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Biomedical subjects

H Kaneto

Publications and source records attributed to H Kaneto.

At least 127 records · Page 7Linked to original sources
PubMed1990

Sandwich enzyme-immunoassay of human urinary trypsin inhibitor (urinastatin) and urinastatin-like immunoreactive substance in mouse urine.

In the enzyme-immunoassay, using rabbit anti-urinastatin (anti-UT) Fab'-beta-D-galactosidase complex and rabbit anti-UT IgG-coupled polystyrene ball as a solid phase, the least measurable amount of UT was 0.3 ng per assay tube. The assay was used to detect UT-like immunoreactivity in the urine of mice. The urine contained a UT-like immunoreactive substance with trypsin inhibitory activity, the concentration of which was 2.3 +/- 0.3 micrograms/l (mean +/- SEM, n = 10). Excretion in the urine was affected by glucocorticoids. There was no immunoreactivity against rabbit anti-UT IgG in the urine of rats, guinea-pigs, rabbits, cats and dogs.

Adolescent↗
PubMed1990

[The muscular architecture at the ureteropelvic junction in congenital hydronephrosis--a stereo-morphometric study].

Ureteropelvic junctions surgically taken from twelve patients with congenital hydronephrosis were submitted to stereo-morphometric studies on the architectural changes of smooth muscle layer. The specimens were opened longitudinally along the ureteral axis, flatly extended on a board, fixed in formalin and embedded in celloidin-paraffin. Serial histological sections in parallel with the wall were prepared; the 3D muscular architecture, visualized in some cases by computer-aided reconstruction, was simplified into vectors of bundles so that their arrangement might be expressed by a vector distribution. Deviation from the norm of architecture at the ureteropelvic junction was disclosed: Reduced muscles with increased connective tissues in four cases and disarrangement of bundles in eight cases, including two with predominantly longitudinal element, three with circular element and another three with irregular orientation. These abnormalities, probably reflecting abnormal maturation of muscles, appear to be related with the urinary obstruction in patients with congenital hydronephrosis.

Humans↗
PubMed1989

Release of substance P by intrathecal KK-3, a newly synthesized Leu-enkephalin derivative.

Intrathecal (IT) injection of KK-3, a leucine-enkephalin analogue with weak, naloxone-reversible analgesic effect, produced behavior consisting of scratching, biting, licking and characteristic convulsion-like symptoms in mice. Naloxone or Mr2266 did not affect the behavior, suggesting a difference in the mechanisms for the production of the behavior and the analgesic effect. The behavior, except the convulsive symptom and the lag time of a couple of min for onset of the behavior, are quite similar to that elicited by IT substance P (SP). D-Pro2-D-Trp7,9-substance P, a SP antagonist, completely suppressed all the behavior induced by KK-3, indicating that the behavior is attributable to SP. By radioimmunoassay, it was found that SP was released by stimulation with KK-3 from the isolated spinal cord preparation of newborn rat. Intrathecal pretreatment with capsaicin, a depleter of SP, suppressed the KK-3-induced behavior, but did not affect the SP-evoked behavior. These results suggest that KK-3 acts as a releaser of SP in the spinal dorsal horn, and consequently produces SP-like behavior. Thus, a novel pharmacological action, the release of substance P from spinal cord by the IT injection of endogenous opioid peptide analogue, was demonstrated.

Animals↗
PubMed1989

Selectivity for opioid receptor subtypes of enkephalin analogues in isolated smooth muscle and in the analgesic effect in mice.

Selectivity for opioid receptor subtypes of enkephalin analogues (KK-1, -2, -3 and -4) of Tyr moiety on the N-terminal, and Phe-ol group on the C-terminal, connected with the methylene group (n = 1-4) were examined in isolated smooth muscle preparations and in the analgesic effect in mice. In the longitudinal muscle preparations of guinea pig ileum (GPI), morphine, U-50488H and all the enkephalin analogues inhibited electrically evoked contractions, and the inhibitory effects of morphine, KK-1, KK-2 and KK-3 were antagonized by naloxone with relatively high pA2 values, while that of U-50488H and KK-3 were preferentially antagonized by norbinaltorphimine. In the rabbit vas deferens preparations (RVD), on the other hand, U-50488H, KK-3 and KK-4 showed weak inhibitory effects and the inhibition of U-50488H and KK-3 were antagonized by norbinaltorphimine. By intracerebroventricularly (i.c.v.) injection, enkephalin analogues produced analgesia in the acetic acid (AcOH) writhing test, and the effect of KK-1 and KK-2 as well as morphine was antagonized by 1 mg/kg naloxone, while those of U-50488H and KK-3 were sensitive to 1 mg/kg Mr2266. In conclusion, enkephalin analogues with a short methylene chain between the functional groups, KK-1 and KK-2, mainly exert their effect through opioid mu-receptors, while those of longer chain, KK-3 and KK-4, act through kappa-receptors preferentially, and KK-3 is situated in the alternating point of the selectivity for mu- and kappa-receptors.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1989

Comparative studies on the inhibitory effect of morphine, pentobarbital and ethanol on the electrically evoked contractions of isolated mouse vas deferens.

To demonstrate the difference in the action mechanisms of morphine (Mor), pentobarbital (Pent) and ethanol (EtOH), comparative studies on the inhibitory effect on the electrical stimulation (ES)-evoked contractions of isolated mouse vas deferens (MVD) were undertaken. All the drugs inhibited the ES-evoked contractions of MVD preparations in a concentration-dependent manner, however, the effects were completely different among 3 drugs in the preparations after incubation in the medium containing each drug and also after acute or chronic treatment with the drugs. The differences among 3 drugs are as follows: 1) The in vitro incubation with Mor, but not with Pent and EtOH developed tolerance. 2) MVD from Mor and EtOH tolerant animals were also tolerant to the inhibitory effect of Mor and EtOH in vitro, respectively. 3) K+ and Ca2+ stimulated the contractions of MVD and the effect was enhanced further after incubation in Mor. 4) The administration of Mor and Pent dose-dependently enhanced the effect of K+ and Ca2+, but this effect of Mor was lost following repeated injections. 5) No cross tolerance was developed among 3 drugs in the inhibitor effect following in vitro incubation or in vivo treatment. Thus, the effects of in vitro incubation with Mor, Pent and EtOH, and acute or chronic administration of the drugs on the response of isolated MVD preparations are different from each other suggesting the difference in the underlying mechanisms of the drugs.

Animals↗
PubMed1989

[Preparation of cerebral ischemia-induced amnesic model in mice and ameliorative effect of several compounds on the model].

A simple and reliable method for the preparation of an ischemia-induced amnesic model was developed in mice and the model animals were employed for screening of the anti-amnesic effect of drugs. Under light thiopental anesthesia the bilateral carotid arteries were exfoliated from the surrounding tissues. Each artery was threaded through a small polyethylene tube, and the incision was sutured, leaving the tip of the tube and both ends of the thread out of the skin. To prevent the tube from falling off, both ends of the thread was ligated at the tip of the tube. Cerebral ischemia was attained by pulling the artery into the tube, and the occlusion was rapidly released by cutting the ligation in the thread and taking off the tube. Twenty-four hours after the surgery, the animals were used for the one trial passive avoidance learning test. In ddY strain mice, the amnesic state was obtained by 5 to 30 min cerebral ischemia, which was applied immediately after the acquisition trial. Mice of the ICR strain were more sensitive to the ischemic treatment and 2 min occlusion of the carotid arteries resulted in a high degree of amnesia. A potent prolyl endopeptidase inhibitor, Z-thiopro-thiazolidine, and 2 novel pyrrolidone derivatives, p-chlorobenzyl-2-pyrrolidone-5-carboxylate and N-(2-pyridylmethyl)-2-pyrrolidone-5-carboxamide, improved the acquisition of the passive avoidance response in the ischemia-induced amnesic models.

Amnesia↗
PubMed1989

Adrenergic function and the development of analgesic tolerance to morphine.

Whether or not the suppressive effect of alpha- and beta-adrenergic blockers, phentolamine and propranolol, on the development of tolerance to morphine could be substituted for each other was investigated in mice. Daily co-administration of either one of the blockers with morphine suppressed the development of analgesic tolerance to morphine as far as the treatment was continued without affecting the analgesic effect per se; however, the suppressive effect was lost from the day of the substitution for the other blocker and tolerance developed as rapidly as in the control group treated with morphine alone. Co-administration of both blockers with morphine also maintained the analgesic effect on the 1st day for 10 days, but when the administration of either one or both blockers was eliminated from the 6th day, the development of tolerance was initiated. These results suggest that the mechanisms of alpha- and beta-blockers for the suppression of the development of analgesic tolerance to morphine are different from each other and that adrenergic blockers may produce a specific alteration in the mechanism for the development of tolerance to morphine.

Analgesics↗
PubMed1989

Role of adrenal glucocorticoids in the blockade of the development of analgesic tolerance to morphine by footshock stress exposure in mice.

To elucidate the mechanism for the suppression by concurrent footshock (FS) exposure of the development of morphine tolerance, the effect of adrenalectomy and a possible participation of glucocorticoids in the mechanism were examined. The analgesic effect of morphine was potentiated in adrenalectomized (ADX) mice, and further enhancement of the effect was shown by the simultaneous exposure to FS (2 mA, 0.2 Hz, 1 sec duration for 15 min) stress, while no such effects were observed in sham-operated (Sham) animals. Daily morphine treatment developed tolerance in Sham and ADX mice. The combined treatment with FS stress suppressed the development of morphine tolerance in Sham mice, whereas such suppression was abolished by adrenalectomy. The suppression of tolerance development was restored in ADX mice by supplement of prednisolone. In contrast to FS stress which produces analgesia through an opioid receptor, forced swimming stress which exerts analgesia through a non-opioid mechanism did not affect the development of morphine tolerance in both Sham and ADX mice. Thus, an opioid mediated stress, FS, could prevent the development of morphine tolerance, and adrenal glucocorticoids play an essential role in the mechanism.

Adrenal Glands↗
PubMed1989

Blockade of the development of analgesic tolerance to morphine by psychological stress through benzodiazepine receptor mediated mechanism.

beta-Carboline-3-carboxylic acid ethyl ester (beta-CCE) dose-dependently potentiated psychological-stress induced analgesia (PSY-SIA), and the effect was reversed by diazepam. Concurrent exposure to PSY stress or concomitant treatment with beta-CCE blocked the development of analgesic tolerance to morphine; the effect of PSY stress was antagonized by diazepam, and that of beta-CCE was reversed by Ro 15-1788. These results suggest that psychological factors which are mediated through benzodiazepine receptors are involved in the mechanism for blocking the development of analgesic tolerance to morphine by PSY stress.

Analgesia↗
PubMed1988

A non-opioid mechanism in the inhibitory effect of ginseng saponins on electrically evoked contractions of guinea-pig ileum and mouse vas deferens.

Both ginseng total saponins (GTS) and one of its constituents, protopanaxatriol saponins (PT), inhibited the electrically evoked contractions of guinea-pig ileum (GPI) in a concentration dependent manner in a range of 1-100 micrograms/ml, and this effect was irreversible at high concentrations of the saponins. Protopanaxadiol saponins (PD) had a transient and weak effect. On the other hand, in mouse vas deferens (MVD), the contractions were increased by PT and PD, however, GTS was almost without effect. The inhibitory effect of morphine was arithmetically increased by pretreatment with 100 micrograms/ml of these saponins in GPI preparations, while the inhibitory effect of the contractions was potentiated in MVD preparations. Neither the inhibition of contractions in the GPI preparation nor the facilitation of contractions in the MVD preparation by these ginseng saponins was reversed by 1 microM naloxone, in contrast to naloxone antagonism of morphine-induced contractions in both preparations. GTS and PT caused a dose-dependent inhibition of BaCl2-induced contraction of GPI. It is concluded that the mechanism on the inhibitory or facilitated effect of ginseng saponins on electrically evoked contractions in GPI and MVD preparations may be separated from the effect of opioids, and the mechanism may be based on the direct action of the saponins on smooth muscles preparations.

Animals↗
PubMed1988

Distinctive effect of ginseng saponins on development of morphine tolerance in guinea-pig ileum and mouse vas deferens.

Studies on the effect of ginseng saponins on the development of tolerance to morphine have been carried out using isolated preparations of guinea-pig ileum (GPI) and mouse vas deferens (MVD). Incubation of GPI preparation with morphine resulted in the development of tolerance to the inhibitory effect of morphine on the electrically evoked contractions. Ginseng total saponins and one of the constituents, protopanaxatriol saponin, suppressed the development of morphine tolerance in a concentration dependent manner in GPI preparation, though another constituent, protopanaxadiol saponin, did not affect the tolerance development substantially. In the MVD preparation, the development of tolerance to the morphine effect was observed as well, but none of the ginseng saponins affected it. It has been well established that electrically evoked contractions of GPI and MVD are mediated by acetylcholine and norepinephrine, respectively, and presumably their release is regulated presynaptically by opioid receptors. The fact that ginseng saponins suppressed the development of morphine tolerance only in the GPI preparation suggest that the inhibitory effect is mediated through and effect on the cholinergic system, without the involvement of direct action on opioid receptors.

Animals↗
PubMed1988

Blockade of the development of analgesic tolerance to morphine by concurrent treatment with opioid- but not non-opioid-mediated stress in mice.

Studies have been carried out to determine how the analgesic effect of morphine and the development of tolerance to the effect would be influenced by concurrent exposure to stresses in mice. Application of footshock (FS) stress, which produces analgesia mediated by opioid mu-receptors, or psychological (PSY) stress, which produces analgesia in a manner more closely related to opioid kappa-receptors, did not affect the analgesic effect of morphine, but completely blocked the development of tolerance during 5 daily concomitant treatments. On the other hand, forced swimming (SW) stress induced analgesia (SIA), which was not antagonized by naloxone, suppressed morphine analgesia, but failed to block the tolerance development. The blockade of the development of tolerance to morphine analgesia by stresses may not be attributed to the analgesic effect induced by the stresses because a combination of weak FS stress, which induces no analgesia, also effectively suppressed the development of morphine tolerance. In addition to the opioid mechanism, an adrenergic mechanism can not be excluded because of the reserpine antagonism of these SIAs.

Animals↗
PubMed1988

Distinctive implication of emotional factors in various types of stress-induced analgesia.

Diazepam, an antianxietic agent, antagonized the stress-induced analgesia (SIA) distinctively depending on the characteristics of the stress. Psychological (PSY, using communication box)-SIA was completely blocked by 1 or 2 mg/kg of diazepam in the tail pinch (TP) method, but not antagonized by 1 mg/kg of the drug in the tail flick test. Swimming-SIA was resistant to diazepam in both methods and footshock-SIA was only suppressed slightly by 2 mg/kg in the TP method. Thus, emotional factors play an essential role in the production of PSY-SIA, although the participation of the factors in the other SIAs can not be excluded.

Analgesia↗
PubMed1988

[Pharmacological interactions between dependence-liable drugs].

Pharmacological interactions between morphine (Mor; analgesia), pentobarbital (Pent; hypnosis), ethanol (EtOH; rotarod adaptability), amphetamine (AMP; ambulation), and cocaine (Coca; ambulation) were examined in mice after a single or repeated administrations. Pretreatment with each drug, even a single dose, resulted in a modification of the effect of succeeding drugs. After 6-day daily treatment with drugs, tolerance developed to Mor, Pent, and EtOH, while reverse tolerance was developed to AMP and Coca. Development of tolerance to Pent was accelerated in the animals that were chronically treated with other drugs. Cross reverse-tolerance was obtained between AMP and Coca, on the other hand, one-way cross tolerance was observed between Mor and EtOH. A marked change was observed in the effect of each drug when administered at the peak time of withdrawal signs of Mor, barbital (Barb), and EtOH. The development of physical dependence on Mor, Barb, and EtOH was not modified by the pretreatment with other drugs. These results may serve to predict the risk of the interactions between various dependence-liable drugs in humans.

Amphetamine↗
PubMed1987

Cross reverse tolerance between amphetamine, cocaine and morphine.

Development of cross reverse tolerance between D-amphetamine, cocaine and morphine to their ambulation accelerating- and swimming time prolonging-effects was investigated in mice. D-Amphetamine and cocaine pretreatment did not increase the ambulation or swimming time by morphine, and pretreatment with morphine produced an increase in the response to D-amphetamine and cocaine. Thus, the difference of the underlying mechanisms between morphine and other drugs for the development of reverse tolerance to their ambulation accelerating and swimming time prolonging effects was demonstrated.

Animals↗