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Biomedical subjects

K Matsuno

Publications and source records attributed to K Matsuno.

At least 289 records · Page 16Linked to original sources
PubMed1986

[Nephrotoxic effect of gold sodium thiomalate in rats--ultrastructual observations using electronmicroscopy and X-ray energy dispersive analysis].

The purpose of this study is to demonstrate renal injuries by gold sodium thiomalate (G) with ultrastructual changes and gold deposition in kidney tissue using X-ray energy dispersive analysis (XEDA). Twenty-five mg of G containing 12.1 mg of Au was injected into rats intraperitoneally. The rats were divided into 5 groups. Group 1 was sacrificed 6 hours after the injection of G, and group 2 after 24 hours, group 3 after 72 hours and group 4 after 144 hours. Group 5 consisted of the control-rats which were provided with injections of saline. Gold contents in kidneys, liver, lungs and spleen were measured using the flameless atomic absorption method. XEDA was also performed in order to confirm the gold deposition in tissue. Among the organs, only the kidney showed remarkable changes with increased weight. Group 1 already showed marked azotemia which reached to the maximum level in group 3. The amount of gold content in the organs did not change significantly in spite of a marked reduction of serum gold concentration among the 4 groups. Histological examinations revealed marked degeneration and necrosis of pars recta in proximal tubules, although no prominent abnormalities of glomeruli could be observed. Using an electron microscope, many electron dense particles in lysosome were noticed, mainly in proximal tubules. We also found these particles in lysosome of glomerular epithelial cells. Using XEDA, these electron dense particles were demonstrated to be gold, since characteristic energy of gold was found. In conclusion, the kidney was shown to be the most accumulative organ of gold. G caused acute extensive necrosis of proximal tubules. Gold was demonstrated as electron dense particles in lysosomes mainly in proximal tubules, but also partly in glomeruli. Therefore, it was confirmed that a large amount of G had a strong nephrotoxic effect in rats.

Animals↗
PubMed1986

Involvement of spinal and supraspinal structures in tizanidine-induced antinociceptive action.

The site of action of tizanidine (5-chloro-4-(2-imidazolin-2-yl-amino)2,1,3-benzothiadiazole) was investigated in a tail-flick test in comparison with clonidine and morphine. Tizanidine and clonidine produced a profound and linear dose-dependent antinociceptive action by i.c.v. administration. The ED50 values for tizanidine, clonidine and morphine were increased 2-4-fold 1 or 3 days after spinalization at C5-C6. These results indicate that the antinociceptive activity of tizanidine arises mainly from activity at the supraspinal level, similar to clonidine and morphine, but these drugs act also at the spinal level at high doses.

Animals↗
PubMed1986

Splenic marginal-zone macrophages and marginal metallophils in rats and mice.

The splenic macrophages of rats and mice were studied by light and fluorescence microscopy to determine their phagocytotic uptake of carbon and neutral polysaccharide (Fic-F), and their lysosomal enzyme activities. In rats, the large macrophages of the marginal zone (MZ) showed a moderate to strong acid phosphatase activity, and took up most of the Fic-F, even though they showed a weak phagocytotic activity to carbon particles. Red-pulp macrophages, however, ingested a large quantity of carbon particles, and are considered to be the major scavengers in the rat spleen. In contrast, the MZ macrophages in the mouse spleen were the major scavengers and showed a vigorous uptake of both carbon and Fic-F. In rats, the marginal metallophils (MM), located at the outer border of the periarterial lymphatic sheath and boundary between the MZ bridging channel and surrounding tissue, ingested Fic-F, whereas those located around the follicular area did not. In mice, on the other hand, the MM never ingested Fic-F. Lightly carbon-ladened small cells were constantly seen in the MZ of both rats and mice. They showed little acid phosphatase activity and did not ingest Fic-F. They were also present in the blood circulation.

Acid Phosphatase↗
PubMed1986

Comparison of tizanidine and morphine with regard to tolerance-developing ability to antinociceptive action.

The antinociceptive, tolerance-developing and anti-withdrawal activities of tizanidine [5-chloro-4-(2-imidazolin-2-yl-amino)-2,1,3-benzo-thiadiazole] were investigated by comparing its effects with those of morphine and clonidine in tail-flick-, hot plate-, acetic acid-induced writhing-, and naloxone-precipitated withdrawal jumping-tests. The antinociceptive action of tizanidine was not altered by naloxone, while that of morphine was antagonized. Tolerance to the tizanidine-induced antinociceptive action and to motor incoordination was developed by successive administration of tizanidine. In the tizanidine-tolerant mice, the antinociceptive action of morphine was significantly decreased, but not sleeping time induced by pentobarbital. The action of tizanidine was not modified in the morphine-tolerant mice. Tizanidine failed to induce morphine-withdrawal jumping and to inhibit naloxone-precipitated withdrawal jumping in the morphine-dependent mice. Cross tolerance to the antinociceptive action induced by tizanidine and clonidine was developed. These results suggest that alpha 2-adrenoreceptors may be involved in the action mechanism of tizanidine, but not opioid receptors. Functional tolerance to tizanidine action may be developed by successive administration of tizanidine.

Analgesics↗
PubMed1986

Pulmonary deposition and clearance of a coal fly ash aerosol by inhalation.

Wistar male rats were exposed to coal fly ash aerosols at average exposure concentration of 10.4 mg/m3 for 7 hr/day, 5 days/week for 1 month. Some rats were sacrificed just after the exposure, while others were kept for 6 or 10 months clearance time before sacrifice. There were no differences in body weight gain between fly ash exposure groups and controls. The burden of fly ash was estimated by the measurement of aluminum contents in rat organs. Aluminum concentrations in lungs of exposure groups were much higher than those of controls. No apparent deposition of fly ash was observed in the liver, kidneys, spleen, and blood, but lung burdens of up to about 0.7 mg of fly ash were found. The apparent deposition fraction was 5.1% after the 1-month exposure. The clearance rate of fly ash deposited in rat lungs may be very slow.

Administration, Inhalation↗
PubMed1986

Marginal zone bridging channels as a pathway for migrating macrophages from the red towards the white pulp in the rat spleen.

The spleen of (PvG/c X DA)F1 rats, intravenously injected with carbon, was investigated. Large heavily carbon-laden (LHC) macrophages, which were found only in the red pulp at 30 min, appeared along marginal zone bridging channels (MZBC) from the red pulp towards the white pulp side successively during 1-6 h after carbon injection. After this time, they appeared in the periarterial lymphatic sheaths (PALS) near MZBC and then in the deeper PALS along the arteries by 5-10 days. Frequently, they were found in rows from MZBC into the white pulp. These findings suggest migration of LHC macrophages from the red towards the white pulp trough MZBC. Possible migration of LHC macrophages through MZBC was observed for a long period--at least 3 months examined. LHC macrophages came together preferentially in PALS and in and around the germinal centers consisting of large pyroninophilic lymphoblastoid cells. Occasionally, possible migration of LHC macrophages from regions around sinuses crossing the marginal zone vertically (vertical sinus) was also observed. Sinuses accompanied by LHC macrophages often ran parallel in close association with MZBC, particularly at sites of MZBC near the red pulp.

Animals↗
PubMed1986

Conditioned suppression and opioid kappa receptor in mice.

Mice exhibited a marked suppression of motility (conditioned suppression) when placed in the same environment in which they had previously received an electric footshock. Furthermore, chronic morphine (mu agonist)-pretreated mice, as well as chronic vehicle-pretreated mice, exhibited the conditioned suppression but chronic ethylketocyclazocine (kappa agonist)- and pentazocine (kappa agonist)-pretreated mice did not. On the other hand, in the synaptic membranes of the chronic vehicle- and morphine-pretreated mice showing conditioned suppression, the specific binding of [3H]phencyclidine (sigma agonist) and [3H]naloxone (mu antagonist) significantly increased, while the specific binding of [3H]ethylketocyclazocine did not change compared to those of the corresponding control groups. However, in the chronic pentazocine- and ethylketocyclazocine-pretreated groups showing non-conditioned suppression, the specific binding of [3H]phencyclidine and [3H]naloxone were not altered. Moreover, a decrease of [3H]ethylketocyclazocine binding was observed in the chronic pentazocine-pretreated group. These results suggest that the binding function of different opioid receptor subtypes may be altered differently by stress, and that the kappa receptor may be important for the conditioned suppression of motility in mice.

Animals↗
PubMed1986

A survey of Streptococcus pneumoniae, Streptococcus zooepidemicus, Salmonella spp., Bordetella bronchiseptica and Sendai virus in guinea pig colonies in Japan.

S. pneumoniae, S. zooepidemicus, Salmonella spp., B. bronchiseptica and Sendai virus were examined in a total of 45 guinea pig colonies (17 institutional and 28 breeder's colonies) of Hartley strain, and found to be positive in 6, 3, 5, 20 and 14 colonies, respectively. Sendai virus was highly prevalent among guinea pigs, showing so high rates positive as 80 to 100% of animals obtained from 11 of the 14 contaminated colonies. B. bronchiseptica was also shown to be prevalent within contaminated colonies by indication of rates positive more than 40% of animals examined in 14 of the 20 colonies. Infection rates of other 3 pathogens, however, ranged from lower than 20% to higher than 80% according to colonies. All strains of Salmonella isolated in this survey were identified as S. typhimurium and those of S. pneumoniae as serotype 19F.

Animals↗
PubMed1986

Effect of tizanidine on body temperature in the mouse.

The effect of tizanidine [5-chloro-4-(2-imidazolin-2-yl-amino)-2,1, 3-benzothiadiazole] on core temperature in the mouse was investigated in comparison with that of clonidine. Tizanidine decreased core temperature in unanaesthetized, freely-moving normal mice. Clonidine produced hypothermia in normal mice. The alpha 2-antagonist yohimbine produced an antagonism to tizanidine- and clonidine-induced hypothermia, while naloxone failed to antagonize the hypothermia. It is concluded that tizanidine and clonidine produce a similar hypothermic effect via an alpha 2-adrenoreceptor, but not an endogenous opioid system.

Animals↗
PubMed1985

Effect of testosterone on the kinetics of the development of suppressor cells in adjuvant arthritis.

The induction of unresponsiveness to mycobacterial adjuvant took a longer time in male DA rats than in female rats. A shift in the induction time of unresponsiveness in males toward the female type was brought about by castration, but could be reverted to the male type by the application of testosterone. The transfer study revealed that cells capable of preventing arthritis required a longer incubation time for their development in males than in females. This suggests that testosterone inhibits the development of suppressor cells in adjuvant arthritis.

Animals↗
PubMed1985

Conformational changes of opioid receptor induced by the electric footshock.

The present electric shock (ES) schedule followed in these experiments produced different functional changes in endogenous putative opioid agonist- and antagonist-type receptors, depending on the type of receptor: the amount of antagonist binding was increased by ES application, while the amount of agonist binding was decreased. In order to elucidate the mechanism of these changes, we investigated whether ES application was able to affect sulfhydryl-groups and phospholipids of endogenous opioid receptors. In comparison to the control membrane, the increased antagonist binding sites of the ES membrane were liable to be inactivated by the sulfhydryl-modifying reagents, N-ethylmaleimide (NEM) and iodoacetamide. However, in the presence of 100 mM Na, the antagonist binding sites of both the control and ES membranes were inactivated by NEM in the same manner. On the other hand, the agonist binding sites of both membranes were similarly inactivated by NEM regardless of the absence or presence of 100 mM Na. Another sulfhydryl-modifying reagent, such as p-chloromercuriphenylsulfonic acid, did not produce any difference between the control and ES membranes. The increased antagonist binding sites of the ES membrane were also liable to be inactivated by phospholipase A2. These results suggest that the present ES schedule followed in these experiments produces conformational changes in endogenous opioid receptors in the rat brain. As a result of these conformational changes, the amount of binding in the antagonist sites may be increased, while the amount of binding in the agonist sites may be decreased. However, the increased antagonist binding sites may be liable to be inactivated by NEM, iodoacetamide and phospholipase A2.

4-Chloromercuribenzenesulfonate↗
PubMed1985

Involvement of different opioid receptor subtypes in electric shock-induced analgesia and motor suppression in the rat.

We have investigated the correlation of electric shock-induced behavioral changes and functional alterations of endogenous opioid receptor subtypes. The degree of electric shock-induced behavioral changes, such as analgesia and motor suppression, was dependent on the duration of and time after electric shock application. The electric shock-induced behavioral changes were completely antagonized by naloxone. The apparent development of tolerance to both behavioral effects as a result of successive daily electric shock was different: Tolerance to electric shock-induced analgesia developed after 2 days' successive electric shock application, while tolerance to motor suppression was not observed even after 7 days' successive electric shock application. There was a decrease of [3H][D-Ala2, Met5]enkephalinamide ([3H]DAMEA, delta agonist) binding and an increase of [3H]naloxone (mu antagonist) binding when potent electric shock-induced analgesia developed. On the other hand, the binding of [3H]DAMEA and [3H]ethylketocyclazocine (kappa agonist) was significantly changed when locomotion was suppressed. These results suggest strongly that different opioid systems may participate in electric shock-induced analgesia and motor suppression: electric shock-induced analgesia and motor suppression may be mediated by mu/delta and kappa/delta receptors, respectively.

Animals↗
PubMed1985

Functional alteration of opioid receptor subtypes in the mice exhibited conditioned suppression in motility.

Mice exhibit a marked suppression of motility (conditioned suppression) when placed in the same environment in which they had previously received the electric footshock. The present study was designed to investigate the functional change of opioid receptor subtypes in the conditioned suppression group using an opioid binding assay technique. In the synaptic membrane of the conditioned suppression group, the binding capacities of [3H]naloxone at high and low affinity binding sites and of [3H]phencyclidine at high affinity binding site were significantly increased compared to those of the control group. On the other hand, the binding capacity of [3H]ethylketocyclazocine at both affinity binding sites in the conditioned suppression group was not changed. These results suggest that the binding function of different opioid receptor subtypes may be altered differently by stress.

Animals↗
PubMed1985

Migration of macrophages from the marginal zone to germinal centers in the spleen of mice.

Histological observations of the mouse spleen were carried out at different times after intravenous carbon injection. Large carbon-laden macrophages appeared in great numbers in the marginal zone soon after injection. They came together favorably around the germinal centers. Possible migration of these cells toward the germinal centers diffusely from the periphery of the white pulp or through the periarterial lymphoid sheath was suggested. These macrophages entered the germinal centers on a large scale and clustered for a long period--at least 180 days. Since the same type of macrophages were observed persistently in the marginal zone, it was thought that some of them might arise from the blood stream. Possible migration of these cells from the marginal zone toward the germinal centers was also persistently observed. A second type of much smaller carbon-laden macrophages was seen in the white pulp. However, they never showed any favorable localization in the germinal centers as did large carbon-laden macrophages.

Animals↗
PubMed1985

Macrophages migrate from the marginal zone into the germinal centre of the rodent spleen.

In the first experiment, histological observation of the mouse spleen was carried out after intravenous carbon injection. Large carbon-laden macrophages were found in the marginal zone soon after injection and then they appeared to migrate into the white or red pulp. Macrophages migrating deeply into the white pulp came together favorably around the germinal centre and entered the majority of the germinal centres by 10 days. In the second and third experiments, syngeneic transfer of rat peritoneal macrophages labeled with carbon were performed. They were injected either retrograde via hepatic artery or directly into the splenic artery. Carbon-laden macrophages were found in the germinal centres in the spleen 12 to 24 hours after injection though in a limited number. Possible migration of intrinsic as well as extrinsic macrophage from the marginal zone into the germinal centre was demonstrated.

Animals↗
PubMed1985

Antinociceptive action of tizanidine in mice and rats.

The antinociceptive action of tizanidine [5-chloro-(2-imidazolin-2-yl-amino)-2,1,3-benzothiadiazole], a centrally acting muscle relaxant, was evaluated after subcutaneous or peroral administration in mice and rats. Tizanidine strongly inhibited the writhing response induced by acetic acid, phenyl-p-benzoquinone and acetylcholine in mice, and its potency was found to be greater than that of morphine. Tizanidine showed antinociceptive action like morphine not only in tail pressure and electrical stimulation tests in mice but also in tail-flick tests in mice and rats. The antinociceptive action of tizanidine was unaffected by pretreatment with naloxone. These findings suggest that tizanidine develops relatively strong antinociceptive action by a nonopioid mechanism.

Analgesics↗