Search PubMed⌕ Search

Biomedical subjects

H Kitagawa

Publications and source records attributed to H Kitagawa.

At least 577 records · Page 32Linked to original sources
PubMed1981

Changes in seizure susceptibility after successive treatments of mice with tryptophol and ethanol.

Changes in leptazol (pentetrazol) seizure susceptibility after successive treatments of mice with tryptophol, a neutral metabolite of indoleamine, in combination with ethanol have been examined. Mice treated with tryptophol plus ethanol became highly susceptible to convulsion. There was little or no difference in seizure susceptibility in mice treated with tryptophol or ethanol alone, compared with the corresponding controls. In the mice treated with tryptophol plus ethanol, a much higher brain tryptophol level was observed, compared with that in mice treated with tryptophol alone. There appeared to be a good correlation between the reduction of the length of the seizure latency time and the time for which the brains were exposed to high levels of tryptophol. These results suggest that elevation of the levels of neutral indoleamine metabolites in the brain may have resulted in the increase in the seizure susceptibility.

Alcoholism↗
PubMed1981

Hypocalcemic effect of acetylsalicylic acid in rats.

Oral administration of acetylsalicylic acid (ASA) at a dose of 200 mg/kg produced a decrease in both total plasma calcium and plasma ionic calcium levels in rats. The percent changes from controls in both total and ionic calcium were similar, being approximately 13% at 3 hr after the administration. A significant (p less than 0.01) decrease in plasma calcium level was also observed at 4 hr after oral administration of salicylic acid at a dose level of 177 mg/kg. However, oral administration of other non-steroidal anti-inflammatory agents such as indomethacin failed to decrease plasma calcium levels in rats. The hypocalcemic effect of ASA was recognized in parathyroidectomized rats, but neither in thyroparathyroidectomized nor in thyroidectomized rats. Therefore, the data suggested that the action of ASA might be mediated by stimulation of calcitonin release, but not by inhibition of prostaglandin biosynthesis.

Animals↗
PubMed1981

Studies of metabolism of tripamide, a new antihypertensive agent. II. Metabolism by the hepatic microsomal enzymes.

1. The metabolism of tripamide, N-(4-aza-endo-tricyclo[5.2.1.0(2.6)]decan-4-yl)-4-chloro-3-sulphamoylbenzamide, has been studied with rat liver microsomal preparations. 2. Hydrolysis of tripamide was induced by phenobarbitone pretreatment and inhibited by O-ethyl O-p-nitrophenyl phenylphosphonothioate (EPN), a classical inhibitor of hepatic microsomal arylamidase. The hydrolysis was also catalysed by partially purified rabbit liver microsomal arylamidase. 3. The hydroxylation of tripamide was induced by 3-methylcholanthrene and inhibited by CO. 4. Inhibition of the hydroxylation of tripamide by antibodies of cytochrome P-450 and P-448 was studied. The 8-hydroxylation was inhibited by both antibodies, but 3-hydroxylation was inhibited by neither.

Aminopeptidases↗
PubMed1981

Purification of liver gamma-glutamyltranspeptidase from the rat.

Gamma-glutamyltranspeptidase (GGT) of adult rat liver was solubilized by treatment with papain and further purified by affinity column chromatography on concanavalin-A Sepharose 4B, followed by ion exchange chromatography on DEAE-cellulose. During DEAE-cellulose chromatography, liver GGT was adsorbed at 0.1M Tris-HCl buffer (pH8.0). The Km value of the liver GGT for L-gamma-glutamyl p-nitroanilide was 1.35mM.

Animals↗
PubMed1981

Interaction of lithium and disulfiram in hexobarbital hypnosis: possible role of the 5-HT system.

The effects of lithium and disulfiram on the 5-hydroxytryptamine (5-HT) system and hexobarbital (HX)-induced hypnosis were studied. Treatment with lithium significantly prolonged HX hypnosis. Disulfiram, a potent inhibitor of brain aldehyde dehydrogenase, also produced a prolongation of HX hypnosis. A combination of lithium treatment for 3 days with disulfiram synergistically potentiated the HX hypnosis and reduced the brain HX levels on awakening. Furthermore, L-tryptophan loading significantly increased the HX sleeping time and reduced the brain HX level on awakening in lithium-pretreated rats, whereas it had not effect on HX hypnosis in controls rats. L-Tryptophan also potentiated HX hypnosis in disulfiram-treated rats. The combination of L-tryptophan, lithium and disulfiram caused the greatest prolongation of HX hypnosis. However, no synergism between lithium and disulfiram was observed in animals treated with lithium for 5 days. after 3 days of lithium treatment, the rate of synthesis of 5-HT was elevated, whereas it had returned to the control level after 5 days of lithium treatment. Tryptophan loading increased the rate of synthesis of 5-HT more than 2-fold in control animals. The increase in the rate of 5-HT synthesis caused by lithium was further potentiated by tryptophan loading. These results suggest that lithium and disulfiram exert their synergistic effect on HX hypnosis by acting on the 5-HT system and that an accumulation of 5-hydroxyindoleacetaldehyde, an active metabolite of 5-HT, may be responsible for the increase in the brain sensitivity to barbiturates caused by these drugs.

Animals↗
PubMed1981

Increase of low-Km NADPH-dependent aldehyde reductase activity in the brain by chronic treatment of rats with barbital.

Kinetics studies showed two apparent Km values for p-nitrobenzaldehyde. The high-Km aldehyde reductase (ALR) had a lower Ki value for barbital than the low-Km ALR. The value for maximal velocity (Vmax) for the high-Km ALR was not changed by chronic barbital treatment. However, the Vmax value for the low-Km ALR was significantly increased by chronic barbital treatment. These results suggest that during barbital treatment low-Km ALR which is less sensitive to barbital is induced in compensation for the decreased aldehyde metabolizing capacity of brain.

Alcohol Oxidoreductases↗
PubMed1981

Induction of hypersensitivity of brain by hydralazine treatment in rats.

Pretreatment with hydralazine caused prolongation of hypnosis induced by hexobarbital (80 mg/kg, i.p.) or intracerebroventricular injection of phenobarbital (1 mg/rat). Under the same condition, brain concentration of hexobarbital was lower than that of no hydralazine treatment. In addition, no appreciable change in liver microsomal drug metabolizing enzyme activities of rats after hydralazine treatment was observed. These findings strongly suggested that hydralazine increases the sensitivity of brain to barbiturates, which leads to prolongation of sleeping time without inhibition of drug metabolizing enzymes.

Animals↗
PubMed1981

[Reflex effects of cough reflex on the tracheobronchial vascular tone (author's transl)].

In a previous paper, it was shown that the cough reflex was accompanied by a slight fall of systemic arterial pressure, tracheal constriction and tracheal vasodilation. In the present study, tracheobronchial muscular and vascular tones during the cough reflex were investigated using the blood perfused canine tracheal and bronchial preparations in situ. The cough reflex was elicited with electrical stimulation of the membraneous wall mucosa of the upper trachea. In the blood perfused tracheal preparation, a close intraarterial injection of atropine or bilateral vagotomy inhibited the tracheoconstriction but had no effect on the tracheal vasodilation during the cough reflex. In the blood perfused bronchial preparation, electrical stimulation of the upper tracheal mucosa induced bronchial constriction but not bronchial vasodilation. Lung inflation with air resulted in a bronchial vasodilation and which persisted even after a close intraarterial infusion of atropine and benzonatate and after bilateral vagotomy. These findings indicate that the tracheobronchial constriction response are primary reflex effects following coughing and the tracheobronchial vasodilation responses are secondary reflex effects induced by increase in internal pressure of the respiratory tract.

Animals↗
PubMed1981

Drug metabolism and fetal toxicity: changes in fetal toxicity of aminopyrine by variation of drug metabolizing enzyme activity in mice.

The influence of hepatic drug-metabolizing enzyme activity on the fetal toxicity of aminopyrine (AM, 200 mg/kg s.c.) was examined in mice. We used the hepatic enzyme inhibitors metyrapon (40 mg/kg s.c.) and SKF-525-A (20 mg/kg s.c.), simultaneously administered with AM on days 7-9 of pregnancy. As hepatic enzyme-inducers we used 3-methyl-cholanthrene (3-MC, 2 mg/kg s.c.) and CoCl2 (40 mg/kg s.c.) were administered on days 5-7 of pregnancy followed by AM on days 7-9. The fetal toxicity of the enzyme inducers and inhibitors was not significantly different from controls. Fetal toxicity of AM (57.1%) was slightly increased and decreased by metyrapon (26.8%). Pretreatment with CoCl2 markedly increased the fetal toxicity of AM (88.6%), particularly by an increase in new abnormalities but the decrease in AM toxicity by SKF-525-A was unclear. The induction of AM N-demethylase and aniline hydroxylase activity was observed in liver microsomes from pregnant mice treated with phenobarbital and AM. From these findings, it appears that the fetal toxicity of AM was altered according to induced changes in maternal hepatic drug metabolizing enzyme activities.

Aminopyrine↗
PubMed1981

Drug sensitivity of rat bladder cancer in syngeneic hosts and athymic nude mice.

The effects of chemotherapeutic agents on BC-47 rat bladder cancer were investigated in nude mice and syngenetic hosts to clarify the influence of host factors on chemotherapy. The BC-47 cancer was rich in stroma and lacked central necrosis in syngeneic ACI/N rats. In contrast, in nude mice it had little stroma and underwent necrosis in the center, and cancer cells proliferated primarily at the periphery in contact with the normal host tissue. The cancer showed similar patterns of sensitivity to bleomycin, 1,3-bis (2-chloroethyl)-1-nitro-sourea, 5-fluorouracil, and mitomycin C in both hosts. In contrast, adriamycin and pyranyl secalonic acid D (pyranyl secalonic acid) had different effects in the two hosts, being significantly effective in rats, but ineffective in nude mice.

Animals↗