters, is closely related to the enhanced activity of the lysosomal system in the hypoplastic jj rat cerebellum severely injured by bilirubin.

Acid Phosphatase↗
PubMed1983

The effect of prostacyclin on increased hydraulic conductivity of pulmonary exchange vessels following microembolization in dogs.

Prostacyclin (PG I2) generated by vascular endothelium is a strong antiaggregating substance. As platelet aggregation and release of humoral factor(s) have been reported to be crucial in the pathogenesis of acute lung injury following pulmonary microembolization, PG I2 could have a protective effect against microembolic lung vascular injury. Following unilateral microembolization, we have observed a large increase in the filtration coefficient in the nonembolized lung with a significant increase in 6-keto PG F1 alpha, the stable metabolite of PG I2, in arterial blood. The pretreatment with indomethacin (10 mg/kg) prevented the increase in 6-keto PG F1 alpha and potentiated the lung injury after microembolization. Exogenously administered PG I2 (20 ng/kg/min) prevented completely the increase in the filtration coefficient without any effects on hemodynamics, although these effects of indomethacin and PG I2 did not relate to their effects on platelet aggregation. Based on these results, we could conclude that prostacyclin could play an important role in preserving cell integrity of the lung and in prevention of increased lung vascular permeability following pulmonary microembolization.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

A pathophysiological role of endogenous prostacyclin in endotoxin induced increase in lung vascular permeability in dogs.

Escherichia coli endotoxin (1 mg/kg) infusion over 30 min into anesthetized artificially ventilated dogs caused a biphasic response: an early phase of pulmonary hypertension and a late phase of increased lung vascular permeability. During an early phase, PG F2 alpha, Tx A2 (as Tx B2) and prostacyclin (as 6-keto-PG F1 alpha) concentrations increased in plasma or right duct lymph of dogs. During a late phase, the concentrations of PG F2 alpha and Tx A2 decreased to near the base-line values, while the concentration of prostacyclin remained elevated. Administrations of PG synthetase inhibitors 45 min prior to endotoxin inhibited the increase in concentration of prostacyclin following the infusion of endotoxin and potentiated the increase in lung vascular permeability at the beginning of the late phase. Continuous infusion of prostacyclin (20 ng/kg/min) starting one hour before endotoxin for 5 hour periods prevented the increase in lung vascular permeability induced by endotoxin. Based on these results, we could conclude that endogenous prostacyclin might play an important role in preserving cell integrity of lungs and counteract the deleterious effects of endotoxin.

Animals↗
PubMed1983

The effect of prostacyclin infusion on increased pulmonary vascular permeability following microembolization in dogs.

Prostacyclin (PG I2) generated by vascular endothelium is a strong antiaggregating substance. As platelet aggregation and release of humoral factor(s) have been reported to be crucial in the pathogenesis of acute lung injury following pulmonary microembolization, prostacyclin could have a protective effect against microembolic lung vascular injury. Following unilateral microembolization, the filtration coefficient in the nonembolized lung increased significantly to 0.14 +/- 0.02 from the base line value of 0.07 +/- 0.01 ml/min/mmHg/100g. Prostacyclin as measured as 6-keto PG F1 alpha in arterial blood increased significantly to 4.15 +/- 1.76 at 30 min from the base line value of 1.90 +/- 0.45 ng/ml and increased further to 5.67 +/- 1.49 ng/ml at 60 min following microembolization. Exogenously administered PG I2 methylester (20 ng/kg/min) prevented completely the increase in the filtration coefficient without any effects on hemodynamics, although the effects of PG I2 methylester did not depend on its action on platelet aggregation. Based on these results, we conclude that prostacyclin could play an important role in preserving cell integrity of the lung and prevention of increased lung vascular permeability following pulmonary microembolization.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Protective effect of a thromboxane synthetase inhibitor, OKY-1581, on increased lung vascular permeability in pulmonary microembolization in dogs.

To evaluate the potential beneficial effect of a thromboxane synthetase inhibitor, OKY-1581, on increased pulmonary vascular permeability in pulmonary microembolization, we have measured the filtration coefficient in the nonembolized lung after unilateral microembolization in dogs. The unilateral microembolization caused marked elevations in pulmonary artery pressure and blood flow to the nonembolized lung, while pulmonary venous pressure in nonembolized lung did not change. The pulmonary vascular resistance in nonembolized lung did not increase significantly. The filtration coefficient (Kf) in nonembolized lung increased to 0.14 +/- 0.02 from the baseline value of 0.07 +/- 0.01 ml/min/mmHg/100g at 30 min after microembolization when the initial hemodynamic changes reduced toward the baseline value. In OKY-1581 treated dogs, similar hemodynamic changes did not result in the increase in the filtration coefficient in nonembolized lung. Platelet aggregation was also inhibited after microembolization in OKY-1581 treated dogs. Based on these results, we could conclude that OKY-1581 could prevent the increase in pulmonary vascular permeability following pulmonary microembolization by inhibiting platelet aggregation and possibly by preventing the release of thromboxane A2.

Acrylates↗
PubMed1982

The potential beneficial effect of a thromboxane synthetase inhibitor, OKY-1581, on increased lung vascular permeability in experimental pulmonary microembolization in dogs.

To evaluate the potential beneficial effect of a thromboxane synthetase inhibitor, OKY-1581, on increased pulmonary vascular permeability in pulmonary microembolization, we have measured the filtration coefficient in the nonembolized lung after unilateral microembolization in dogs. The unilateral microembolization caused marked elevations in pulmonary artery pressure and blood flow to the nonembolized lung, while pulmonary venous pressure in nonembolized lung did not change. The pulmonary vascular resistance in nonembolized lung did not increase significantly. The filtration coefficient (kf) in nonembolized lung increased to 0.14 +/- 0.02 from te base line value of 0.07 +/- 0.01 ml/min/mmHg/100 g at 30 min after microembolization when the initial hemodynamic changes reduced toward the base line value. In OKY-1581 treated dogs, similar hemodynamic changes did not result in the filtration coefficient in nonembolized lung. Platelet aggregagation was also inhibited after microembolization in OKY-1581 treated dogs. Based on these results, we could conclude that OKY-1581 will serve as a potent beneficial protective drug against pulmonary edema by inhibiting the release of thromboxane A2 following microembolization in the pulmonary vascular bed.

Acrylates↗
PubMed1981

Scanning electron microscopic and enzyme histochemical observations on the cadmium-affected gastrointestinal villi of mice.

Orally administered cadmium has been known to cause diarrhea and flatulence of the gastrointestinal tract. Scanning electron microscopic observations revealed that the absorptive cells on the tip of the intestinal villi were affected to some extent by administration of 2.5 microgram CdSO4/10 g of body weight (b. w.). Administration of higher doses of CdSO4 made the microvilli of the absorptive cells sparse and caused degeneration of the cells. Strong enzymic activities of alkaline phosphatase, acid phosphatase, magnesium-dependent ATPase, and sodium-potassium-dependent ATPase were recognized at the microvilli of the absorptive cells of the villi in the control mice. The enzymic activities of magnesium-dependent ATPase and sodium-potassium-dependent ATPase became weak with increasing dosages of CdSO4. The microvilli of the absorptive cells showed a strong alkaline phosphatase activity at a dose less than 25 microgram CdSO4/10 g of b. w., while some inhibitory effects could be recognized with 50 microgram/10 g of b. w. After administration of 2.5 microgram CdSO4/10 g of b. w., no acid phosphatase reaction products were found only at the absorptive cells located on the tip of the villi. Administration of a large quantity more than 5 microgram/10 g of b. w. strongly affected the acid phosphatase activity. It may be possible that the digestive functions are impaired by low cadmium administration.

Adenosine Triphosphatases↗