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K Furuno

Publications and source records attributed to K Furuno.

At least 19 recordsLinked to original sources
PubMed1999

Determination of plasma phenobarbital concentration by high-performance liquid chromatography in rat offspring.

Plasma phenobarbital (PB) concentrations in rat offspring were determined using a 9 microl capillary by high-performance liquid chromatography (HPLC). Capillary plasma which was put into a Bond Elut cartridge column by using 1 ml of 0.01 M KH2PO4 was applied to the column with 50 microl of 2 microg/ml of acetanilide (internal standard, I.S.). After washing the column, PB and I.S. were eluted with methanol and injected into the HPLC system. There were excellent linear correlation between the amount of PB and length of the capillary at three different concentrations. Calibration for PB was linear in the range of 0-50 microg/ml. The coefficients of variation were 3.4-5.0% and 5.9-7.5% in the within-day and between-day assays, respectively. The extraction recovery rates were 87.5-105.4%. By this method, it was possible to measure plasma PB concentrations in rat offspring without killing. These results suggested that this method is very useful to determine the plasma PB concentration derived from mother's milk in newborn rats.

Animals↗
PubMed1998

Lipid peroxidation induced by adriamycin in linolenic acid-loaded cultured hepatocytes.

Addition of more than 10 microM of adriamycin to cultured rat hepatocytes loaded with alpha-linolenic acid (linolenic acid-loaded hepatocytes) caused marked lipid peroxidation as measured by an accumulation of malondialdehyde during a 9 hr incubation. After addition of 50 microM of adriamycin to linolenic acid-loaded hepatocytes, malondialdehyde accumulation significantly increased at 3 hr, followed by cellular reduced glutathione decrease and lactate dehydrogenase leakage after 6 hr. Inhibition of adriamycin-induced lipid peroxidation by addition of N,N'-diphenyl-p-phenylenediamine or alpha-tocopherol, both lipid radical scavengers, or deferoxamine, which is a Fe ion chelator, prevented both glutathione decrease and lactate dehydrogenase leakage, indicating that lipid peroxidation caused cellular damage to linolenic acid-loaded hepatocytes exposed to adriamycin. The effect of SKF 525-A, which is a cytochrome P450 inhibitor, on adriamycin-induced lipid peroxidation and on 7-ethoxycoumarin O-deethylase activity was determined by 6 hr incubation of linolenic acid-loaded cells. Addition of SKF 525-A suppressed adriamycin-induced lipid peroxidation comparably with its 7-ethoxy-coumarin 0-deethylase inhibitory activity. These results suggest that cytochrome P450 contributes to the one-electron bioreduction of adriamycin into its semiquinone radical in rat hepatocytes.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1998

Effect of potassium sorbate on cellular GSH level and lipid peroxidation in cultured rat hepatocytes.

Change in cellular reduced glutathione (GSH) level was examined after the addition of 1-10 mM potassium sorbate (SA-K) to cultured rat hepatocytes. The cellular GSH content was decreased to the lowest level at 6 h after the addition of SA-K, and then gradually returned to the normal level except for hepatocytes exposed to 10 mM SA-K. Although the decrease in GSH level was not associated with lactate dehydrogenase (LDH) leakage in hepatocytes exposed to SA-K up to the concentration of 5 mM, cell injury was caused in cells exposed to 10 mM SA-K. When eicosapentaenoic acid was added in conjunction with various concentrations of SA-K to hepatocytes, peroxidation of the fatty acid was accelerated in parallel with the decrease in cellular GSH level. The enhanced lipid peroxidation in the hepatocytes co-exposed to SA-K and eicosapentaenoic acid (EPA) induced the development of cell injury. These results suggest that hepatocytes exposed to SA-K become susceptible to oxidative stress such as lipid peroxidation.

Animals↗
PubMed1998

Steady-state serum concentrations of carbamazepine and valproic acid in obese and lean patients with epilepsy.

Steady-state serum concentrations of carbamazepine (CBZ) and valproic acid (VPA) were investigated in normal weight (body mass index; BMI 20 to 25), lean (smaller than 20 BMI) and moderately obese subjects (greater than 25 BMI) who received either 400 mg/day of CBZ or 800 mg/day of VPA. The CBZ serum concentration in lean subjects was significantly higher than that in normal weight subjects. However, no significant differences in VPA serum concentration were found between the three groups. The CBZ serum concentration decreased with increases in total body weight, and the VPA serum concentration decreased with increases in ideal body weight. However, both serum concentrations were not correlated with BMI. These results suggest that VPA doses should be calculated using ideal body weight and that degree of obesity may affect CBZ serum concentration rather than VPA serum concentration.

Adolescent↗
PubMed1998

[Orbital and stomach metastasis from invasive lobular breast carcinoma].

Orbital or ocular metastatic tumors may originate from breast cancer. Few studies have been made regarding their histopathological classification. A 71-year-old female noted a tumor in the right orbital region. She had had bilateral breast cancer 2 years before and gastric cancer 5 months before. Histopathology had shown stage II invasive ductal cancer (scirrhus) in the right breast and stage III invasive lobular cancer in the left. Signet-ring cells were present in the breast and gastric cancers. Biopsy of the right lower eyelid showed poorly differentiated adenocarcinoma with signet-ring cells. Indian file pattern, which is specific for invasive lobular cancer, was also present, suggesting that the orbital tumor had metastatized from the left breast cancer. Genetic analysis of the gastric cancer using polymerase chain reaction showed a mutation at exon 8 of the p53 tumor suppressor gene, indicating the cancer to be metastatic. These results led to the conclusion that invasive lobular cancer of the left breast was the primary lesion for the gastric and orbital metastases. This case also illustrates that signet-ring cells, which are usually seen in gastric cancer, may be present in invasive lobular breast cancer and in orbital metastasis.

Aged↗
PubMed1997

Cytotoxicity of food preservatives in cultured rat hepatocytes loaded with linolenic acid.

We investigated the ability of eight food preservatives to induce lipid peroxidation in normal and alpha-linolenic acid (LNA)-loaded cultured rat hepatocytes. On the addition of sodium dehydroacetate (DHA-Na), potassium sorbate (SA-K) or thiabendazole (TBZ) to the cell culture, lipid peroxidation, assessed in terms of the production of malondialdehyde (MDA), was induced in LNA-loaded cells, but not in normal cells. At the low concentrations, induction of lipid peroxidation in LNA-loaded cells was highest with TBZ, whereas at high concentrations DHA-Na greatly induced lipid peroxidation. The occurrence of lipid peroxidation in LNA-loaded cells was accompanied by a decrease in cellular GSH levels with the three preservatives and by a decrease in cellular protein-SH levels with DHA-Na and TBZ. Furthermore, cell injury, measured by the release of LDH, was produced in LNA-loaded cells exposed to DHA-Na and SA-K. The addition of TBZ caused substantial cell injury in normal cells, and even greater injury in LNA-loaded cells. The prevention of lipid peroxidation in LNA-loaded hepatocytes by addition of an antioxidant, N,N'-diphenyl-p-phenylenediamine (DPPD) almost completely prevented DHA-Na- and SA-K-induced cell injury, and reduced TBZ-induced cell injury. The addition of diphenyl (DP), o-phenylphenol (OPP) or butyl p-hydroxybenzoate (BHB) caused severe cell injury, in association with a marked decrease in cellular levels of both of GSH and protein-SH in both groups of cells. However, lipid peroxidation was not detectable in either group of cells exposed to these preservatives. Sodium propionate (PA-Na) and sodium benzoate (BA-Na) had little effect on any cytotoxic parameter in either group of cells.

Animals↗
PubMed1997

Effects of various antiepileptic drugs on plasma levels of lamotrigine, a novel antiepileptic, in rats.

The pharmacokinetics of lamotrigine (LTG) and effects of carbamazepine (CBZ), valproic acid (VPA) and zonisamide (ZNS) on LTG kinetics were investigated in rats. LTG plasma levels were measured by high-performance liquid chromatography (HPLC). A single oral administration of LTG at 2.5-10 mg/kg showed linear disposition kinetics. In the pharmacokinetic parameters of LTG when combined with CBZ, the maximal plasma concentration (Cmax) and the area under the plasma concentration curve (AUC0-36) values were significantly lower and the time to maximal plasma concentration (Tmax) value was significantly higher than those in LTG alone. Furthermore, the Cmax and AUC0-36 values of LTG when pretreated with CBZ for 7 days were significantly lower than those from simultaneous treatment with CBZ. The Cmax and AUC0-36 values of LTG when combined with VPA were significantly lower than those for LTG alone. There was no significant difference in the Tmax or time of elimination half-life (t1/2) values of LTG between simultaneous and pretreatment with VPA. Of the pharmacokinetic parameters of LTG with ZNS combination, the Cmax value of LTG after long-term dosings of ZNS decreased significantly, whereas no significant change in Cmax was observed after the combined single administration of LTG and ZNS. Single and chronic ZNS treatment did not significantly affect the Tmax, t1/2 and AUC0-36 values of LTG. The LTG trough level was significantly reduced by CBZ administration, reached the bottom level at 6 days after starting CBZ administration, and recovered gradually after withdrawal of CBZ. These results suggest that CBZ, VPA and ZNS causes changes in the plasma LTG level. They also suggest that in therapy combining LTG with one of these antiepileptics, especially CBZ, the LTG concentration in plasma should be monitored carefully.

Administration, Oral↗
PubMed1997

Influence of lactation on plasma phenobarbital concentrations in rats.

The effect of lactation on the pharmacokinetics of phenobarbital (PB) after delivery was studied in female rats. Non-pregnant animals received PB 20 mg/kg/day twice for 6-7 days before mating, during pregnancy and after delivery. Chronic PB did not significantly influence changes in the body weight of rats after delivery. On the first post-delivery day, the plasma PB concentration in the PB-treated rats was significantly higher than that in PB-treated, non-pregnant rats (non-pregnant rats); and thereafter, it gradually decreased until ablactation on the 20th day. After ablactation, plasma PB concentrations gradually returned to the level before delivery. In PB-treated rats, pharmacokinetic parameters (Cmax, AUC0-12) of PB between 0 and 12 hr after a single oral administration were significantly decreased during lactation. These results suggest that PB administered during lactation is transferred in part to offspring through maternal milk.

Administration, Oral↗
PubMed1997

Effects of cigarette smoke inhalation on plasma diltiazem levels in rats.

A rapid and sensitive method for the assay of plasma diltiazem was developed using a solid-phase extraction technique followed by high-performance liquid chromatography. The effects of cigarette smoke on plasma levels of orally administered diltiazem was investigated in rats. The animals were exposed to cigarette smoke for 10 min using a Hamburg II smoking machine, immediately after oral administration of diltiazem (10 mg/kg). In the nonsmoking nonrestrained rats, plasma diltiazem levels increased rapidly and reached the maximum (7.1 micrograms/kg) 2 h after administration and decreased gradually thereafter. In the nonsmoking restrained rats, plasma diltiazem levels increased rapidly, but showed almost constant levels between 1 h and 8 h after administration. The maximum level (5.4 micrograms/kg) was shown after 2 h. On the other hand, plasma diltiazem levels in the rats exposed to cigarette smoke reached the maximum (4.3 micrograms/kg) after 4 h. These results suggest that absorption of orally administered diltiazem is inhibited and delayed by cigarette smoke.

Animals↗
PubMed1996

Pharmacokinetic evaluation of omeprazole suspension following oral administration in rats: effect of neutralization of gastric acid.

In order to evaluate a clinical use of omeprazole suspension, we examined the pharmacokinetics of omeprazole after oral administration in rats. Although the administration of omeprazole suspension buffered by NaHCO3 solution did not produce a significant increase in the area under the concentration-time curve (AUC) value compared with non-buffered group, the administration of NaHCO3 buffer immediately after dosing of omeprazole suspension buffered by NaHCO3 caused a significant increase in the AUC value. These results suggest that the NaHCO3 treatment following the administration of omeprazole buffered suspension effectively decreased the degradation of the compound by gastric acid. Therefore, the successive administration of NaHCO3 solution after the omeprazole dosing seems to be a simple and useful method for the administration to patients who cannot receive tablets.

Administration, Oral↗
PubMed1996

Effects of nicotine and exposure to cigarette smoke on suppression of local graft-versus-host reaction induced by immobilization stress in mice.

To study the effects of emotional stress on immunological activities and modification of these effects by nicotine or cigarette smoke, we evaluated the effects of immobilization stress on local graft-versus-host (GVH) reaction, a cell-mediated immune response, and the effects of nicotine and cigarette smoke on them. The effects of immobilization stress on GVH reaction and the effects of nicotine and cigarette smoke on them were evaluated in two experiments: in Experiment 1 by applying the stimulations before and immediately after spleen cell transplantation, and in Experiment 2, by applying stimulations after transplantation. Spleen cells of BALB/C mice were injected into the footpad of CBF1 mice, and GVH reaction was examined after 7 days by weighing the popliteal lymph nodes. Immobilization, nicotine administration and inhalation of cigarette smoke were performed either for 5 days before and immediately after the transplantation (Experiment 1) or for 5 days after transplantation (Experiment 2). The weight of the lymph nodes was markedly increased in the control group, indicating GVH reaction, but the reaction was suppressed by immobilization in both experiments. This suppression of GVH reaction by immobilization was antagonized by nicotine administration and exposure to cigarette smoke in Experiment 1 but not in Experiment 2. These findings suggest that nicotine and cigarette smoke induce recovery of immune response suppressed by immobilization stress, especially by increasing the competence of antigen recognition.

Animals↗