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Biomedical subjects

T Urano

Publications and source records attributed to T Urano.

At least 289 records · Page 16Linked to original sources
PubMed1985

A simple and rapid method for preparation of 203Hg-labeled methylmercury from 203HgCl2 and methylcobalamin.

A rapid and simple method for preparation of 203Hg-labeled methylmercuric chloride (CH3(203)HgCl) from 203HgCl2 and methylcobalamin is described. More than 99% of 203Hg was methylated with methylcobalaminin 0.01 N HCl during 1 h. CH3(203)HgCl formed during the reaction was rapidly and completely separated from cobalamins and unreacted 203HgCl2 by CM-Sephadex C-25 minicolumn. The low cost procedure for preparation of CH3(203)HgCl can be completed within 2 h and yields an inorganic 203Hg-free CH3(203)HgCl which is useful in methylmercury toxicology.

Isotope Labeling↗
PubMed1985

The bursa of Fabricius: a trapping site for environmental antigens.

The entry of environmental antigens into the lumen of the bursa of Fabricius was prevented by ligating the bursal duct prior to hatching (BDL: bursal duct ligation). The development of 'natural' serum agglutinins for bacteria and heteroerythrocytes was markedly suppressed by BDL. The antigen-specific recovery was observed by simultaneous administration of sterile antigens into the bursal lumen at the time of BDL. These results strongly suggest that the bursa of Fabricius is a major channel through which environmental antigens stimulate the immune system and induce the formation of 'natural' serum agglutinins.

Agglutinins↗
PubMed1984

The enhanced activation of Glu-plasminogen by urokinase in the presence of fibrin or des A fibrin as measured by the release of B beta peptide and FDP.

Fresh plasma was incubated either with urokinase (UK) alone or the mixture of UK and human thrombin or Reptilase. In a purified system Glu-plasminogen (Glu-plg) was incubated with fibrinogen or fibrinogen plus thrombin in the presence of UK. At intervals, aprotinin was added to stop the reactions and the amounts of B beta peptide and fibrin(ogen) degradation products (FDP, FgDP) were measured by radioimmunoassay and enzyme immunoassay, respectively. Results obtained by using plasma showed that fibrin was degraded faster than fibrinogen upon the addition of UK to the plasma or plasma clotted with thrombin. B beta peptide was released faster from the clot than plasma. The clot formation caused by Reptilase (release of fibrinopeptide A) was accompanied by increase in the release of B beta 1-42 from des A fibrin (fibrin without fibrinopeptide A). In a purified system, fibrin was degraded faster than fibrinogen upon the activation of Glu-plg by UK. These results may correlate well with the observation that Glu-plg was activated better by UK in the presence of fibrin than fibrinogen.

Aprotinin↗
PubMed1984

Interaction of prostaglandin E2 and bradykinin in the induction of afferent splanchnic nerve discharges in cats.

In anesthetized cats, the administration of either bradykinin (BK) (0.3-3 micrograms/kg) or prostaglandin E2 (PGE2) (1-30 micrograms/kg) into the cranial mesenteric artery dose-dependently evoked the firing discharge in the proximal end of the afferent greater splanchnic nerves with a latency of about 10 sec, the pronounced contraction of the longitudinal muscle of the jejunum, and changes in blood pressure. PGE2 at the doses of 1-10 micrograms-kg i.a. potentiated the BK (1 microgram/kg i.a.)-induced firing discharge of the afferent splanchnic nerves of which latency was also shortened, but did not alter the BK-induced jejunal contraction and blood pressure change. However, trimoprostil (30 micrograms/kg i.a.), a trimethyl PGE2 derivative, did not change all of these responses to BK. Aspirin at 50 mg/kg i.v. markedly prevented the BK-induced nerve discharges, but not the BK-induced jejunal contraction. These results taken together indicate that PGE2 may be involved in the facilitatory response of afferent splanchnic nerve discharges to BK, but not involved in the BK-induced jejunal contraction and blood pressure change. The findings on trimoprostil present the possibility that derivatization of PGE2 could modify its inherent ability to produce adverse side-effects.

Animals↗
PubMed1984

Drug resistance in Streptococcus faecalis, Streptococcus faecium and Staphylococcus epidermidis isolated from laboratory animals.

A total of 1,278 strains of Streptococcus faecalis, 688 of Str. faecium and 796 of Staphylococcus epidermidis were collected from laboratory animals of 20 colonies in 1980, and tested for their resistance to 20 drugs. Thirteen percent of Str. faecalis, 12% of Str. faecium and 25% of Staph. epidermidis were drug resistant. Multiple drug resistant organisms were frequently detected in laboratory animal colonies where antibiotic treatment had been undertaken. TC-resistant streptococci and EM-resistant Staph. epidermidis were distributed in about half of the colonies regardless of the history of antibiotic usage.

Animals↗
PubMed1984

[Functional changes of the central nervous system in rat offspring treated with ethanol during lactating period].

The present study was made to investigate the developmental toxicity of ethanol administered to rat pups via dams for 18 days (day 3-21 after parturition) from the relatively early postnatal stage in terms of changes in the threshold for pentylenetetrazol-induced convulsions, the sleeping time with barbital, preference for morphine or ethanol and tolerance to phenobarbital. The threshold of pentylenetetrazol-induced convulsions in ethanol-experienced off-spring were similar to that in the naive group. The sleeping time with barbital in ethanol-experienced offspring were prolonged in comparison with that in the naive offspring. Pups whose dams were treated with ethanol showed high preference for ethanol. The inhibition of rotarod performance in ethanol-experienced offspring were accelerated. The present results suggest that the inhibition of functional development in the central nervous system may have occurred in the ethanol-experienced offspring.

Animals↗
PubMed1983

Effects of central monoamine compounds on tranylcypromine-induced barbital-withdrawal convulsions.

Challenge with tranylcypromine (Tcp) during barbital (B) withdrawal induces dose-related clonic-tonic convulsion (C-TC), which is also related to the severity of withdrawal signs and their changes with the passage of time. The effects of neuropharmacological agents on the Tcp-induced convulsions were observed. dl-Propranolol, phentolamine, phenoxybenzamine and methysergide had been administered intraperitoneally 20 approximately 30 minutes before Tcp challenge. B-withdrawn rats had been pretreated with alpha-methyl-p-tyrosine, 5-hydroxytryptophan, p-chlorophenylalanine or reserpine, or with the combination of iproniazid and reserpine (5 hrs after iproniazid administration) before Tcp challenge. alpha-MT and dl-propranolol inhibited B withdrawal convulsion markedly, though high doses of dl-propranolol rather tended to show a less effect on the convulsion. alpha-Adrenoceptor blockers scarcely inhibited the convulsion. Methysergide or 5-HTP failed to inhibit, but PCPA intensified the convulsion. Reserpine, when administered alone, aggravated the convulsion, but when administered after iproniazid, inhibited it significantly. These findings suggested that the balance between the activities of noradrenergic and serotonergic neurons might be of importance in the manifestation of B withdrawal convulsions, the former probably being excitatory and the latter, inhibitory.

Animals↗
PubMed1983

Effects of propranolol on barbital dependence formation and withdrawal signs.

We studied the involvement of beta-adrenoceptors in the physical dependence formation of barbital. 1. Propranolol (at a dose of 0.5 or 1.0 mg/g food) and barbital were applied simultaneously as a mixture with animal food (barbital-propranolol combination). Barbital was applied on a schedule of gradually increasing dosages from 0.5-and-1.0 to 6-and-8 mg/g food over 36 days. Only the animals dosed with barbital exhibited severe withdrawal signs such as spontaneous withdrawal convulsions. The animals dosed with propranolol alone showed no changes even on withdrawal of the drug. The formation of physical dependence on barbital was obviously inhibited by the combination of barbital and propranolol. 2. Cross-application of propranolol (30 and 60 mg/kg, p.o., and 10 and 30 mg/kg, i.p.) following withdrawal of barbital resulted in the inhibition of the spontaneous withdrawal convulsions, muscle rigidity and hyperirritability. It also inhibited significantly tranylcypromine-induced convulsions, while it failed to inhibit similarly induced hyperthermia. These results including previous findings of effects of monoamine-related compounds on barbital withdrawal convulsions suggest that the balance of activities of noradrenergic neurons, especially that of alpha- and beta- receptors, has great influence on both the formation of physical dependence on barbital and the manifestation of withdrawal convulsions.

Animals↗
PubMed1983

Formation of physical dependence on barbiturates and cerebral monoamines.

The effects of cerebral monoamine-related substances during the course of formation of barbital (B) dependence were studied in male S.D. rats by the B-admixed food method. The monoamine-related substances, p-chlorophenylalanine (PCPA), tranylcypromine (Tcp), alpha-methyl-p-tyrosine (alpha-MT), methamphetamine (MA) and reserpine were administered during each B treatment period, except in the control group that was fed a food admixed with B only. All groups were examined for B withdrawal signs during each of 2 B withdrawal periods. Compared with the control group, B withdrawal signs tended to be mild in the PCPA-treated group, remained similar in the Tcp-treated group, were severe in the alpha-MT-treated group, very mild in the MA-treated group, and very severe in the reserpine-treated group. These findings suggested B withdrawal signs may tend to be reduced in severity if the activity of catecholaminergic neurons is kept elevated during the course of formation of physical dependence on B, and they suggested that acquisition of tolerance to and formation of dependence on barbiturates tend to be reduced under a condition of reduced cerebral 5-HT activity.

Animals↗
PubMed1983

Cross-physical dependence liability of psychotropic drugs in rats dependent on barbiturates.

Rats were rendered physically dependent on phenobarbital by phenobarbital-admixed foods. Barbital, phenobarbital, ethanol, diazepam, nitrazepam, meprobamate, methaqualone, chlorpromazine, diphenylhydantoin, mephenesin, reserpine and clonidine were cross-administered to evaluate the mode of suppression of withdrawal signs and cross-physical dependence liability. The drugs were administered several times during the period from 17-18 hr (when withdrawal signs began to appear) to about 48 hr after the withdrawal of phenobarbital. From the mode of suppression and severity of relapsed withdrawal signs, these drugs were classified into the following 3 types: Type 1: drugs suppressing withdrawal signs of phenobarbital (WSP) almost completely and followed by the relapse of severe WSP. Type II-a: drugs suppressing WSP partially and followed by the relapse of moderate WSP. Type II-b: drugs suppressing WSP partially and followed by the relapse of only mild or practically no signs. Type III (III-a and -b): drugs practically failing to suppress or rather aggravate WSP. Consequently, we found that it was possible to evaluate precisely the cross-physical dependence on sedative-hypnotics by means of investigation for the method of suppression of WSP and the relapse of such signs upon their withdrawal.

Animals↗
PubMed1982

Specific action of tranylcypromine to precipitate barbital withdrawal convulsions.

This research was designed to determine whether the convulsion-eliciting action of tranylcypromine (TCP) during bartibal (B) withdrawal was specific to physical dependence on B, and to compare the findings with the action of pentetrazol (PTZ). Challenge with 15-20 mg/kg IP TCP at 48 or B withdrawal resulted in the elicitation of clonic-tonic convulsion (CTC) in all rats (n = 6) within 10 min. Another challenge with 5-20 mg/kg TCP led to the dose-related precipitation and intensification of CTC. The CTC-inducing action of TCP was relatively reduced as the B withdrawal signs were gradually mitigated. In other words, when challenge with the drug was made at 72h of B withdrawal, the time of CTC onset was prolonged, and the incidence was reduced to 50% in parallel with abolition of the other withdrawal signs. A challenge at 120 h of B withdrawal when the vital signs had almost recovered to prewithdrawal level failed to induce even the prodromal signs of convulsion. In all rats exhibiting only mild to moderate withdrawal signs (such as hyperirritability, hyper-reflexia, anorexia, weight loss), 40 mg/kg TCP was required to induce CTC during B withdrawal, which was twice the dose required in severely dependent rats. Other monoamine oxidase inhibitors, i.e., pargyline, iproniazid, and clorgyline, elicited no CTC during B withdrawal. Methamphetamine was without effect on B withdrawal convulsions. From these findings, the convulsive threshold for TCP during B withdrawal proved well correlated to the grade of B-dependence and the duration of B-withdrawal signs.

Animals↗
PubMed1982

Participant of serotonin turnover rate in the brain on barbital withdrawal convulsion.

The correlation between the development of barbital (B)-withdrawal signs and alterations in the metabolism of brain 5-hydroxytryptamine (5-HT) was studied. Barbital (B)-dependent rats were prepared by the B-Admixed Food method (DAF method). The B-dependent rats were grouped according to the following 5 states: G-I, B-dependent state; G-II, B-withdrawn state; G-III, cross-administration of nitrazepam (NZP) following B-withdrawal; G-IV, cross-administration of chlorpromazine (CPZ) following B-withdrawal; and G-V, cross-administration of phenytoin following B-withdrawal. The controls were comprised of naive rats (G-VI) and naive rats dosed in the same manner as the dependent rats. The brain 5-HT synthesis rate and the brain 5-hydraxyindole acetic acid (5-HIAA) elimination were measured at 44 to 48 hr after B-withdrawal in all groups (when withdrawal convulsion was still persisting in the B-withdrawn rats of the G-II group). The brain 5-HT synthesis rate was elevated significantly (P less than 0.001) in the rats with persistent B-withdrawal convulsion (G-II) as compared with that in the B-dependent rats (G-I). Cross-administration of nitrazepam caused the elevation of 5-HT synthesis rate with B-withdrawal to be inhibited to the dependent level in parallel with the inhibition of B-withdrawal signs. On the other hand, CPZ and phenytoin, which inhibit B-withdrawal convulsion slightly, failed to recover completely the 5-HT turnover rate during B-withdrawal. From these results, it is obvious that the elevation of the brain 5-HT synthesis rate with B-withdrawal plays an important role in eliciting B-withdrawal convulsion.

Animals↗
PubMed1982

Alteration of convulsive threshold and sensitivity to CNS acting drugs in sedative-hypnotics-experienced rat offspring.

The present study was made to investigate the developmental toxicity of ethanol and several sedative-hypnotics (barbital, diazepam, phenobarbital) administered to rat pups via dams for 18 days (day 3-21 after parturition) from the relatively early postnatal stage in terms of changes in the threshold for pentetrazol (PTZ)-induced convulsion, tolerance to, and physical dependence on barbital (B). In the pups of all dosed groups, the convulsive threshold for PTZ is reduced significantly compared with that in the naive group. The sleeping time with B in phenobarbital-exposed offspring was also reduced significantly compared with that in the naive pups. No difference was however, noted in the B concentration of the brain or plasma upon awaking between these groups of pups, which proved that the phenobarbital-exposed pups had obviously acquired a functional tolerance to B. B-dependence formation and the ensuring weight loss and appearance of withdrawal signs, especially clonic-tonic convulsion, were made intense in the phenobarbital-experienced pups. From these results, it may be concluded that exposure to sedative-hypnotics from the early CNS developing stage makes a lowered state of convulsive threshold for PTZ, and therefore, tends to enhance B-withdrawal convulsion. These phenomena were discussed from the viewpoint of monoamine metabolism in the brain.

Animals↗
PubMed1982

Biphasic action of pentazocine in morphine-dependent rats.

The characteristic actions of pentazocine in morphine-dependent rats were investigated by a drug-admixed food (DAF) method. Pentazocine did not cause evident withdrawal signs when stopped after a continuous administration for 2 months at 3 different dose levels. A state of physical dependency on morphine was produced in rats by feeding them for 3 weeks with food that contained different levels of morphine. Animals exhibiting a moderate degree of morphine-withdrawal signs (17-18 hr after withdrawal) received a s.c. cross-administration with pentazocine at 0, 5, 10, 20, 40, 80, and 150 mg/kg. This drug at 20 mg/kg proved most supressive of morphine-withdrawal signs, being about 1/4 as potent as codeine. In a dose range from 20 to 40 mg/kg, the action of pentazocine on the withdrawal signs was reserved, that is, doses not less than 40 mg/kg exerted a dose-related antagonistic action in all the 3 levels of morphine dependent rats. The challenge with levallorphan (2 mg/kg, s.c.) during the chronic application of pentazocine has biphasic action on morphine dependence and suggests that this type of drug must have different properties from morphine type drugs.

Animals↗