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Biomedical subjects

K Asai

Publications and source records attributed to K Asai.

At least 217 records · Page 12Linked to original sources
PubMed1991

Comparison of plasma clearance of low density lipoprotein with beta-very low density lipoprotein or acetoacetylated low density lipoprotein in cholesterol-fed rabbits.

The plasma clearance and tissue distribution of radioiodinated low-density lipoprotein (LDL), beta-very low density lipoprotein (beta-VLDL), and acetoacetylated LDL were studied in cholesterol-fed rabbits. Radioiodinated LDL ([125I]LDL) was cleared more slowly than either [125I]beta-VLDL or acetoacetylated-[125I]LDL and its fractional catabolic rate was one-half that of [125I]beta-VLDL and one-ninth that of acetoacetylated-[125I]LDL. Forty-eight hours after the injection of the labeled lipoproteins, the hepatic uptake was the greatest among the organs evaluated with the uptake of [125I]LDL being one-third that of either [125I]beta-VLDL or acetoacetylated-[125I]LDL. The reduction in the hepatic uptake of LDL due to a down-regulation of the receptors would account for this retarded plasma clearance.

Animals↗
PubMed1991

Antioxidants stimulate endothelial cell proliferation in culture.

The effect of antioxidants on the proliferation of cultured endothelial cells (ECs) were studied. Probucol, a lipid-lowering drug with antioxidant properties, added to the growth medium stimulated the proliferation of ECs. D1-alpha-tocopherol (tocopherol), a natural antioxidant, and butylated hydroxytoluene, a synthetic antioxidant also had the same effect on the proliferation of ECs. There was no significant difference in the content of thiobarbituric acid-reacting substances between the probucol-containing growth medium and control medium during the growth assay. Pretreatment of ECs with probucol or tocopherol also enhanced ECs proliferation in medium without any added antioxidants. The addition of free radical scavengers superoxide dismutase, catalase and mannitol to the growth medium did not enhance the proliferation of ECs. These findings indicate that the stimulatory effect on ECs proliferation of antioxidants in the growth medium appears to be unrelated to preventing free radical reactions in the medium itself, but rather may be related to the uptake of antioxidants by ECs.

Animals↗
PubMed1991

Probucol prevents oxidative injury to endothelial cells.

We evaluated the effect of the antioxidant, probucol, on the cytotoxic effects of oxidized low density lipoprotein (OX-LDL) or of cumene hydroperoxide (CumOOH) on cultured bovine endothelial cells (EC). The addition of CumOOH to EC caused the release of lactate dehydrogenase and the accumulation of thiobarbituric acid-reacting substances (TBARS), effects that were protected against by preincubation with either probucol or tocopherol. Similarly, preincubation of EC with those antioxidants protected against OX-LDL toxicity and the accumulation of TBARS. The content of probucol in EC measured by high performance liquid chromatography was directly correlated with the extent of protection against OX-LDL toxicity. We also found that treatment of EC with serum from patients receiving treatment with probucol resulted in the detection of probucol in the cells. We conclude that probucol is transported and incorporated into EC membranes to act as a radical-trapping antioxidant, protecting the EC against oxidative stress. Our results also indicate that lipid peroxidation in cellular membranes involves cell injury inflicted by OX-LDL.

Animals↗
PubMed1990

Effects of fibrinogen and fibrin on the migration of vascular smooth muscle cells in vitro.

The migration of vascular smooth muscle cells from the media into the intima and their proliferation in the intima play an important role in the pathogenesis of atherosclerosis. We examined the effects of fibrinogen and fibrin on the migration of cultured bovine aortic smooth muscle cells using a modified Boyden chamber assay. The cells migrated to a gradient of soluble fibrinogen. Checkerboard analysis indicated that the effect was largely directional in nature (chemotaxis). The cells also migrated in a dose-dependent manner to a gradient of substrate-bound fibrinogen (haptotaxis). Fibrin, converted from substrate-bound fibrinogen by thrombin, also induced haptotaxis of smooth muscle cells. These observations suggest that, by recruiting smooth muscle cells from the media into the intima, fibrinogen and fibrin may be involved in the pathogenesis of arterial intimal thickening, atherosclerosis, and the organization of a thrombus.

Animals↗
PubMed1990

Clinical and experimental approaches to the prevention of atherosclerosis by immunological regulations.

To evaluate the involvement of the complement system in atherogenesis, we investigated the effect of camostat mesilate (CM), C1r, and C1 esterase inhibitor on cholesterol-induced atherosclerosis in rabbits. We also examined the effect of sodium dextran sulfate (DS, molecular weight: 7000), which is reported to be effective in preventing arteriosclerotic diseases and in inhibiting cholesterol-induced atherosclerosis in experimental animals, on complement activation in vitro and in vivo. The administration of CM reduced the formation of atherosclerotic lesions in cholesterol-fed rabbits. DS inhibited complement pathway in vitro, and the administration of DS reduced the C3a level in subjects. These results suggest that complement activation may possibly be involved in the atherosclerotic process.

Aged↗
PubMed1990

Intimal thickening of jugular and femoral veins vs arteries in the rabbit following investment.

The authors induced intimal thickening in the jugular and femoral veins and in the common carotid and femoral arteries of rabbits by placement of a polyethylene tube cuff. The comparative effects on the intima were studied by light and electron microscopy. Even in the veins, thickening resulted from the migration of medial smooth muscle cells into the intima with subsequent proliferation. Thickening in the arteries consisted of tightly packed smooth muscle cells and a few elastic fibers, whereas that in the veins was characterized by an abundance of collagen fibers, layers of smooth muscle cells, and a few elastic fibers. Capillaries were often observed in the thickened intima of the veins but not of the arteries.

Animals↗
PubMed1990

Effect of pretreatment with antibiotics on the hydrolysis of salicyluric acid in rabbit intestinal microorganisms.

The effect of pretreatment with antibiotics on the hydrolysis of salicyluric acid in rabbit intestinal microorganisms was investigated. Latamoxef sodium (LMOX, 25 mg/kg/d, intravenously) and cephalexin (CEX, 16.7 mg/kg/d, orally) were administered for 1 or 3 d. The blood concentration of salicyluric acid and salicylic acid following oral, intracecal and rectal administration of salicyluric acid was determined. By the pretreatment with LMOX for 1 or 3 d, the blood concentration of salicylic acid following oral administration of salicyluric acid was slightly decreased. In rabbits pretreated with CEX for 3 d, the blood concentration of salicylic acid was detected at low concentration. By the pretreatment with LMOX and CEX, however, the decrease in the blood concentration of salicylic acid following rectal administration of salicyluric acid was not observed. Although the examination of population of intestinal microorganisms induced by the pretreatment with antibiotics was not performed, the metabolic activity of intestinal microorganisms may be changed.

Administration, Oral↗
PubMed1990

Probable assignment of the dihydropteridine reductase gene to 4p15.31.

We report the dihydropteridine reductase (DHPR) activity in cases with interstitial deletion of the short arm of chromosome 4. Case 1 with the segment 4p15.32-4p16 deleted has normal DHPR activity. Case 2 with 4p15.2-4p15.32 deleted has reduced DHPR activity, less than 50% of normal.

Chromosome Banding↗
PubMed1990

[A controlled study on edema in elderly inpatients].

The clinical background relating to edema in elderly inpatients was investigated, in terms of various items in elderly (aged greater than or equal to 65) cases with edema (n = 96) and without edema (controls, n = 95). Both groups were matched for sex, age, and underlying diseases. As compared with the control patients, the patients with edema had longer hospital stays with more disabled status, and showed less activity of daily living (ADL). The rates of bed-restricted patients, dementia patients, and patients with decubitus, muscle atrophy, or incontinence were found to be significantly higher in the patients with edema. The measurement of biochemical parameters revealed that the patients with edema had significantly lower levels of serum albumin, Na, Cl, creatinine, and uric acid, in contrast to higher levels of C-reactive protein. According to the classification of the assumed causes of edema, we divided the patients with edema into five groups; group 1 (n = 33): edema associated with immobilization, group 2 (n = 18): edema due to heart failure, group 3 (n = 15): edema on paretic limbs, group 4 (n = 6): edema due to hypoproteinemia, group 5 (n = 5): edema associated with liver cirrhosis. Both group 1 and group 4 patients had lower levels of hemoglobin and albumin, whereas group 3 patients had higher scores of ADL, higher blood pressure, and higher levels of hemoglobin and albumin. These results suggest that immobilization and restriction in bed, as well as malnutrition, were important factors in causing edema in elderly inpatients.

Activities of Daily Living↗
PubMed1990

Involvement of intracellular iron in the toxicity of oxidized low density lipoprotein to cultured endothelial cells.

We evaluated the role of iron in the toxicity of oxidized low density lipoprotein (Ox-LDL) to cultured vascular endothelial cells. Exposure of the endothelial cells to Ox-LDL led to cell lysis as judged by the release of lactate dehydrogenase into the medium. The presence of deferoxamine, an iron chelator, in the reaction medium containing Ox-LDL prevented the lysis of cells by Ox-LDL. Pretreatment of the cells with deferoxamine also reduced their susceptibility to the cytotoxicity of Ox-LDL. The formation of thiobarbituric acid-reacting substances (TBARS) was observed in the cells exposed to Ox-LDL. Pretreatment of cells with deferoxamine reduced the formation of TBARS which was induced by Ox-LDL. These observations suggest that the toxicity of Ox-LDL to cultured endothelial cells involves the lipid peroxidation of cellular membrane catalyzed by iron derived from the target (endothelial) cells.

Animals↗
PubMed1990

Delayed clearance of beta-very low density lipoprotein after feeding cholesterol to splenectomized rabbits.

The role of the spleen on the metabolism of lipids in cholesterol-fed rabbits was evaluated. Rabbits were divided into two groups: splenectomized and control (sham-operated) groups. After the operation, all rabbits were fed a 1% cholesterol diet for 12 weeks and the changes in serum lipids were observed. In a separate experiment, a study of the clearance of 125I-labeled lipoproteins, including beta-migrating very-low density lipoprotein (beta-VLDL), low density lipoprotein (LDL), and acetoacetylated-LDL, was carried out in both groups of rabbits. After cholesterol feeding, all rabbits showed marked hyperlipidemia; however, the splenectomized animals showed a significantly higher level of serum total cholesterol, triglycerides, and phospholipids together with a lower level of high-density lipoprotein cholesterol. A lipoprotein clearance study showed that beta-VLDL was cleared more slowly from the plasma of the splenectomized rabbits than of the controls fed a 1% cholesterol diet. Without cholesterol feeding, beta-VLDL was cleared more rapidly, and to a similar extent in both groups. The plasma clearance of either LDL or acetoacetylated-LDL did not differ between the two groups. These findings suggest that the spleen may play a role in catabolizing the excessive beta-VLDL in rabbits with dietary-induced hyperlipidemia.

Animals↗
PubMed1989

Protective role of intracellular glutathione against oxidized low density lipoprotein in cultured endothelial cells.

We examined the role of intracellular glutathione (GSH) in the defense of endothelial cells against oxidized low density lipoprotein (OX-LDL). Incubation of cultured bovine endothelial cells with OX-LDL produced a loss of intracellular GSH, followed by lysis. A decrease in the cellular stores of GSH by treating the endothelial cells with buthionine sulfoximine, an irreversible inhibitor of gamma-glutamylcysteine synthetase, increased the susceptibility of endothelial cells to lysis by OX-LDL. In contrast, an increase in cellular GSH level by treatment with L-2-oxothiazolidine-4-caboxylate, an effective intracellular cysteine delivery agent, reduced the toxicity of OX-LDL. These findings suggest that intracellular GSH plays an important role in the defense of endothelial cells against OX-LDL, and that the mechanism of OX-LDL toxicity is related to the depletion of intracellular GSH.

Animals↗