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Biomedical subjects

T Kihara

Publications and source records attributed to T Kihara.

At least 145 records · Page 8Linked to original sources
PubMed1989

[Postoperative pyuria after TUR-P: the study of postoperative pyuria by using NFLX].

The postoperative duration of pyuria was studied in 35 patients who underwent transurethral resection of the prostate (TUR-P). The average postoperative duration of pyuria was 58.0 +/- 23.6 days. The age over 70 years, preoperative indwelling of urethral catheter and the preoperative urinary tract infection did not make the duration of pyuria longer. The volume of resected prostatic tissue over 20 g and the existence of diabetes mellitus make it significantly longer. It is effective and safe to use a low-dose antibacterial agent such as NFLX which has a broad spectrum and hardly develops bacterial resistance after TUR-P. It is suggested unnecessary to change the anti-bacterial agent even when pyuria continues.

Aged↗
PubMed1988

General pharmacological studies on N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate. 1st communication: effect on the central nervous system.

The pharmacological actions of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165), a new antiarrhythmic agent, on the central nervous system were studied in various experimental animals as compared with those of disopyramide, mexiletine and lidocaine, and the following results were obtained. 1. Acute toxicity of SUN 1165 in mice was similar to that of mexiletine, and twice as potent as compared with that of disopyramide and lidocaine. Main acute toxic symptoms of SUN 1165 were muscle relaxation, ataxia, clonic convulsions, tremor and a decrease in spontaneous activity in mice, rats and rabbits. In addition to these symptoms, vomiting in dogs was observed. These toxic symptoms were similar to those of lidocaine. In the case of disopyramide, ataxia, tremor and a decrease in spontaneous activity were observed in mice and rats. On the other hand, mexiletine caused central nervous excitatory symptoms, that is, tremor, Straub tail, clonic convulsions, jumping, running and opisthotonus in mice and rats, and vomiting in dogs. 2. SUN 1165 even at large doses (50-100 mg/kg p.o.) exerted no significant effects on the following changes: hexobarbital-induced induced hypnosis, oxotremorine-induced tremor, apomorphine-induced hypothermia, reserpine-induced ptosis and hypothermia, 5-hydroxytryptophan syndrome and fighting behavior in mice, and conditioned avoidance response in rats. 3. An ineffective dose of SUN 1165 (12.5 mg/kg p.o.) on spontaneous locomotor activity was lower than of disopyramide and lidocaine, however, higher than that of mexiletine. 4. SUN 1165 at large doses showed antagonistic action on toxic extensor seizures induced by maximal electroshock, picrotoxin, or strychnine in mice, but anticonvulsive effects of SUN 1165 were less potent than those of mexiletine and lidocaine. SUN 1165 had no effect on clonic convulsions induced by pentetrazol and pictrotoxin in mice, while both mexiletine and lidocaine prolonged the duration of clonic convulsions. 5. The muscle relaxant effect of SUN 1165 (50%-toxic dose, TD50 = 30 mg/kg p.o.) was more marked than that of lidocaine (TD50 = 92 mg/kg p.o.) on traction test in mice. However, effect of SUN 1165 (TD50 = 62 mg/kg p.o.) on motor incoordination was similar to that of disopyramide, mexiletine and lidocaine on the rotarod test in mice. 6. The analgesic effect of SUN 1165 was as weak as that of disopyramide, mexiletine and lidocaine on chemically and mechanically-induced pain response in mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1988

General pharmacological studies on N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate. 2nd communication: effect on the peripheral nervous system and peripheral organs.

The pharmacological actions of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165), a new antiarrhythmic agent, on the peripheral nervous system and peripheral organs were studied in various laboratory animals in comparison with those of disopyramide and mexiletine, and the following results were obtained. 1. Large doses (50 or 100 mg/kg p.o.) of SUN 1165 as well as mexiletine had little effects on the pilocarpine-induced hypersalivation and the pupil size in mice. At higher concentration (10(-5) g/ml), SUN 1165 had no effects on the various spasmogen acetylcholine (ACh)-, histamine- or BaCl2-induced contractions in the isolated guinea pig ileum, tracheal smooth muscle and urinary bladder. Disopyramide caused mydriasis, inhibited the pilocarpine-induced hypersalivation at antiarrhythmic doses (10-30 mg/kg p.o.), and suppressed ACh-induced contractions in the various organs. 2. SUN 1165, like disopyramide and mexiletine, decreased the contractile amplitude and diastolic tone of the isolated rabbit ileum. SUN 1165 as well as disopyramide had no effect on the intestinal propulsion even at a large dose (100 mg/kg p.o.). Mexiletine inhibited it at antiarrhythmic doses (10-30 mg/kg p.o.). SUN 1165 only at a large dose (100 mg/kg i.d. or p.o.) inhibited volume of pepsin output in the gastric juice in pylorus-ligated rats and caused a damage to the gastric mucosa. 3. SUN 1165, like disopyramide and mexiletine, slightly potentiated the norepinephrine-induced contraction of the rat vas deferens in vitro. Moreover, SUN 1165 as well as disopyramide and mexiletine slightly potentiated the serotonin-induced contraction of the rat isolated fundus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Developmental anomalies induced by all-trans-retinoic acid in fetal mice: II. Induction of abnormal neuroepithelium.

All-trans-retinoic acid (RA) in olive oil was given in doses of 0, 40, or 60 mg/kg of body weight to pregnant mice on day 8 of gestation, and 2-6 hr later embryos were fixed in solutions with or without cetylpyridinium chloride (CPC). The neuroepithelium of the presumptive midbrain was processed for light and electron microscopy. Distorted contours of the neuroepithelium were induced by both doses of RA and the incidence and the severity of the disorganized neuroepithelium showed dose-related results. Abnormal neuroepithelium showed wide intercellular spaces with degenerated cytoplasmic processes or cell debris, separation of the apical side from adjacent cells, retention of mitotic and/or postmitotic cells on the apical side, presence of mitotic cells on the basal side, and detachment of degenerated structures from the neuroepithelium. Ultrastructurally, the affected neuroepithelium showed (1) appearance of degenerating filamentous or tubular coagulating bundles in the cytoplasm and the cytoplasmic process of the neural crest cells, (2) dispersal of polysomes into monosomes especially in the degenerating neural crest cells, (3) and a collecting of microfilament-like structures at the contact area between the neural crest cell and the presumptive neuroblast. These morphological changes suggest that RA affects the nature of cytoskeletal elements and the protein synthesis of the neuroepithelial cells. The selective susceptibility of neural crest cells to RA causes more degenerating neural crest cells in the neuroepithelium, which causes nonapproximation of the neural folds and scantiness of the migrating neural crest cells; these results lead to neural tube defects and craniofacial anomalies, respectively.

Actin Cytoskeleton↗
PubMed1986

Developmental anomalies induced by all-trans retinoic acid in fetal mice: I. Macroscopic findings.

The administration of a single dose of all-trans retinoic acid on day 8 of gestation to pregnant mice, ICR strain, led to malformed fetuses in all of the litters. All-trans retinoic acid (RA) was dissolved in olive oil and given in doses of 60 or 40 mg/kg of body weight. The control mice were given vehicle alone. Examination on day 18 of gestation of the fetuses exposed to 60 mg/kg showed various malformations, such as exencephaly, exophthalmus, micrognathia, agnathia, cleft palate, cleft lower lip, spina bifida, atresia ani, tail anomalies, agenesis of the kidneys, or hydronephrosis. In the fetuses exposed to 40 mg/kg, isolated cleft palate was much more common than in those exposed to 60 mg/kg. Double-stained preparations of bone and cartilage showed cranio-facial anomalies and axial skeletal anomalies: a- or hypogenesis of palatine or maxillary bones, tympanic ring, squamosal temporal bone or otic ossicles in cartilage, and fusion of basioccipital to basisphenoid and maxilla, zygomatic and mandibular bones; a- or hypogenesis of caudal vertebrae and supernumerary thoracic and lumbar vertebrae. These results indicate that anomalies comparable to those seen in the infants of mothers treated with isotretinoin, 13-cis retinoic acid, during pregnancy can also be induced in mice and suggest that the site affected by RA may be neural crest cells, including those in the cephalic and caudal regions, and cells committed to somitic mesoderm in the trunk region.

Abnormalities, Drug-Induced↗
PubMed1986

Morphine analgesia without development of tolerance in reserpinized mice.

The relationship between the brain monoaminergic mechanism and morphine tolerance was examined in reserpinized mice. In parallel with the reduction of brain monoamine content, the analgesic effect of morphine was reduced in reserpinized animals. At the peak of the reserpine effect, 24 hr after a single dose of 2.5 mg/kg reserpine, i.p., the analgesic effect of morphine was lowered to about 45% of that in naive animals; and 5 days after reserpine treatment, it recovered to about 60% of the control activity. In these animals, the lowered effect of morphine was maintained at the same range during 6 daily repetitions, and the development of tolerance was suppressed. When daily morphine injection was started from 10 days after reserpine treatment, at the time when the brain level of monoamines was still reduced to 60 to 80% of the control, tolerance developed as rapidly as in control animals. On the other hand, daily treatment with a small dose of reserpine, 0.1 mg/kg, neither affected the brain level of norepinephrine and dopamine nor modified morphine analgesia, but completely blocked the development of tolerance. These results may suggest that suppression of the development of tolerance to morphine analgesia is not attributed to the reduction of brain norepinephrine and dopamine by reserpine. Morphine analgesia without development of tolerance in reserpinized mice may indicate the dissociation of the analgesic effect from tolerance liability.

Animals↗
PubMed1986

Important role of adrenergic function in the development of analgesic tolerance to morphine in mice.

The involvement of a catecholaminergic mechanism in the production of morphine analgesia and the development of tolerance to the effect has been suggested. Here, using various adrenergic blockers, the role of adrenergic function in the mechanism was examined. Phentolamine (alpha 1 + alpha 2-blocker, 10, 1 and 0.5 mg/kg), prazosin (alpha 1-blocker, 0.1 and 0.02 mg/kg), propranolol (beta 1 + beta 2-blocker, 10, 1 and 0.5 mg/kg), metoprolol (beta 1-blocker, 10 and 1 mg/kg) did not affect morphine analgesia, but dose-dependently suppressed the development of tolerance to morphine. Yohimbine (alpha 2-blocker, 5 and 1 mg/kg) dose-dependently antagonized morphine analgesia in naive animals and delayed the development of tolerance to morphine. Pindolol (beta 1 + beta 2-blocker but is devoid of membrane stabilizing activity) suppressed the development of tolerance to morphine analgesia; however, d-propranolol, which possesses membrane stabilizing activity but lacks beta-blocking activity, could not prevent the development of tolerance. Thus, the suppressive effect of propranolol on the development of tolerance is not due to membrane stabilizing properties. Not only the non-selective adrenergic blockers, phentolamine and propranolol, but also the selective blockers of each receptor subtype, prazosin and metoprolol, suppressed the development of tolerance. This fact may suggest the importance of the equilibrated state of adrenergic functions in the mechanism for the development of tolerance to morphine.

Adrenergic alpha-Antagonists↗
PubMed1985

Effect of ethinyl estradiol on the differentiation of mouse fetal testis.

In an evaluation of the effect of ethinyl estradiol (EE) on the differentiation of fetal mouse testes, the ratio of the seminiferous tubular region to the testicular tissue region, the ratio of Sertoli cells to gonocytes in tubule cross sections, and the size of Leydig cells were determined by the Texture Analyse System (T.A.S., Leitz) in histological preparations of the testes. The testes were those of fetuses taken from dams given orally 0, 0.02, 0.2 or 2.0 mg/kg of body weight of EE in olive oil from day 11 through day 17 of gestation and killed at term. From experimental and the control testes, five sections were taken at 40-micron intervals. The areas of the seminiferous tubular region and the testicular region were determined and the Sertoli cells and gonocytes in tubule cross section were counted in each of the five sections. The diameters of 100 Leydig cells selected at random were averaged. These data were analyzed by Student's t test. The seminiferous tubular region was significantly increased in the testes treated with 0.02 mg/kg of EE and significantly decreased in those treated with 0.2 mg/kg of EE. The number of gonocytes per tubule cross section was significantly increased in the testes treated with 0.02 or 2.0 mg/kg of EE. The number of Sertoli cells per tubule cross section and the number of Sertoli cells per gonocyte were significantly decreased in the experimental testes. The size of the Leydig cells was significantly decreased in the testes treated with 0.2 mg/kg of EE. These findings suggest that prenatal exposure to EE before testicular differentiation affects tubular formation, the proliferation of fetal Sertoli cells, and Leydig cell differentiation, resulting in disturbances of spermatogenesis.

Animals↗
PubMed1985

Gonadal dysgenesis induced by prenatal exposure to ethinyl estradiol in mice.

Daily oral administration of ethinyl estradiol (0.02, 0.2, or 2.0 mg/kg of body weight) to pregnant Jc1:ICR mice resulted in ovotestis and intra-abdominal testis with persistent Müllerian duct and Wolffian duct in male fetuses and ovarian hypoplasia in female fetuses when it was given from day 11 through day 17 of gestation (before gonadal differentiation in the fetus). The ovotestis consisted of testicular and ovarian portions. In the testicular portion, a few solid seminiferous tubules containing spermatogonia, some with pachytene nuclei with Sertoli cells and compact interstitial tissue including Leydig cells, were seen. In the ovarian portion, pachytene nuclei were seen. The intra-abdominal testis was smaller and contained more spermatogonia per tubule in cross section than the control testis. These findings suggest that in male fetuses ethinyl estradiol affects Sertoli cell differentiation resulting in suppression of Müllerian inhibiting factor. On the other hand, in the ovarian hypoplasia, the primordial follicles and follicular cells in a primordial follicle were significantly decreased in number, and the number of the degenerated primordial follicles was significantly increased. It seems likely that ethinyl estradiol affects the intimate contact between follicular cells and oocytes to cause degeneration of primordial follicles.

Animals↗
PubMed1985

Evidence for the dissociation of morphine analgesia, tolerance and dependence.

A single large dose of morphine produced profound analgesia accompanied by the development of tolerance and physical dependence. The tolerance developed acutely within 24 h and was further intensified, reaching a peak on the 5th day, then gradually disappeared. Partial or complete masking of morphine analgesia by naloxone inhibited the development of the acute, but could not prevent the development of the delayed, tolerance. These results suggest there are two kinds of tolerance and that the analgesic effect is separate from tolerance. Similarly, treatment with morphine produced physical dependence which was precipitated by naloxone. Unlike tolerance, dependence did not develop when morphine analgesia was completely masked by naloxone. The findings provide for the dissociation or morphine analgesia, tolerance and dependence.

Analgesics↗
PubMed1984

Distribution of 35S-taurine in rat neonates and adults. A whole-body autoradiographic study.

The distribution of 35S-taurine in rat neonates and adults was investigated by wholy -body autoradiography. The neonates (4-day-old) were frozen in dry-ice hexane at 30 min, 1, 3 and 6 h after an intraperitoneal injection of 35S-taurine, whereas survival intervals for adult rats were 1 and 3 h. Whole-sagittal sections of the frozen rat, obtained by using a cryostat microtome were dried in situ and autoradiographed. In rat neonates and adults, 35S-taurine was mainly accumulated in the renal cortex, urine, feces, liver, eye (lens, vitreous fluid, retina), hypophysis, thymus, adrenal glands, nasal mucous membrane, salivary glands, gastric mucosa, small and large intestinal mucosa, choroid plexus, myocardium and sebaceous glands. In the rat neonate, such regions as the olfactory bulb, cerebrum, and cerebellum showed relatively high optical density.

Aging↗