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Y Kasuya

Publications and source records attributed to Y Kasuya.

At least 163 records · Page 9Linked to original sources

Phorbol ester (PMA) activates voltage-dependent Ca(2+)-channels in helical but not ring preparation of the rat aorta.

Effects of phorbol 12-myristate 13-acetate (PMA) on the helical and ring preparations from rat thoracic aorta was investigated in the present study. In helical strips, PMA produced biphasic contraction, i.e., sustained contraction followed by a phasic response superimposed on the sustained contraction. The phasic contraction was completely inhibited by removal of external Ca2+, whereas sustained contraction was not affected by the treatment. In the ring preparation, PMA produced only sustained contraction, whereas phasic contraction was not induced. On the other hand, in the ring preparation which had been treated with 15 mM K+, PMA was able to produce phasic contraction. Contractile response of the aorta to norepinephrine (NE) or clonidine in the ring preparations was significantly weaker than that in the helical strips. In the presence of nifedipine, however, these different sensitivity to NE between ring and helical preparations was not shown. These results suggest that an activation of C-kinase by PMA is able to stimulate voltage-dependent Ca(2+)-channels in the helical strips but not ring preparation of the aorta. An increased contractile response of the aorta to agonists in helical strips may be responsible for an increased activities of voltage-dependent Ca(2+)-channels.

Animals↗

Antitussive effect of captopril, an angiotensin converting enzyme inhibitor, in the rat.

The effects of acute treatment with captopril, an angiotensin converting enzyme inhibitor, on the capsaicin-induced cough reflex were examined in rats. Intraperitoneal injection of captopril in doses of 3 and 10 mg/kg decreased the number of coughs dose-dependently. Although the peak effect was similar to that of morphine (0.5 mg/kg), the duration of captopril's effect (10 mg/kg) was longer than that of morphine. Furthermore, while pretreatment with naloxone significantly decreased the duration of the antitussive effect of captopril, it had no significant effect on the early-phase (within 60 min) effect of captopril. These results suggest that the mechanism which underlies the antitussive effect of captopril involves mediation by both nonopioid and opioid systems.

Animals↗

[Obstetric anesthesia in Gifu].

Improvement of perinatal mortality rate in Japan is remarkable for the last two decades, but maternal mortality rate is still relatively high in comparison with the improvement of the perinatal mortality rate. Maternal mortality rate 1991 in Japan was 8.5. Maternal deaths occurred mostly in perinatal period. The causes of death include pre- and postpartum hemorrhage, pulmonary embolism, and hypertension. This means an intensive, vigorous therapy including anesthesia management is necessary during peripartum period. Questionnaires were mailed to 63 maternity clinics in Gifu area. Some of the questions requested as many answers as applicable. We received 51 replies to questionnaires. Average Cesarean rate in Gifu was 7.3%. Spinal anesthesia was used in 74.5% of maternity clinics. Dibucaine was the most widely used local anesthetic for spinal anesthesia. Antacid medications were rare in our study group. After induction of general anesthesia, airway was maintained by masks (36.0%) or endotracheal tube (64.0%). Obstetric analgesia by local anesthetics was not used widely.

Anesthesia, Obstetrical↗

[A case of pulmonary alveolar proteinosis--evaluation of a Swan-Ganz catheter in bilateral lung lavage].

Lung lavage, known to be effective for alveolar proteinosis, brings about significant hypoxemia immediately after evacuation of lavage fluid. Impeding blood flow of even a distal branch of a pulmonary artery by using a Swan-Ganz catheter (SGC) successfully prevented this hypoxemia. And this SGC procedure could be safely carried out to make lavage of each lung successively in one day.

Adult↗

The antitussive effect of cromakalim in rats is not associated with adenosine triphosphate sensitive K+ channels.

The effects of cromakalim, a K+ channel opener, on the capsaicin-induced cough reflex in rats were studied. I.P. administration of cromakalim in doses of 0.1 to 1.0 mg/kg decreased the number of induced coughs in a dose- dependent manner. Neither glibenclamide, an adenosine triphosphate-sensitive K+ channel blocker, nor tetraethylammonium, a blocker of other types of K+ channels, affected the antitussive effect of cromakalim. However, the antitussive effect of cromakalim was antagonized by methysergide, a 5-HT antagonist. Although Bay K 8644, a dihydropyridine Ca2+ channel activator, had a marked cough-depressant effect, it had no effect on the antitussive effect of cromakalim. These results suggest that the antitussive effect of cromakalim is primarily mediated by activation of the serotonergic system through the inhibition of voltage-dependent Ca2+ channels, and not through the activation of K+ channels.

Adenosine Triphosphate↗

Effects of diabetes on the antinociceptive effects of intrathecally administered endothelin-1.

Intrathecal administration of endothelin-1 (ET-1) produced a dose-dependent increase in tail-pinch latency, i.e., antinociception, in both diabetic and non-diabetic mice. The dose ranges which produced a significant antinociception in diabetic mice (0.0001 to 0.0003 nmol) were lower than those in non-diabetic mice (0.001 to 0.003 nmol). Furthermore, the antinociceptive effect of ET-1 in diabetic mice was decreased when the doses of ET-1 were increased. Indeed, when ET-1 in a dose of 0.003 nmol, which produced significant antinociception in non-diabetic mice, it had no antinociceptive effect in diabetic mice. These results suggest that the mechanism which underlies the antinociceptive effects of ET-1 is up-regulated in diabetic mice, as compared with that in non-diabetic mice.

Animals↗

Involvement of haloperidol-sensitive sigma-sites in antitussive effects.

The effects of selective sigma-ligands on the capsaicin-induced cough reflex in rats were studied. Intraperitoneal injection of (+)-N-allylnormetazocine ((+)-SKF-10,047) and N,N'-di(ortho-tolyl)guanidine (DTG) in doses that ranged from 0.3 to 3.0 mg/kg decreased the number of coughs dose dependently. The antitussive effects of these sigma-ligands were significantly attenuated by pretreatment with haloperidol. Pretreatment with haloperidol also markedly reduced the antitussive effects of (+/-)-pentazocine and dextromethorphan. These results suggest that haloperidol-sensitive sigma-sites may be involved in the regulation of coughs.

Animals↗

Complete primary structure and tissue expression of chicken pectoralis M-protein.

M-Protein (165 kDa) is a structural constituent of myofibrillar M-band in striated muscle. We generated a monoclonal antibody which recognized a 165-kDa protein from chicken pectoralis muscle in immunoblot analysis and stained the M-band under immunofluorescence microscopy. By screening a lambda gt11 cDNA library from chicken embryonic pectoralis muscle with this antibody, we isolated a cDNA clone encoding the M-protein. Northern blot analysis showed that M-protein mRNA is expressed in pectoralis and cardiac muscle but not in gizzard smooth muscle or non-muscle tissues. Moreover, the anterior latissimus dorsi muscle, which consists almost exclusively of slow fiber types, contains no detectable levels of the mRNA. The full-length cDNA sequence predicted a 1,450-amino acid polypeptide with a calculated molecular weight of 163 x 10(3). The encoded protein contains several copies of two different repetitive motifs: five copies of fibronectin type III repeats are in the middle part of the predicted molecule, and two and four copies of the immunoglobulin C2-type repeats are located toward the NH2-terminal and COOH-terminal regions, respectively. This indicates that M-protein, along with other thick filament-associated proteins such as C-protein, twichin, and titin, belongs to the superfamily of cytoskeletal proteins with immunoglobulin/fibronectin repeats.

Amino Acid Sequence↗

Paradoxical analgesia produced by naloxone in diabetic mice is attributable to supersensitivity of delta-opioid receptors.

The effects of naloxone on the analgesic response were examined using the tail-flick test, in mice with streptozotocin-induced diabetes. Subcutaneous injection of naloxone (5 mg/kg, s.c.) produced a marked analgesia in diabetic mice but not in age-matched non-diabetic mice. Naloxone-induced analgesia in diabetic mice was significantly reduced by pretreatment with naltrindole (0.1 mg/kg, s.c.), a selective antagonist of delta-opioid receptors. By contrast, no significant naloxone-induced increase in tail-flick latency in diabetic mice was observed after chronic treatment with naloxone (5 mg/kg, s.c.) for 5 days. However, the tail-flick latency was significantly increased by chronic treatment with naloxone in non-diabetic mice. Furthermore, the significant naloxone-induced increase in tail-flick latency in non-diabetic mice that had been chronically treated with naloxone was also antagonized by pretreatment with naltrindole. Chronic pretreatment with 5 mg/kg of naloxone for 5 days markedly attenuated the analgesic effect of the delta-agonist DPDPE in diabetic mice, whereas this pretreatment significantly enhanced the effect of DPDPE in non-diabetic mice. These results suggest that naloxone-induced 'paradoxical' analgesia in mice may be mediated predominantly by delta-opioid receptors.

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

Stable isotope dilution mass spectrometry for the simultaneous determination of cortisol, cortisone, prednisolone and prednisone in plasma.

A capillary gas chromatographic-mass spectrometric method for the simultaneous determination of cortisol, cortisone, prednisolone and prednisone in human plasma is described. [1,1,19,19,19-2H5]Cortisol, [1,1,19,19,19-2H5]cortisone, [1,19,19,19-2H4]prednisolone and [1,19,19,19-2H4]prednisone were used as internal standards. Formation of the bismethylenedioxy-3-heptafluoro-n-butyryl (BMD-HFB) derivatives made possible the separation of the four corticosteroids with good gas chromatographic behaviour. The new double derivatization has been demonstrated to be of value for sensitive and selective quantification by this technique. Detection was performed by monitoring the molecular ion (M+) of the BMD-HFB derivatives for cortisone and prednisolone, the [M - 18]+ ion for cortisol, and the [M - 30]+ ion for prednisone. The method requires no complex corrections for contributions and provides good accuracy and precision.

Cortisone↗

Periaqueductal gray matter stimulation-produced analgesia in diabetic rats.

The effect of diabetes on periaqueductal gray matter (PAG) stimulation-produced analgesia (SPA) was examined in rats. PAG SPA was assessed using the tail-pinch test. PAG stimulation produced marked analgesia in both naive and diabetic rats. Furthermore, the degree of PAG SPA did not differ between naive and diabetic rats. PAG SPA was significantly attenuated by a low dose (0.5 mg/kg, s.c.) of naloxone in naive rats, but not in diabetic rats. However, a high dose (5 mg/kg, s.c.) of naloxone significantly and equally attenuated PAG SPA in both naive and diabetic rats. On the other hand, the analgesic potency of morphine (3 mg/kg, s.c.) was significantly reduced in diabetic rats as compared with naive rats. These results suggest that PAG SPA in diabetic rats may be mediated by different opioid receptor interactions as compared with naive rats.

Animals↗

Level of ETB receptor mRNA is down-regulated by endothelins through decreasing the intracellular stability of mRNA molecules.

Using ROS17/2 rat osteosarcoma cells as a model system, we examined the possibility that endothelin (ET)-induced down-regulation of ETB receptor was accompanied by a decrease in levels of ETB receptor mRNA. Northern blot analysis showed that low doses of ET-1 and ET-3 caused a transient decrease in ETB receptor mRNA in the cells. The maximum decrease in the levels of ETB receptor mRNA (80%) occurred after 2-4 h of exposure of the cells to ETs and was followed by a gradual recovery to control levels by 24 h. The effects were dose-dependent (EC50-1 nM), and ET-1 and ET-3 were almost equipotent in eliciting the response. The addition of either ionomycin, a Ca2+ ionophore, or phorbol dibutyrate, a protein kinase C activator, mimicked the effect of ETs. These results suggested that ETs-induced down-regulation of ETB receptor mRNA was mediated by the activation of ETB receptor and that it may have involved ETB receptor coupled second messenger pathways. We also showed that ETB receptor mRNA had a long intracellular life span which suggested that ETs-induced down-regulation of ETB receptor mRNA may have been due to a decrease in the stability of mRNA, rather than inactivation of the transcription of mRNA.

Animals↗

Action of endothelin-1 on rat astrocytes through the ETB receptor.

We investigated the effect of ET-1 on the state of rat cerebral astrocytes (AC) differentiation. AC ceased to proliferate and changed into its differentiated state by treatment with dibutyryl cyclic AMP (DBcAMP). The cell growth activity in DBcAMP-treated AC was stimulated by ET-1 in a dose-dependent manner. Over similar dose ranges, ET-1 suppressed the glutamine synthetase activity in DBcAMP-treated AC. The molar potency of ET-1 in this action was at least 3 orders of magnitude higher than that in mitogenic action in AC under the proliferative state previously reported. Northern blot analysis revealed that ETB receptor mRNA level in DBcAMP-treated AC was markedly higher than that in AC untreated with DBcAMP. Consistently, binding studies showed that the Bmax value for [125I]ET-1 in DBcAMP-treated AC was 16 times higher than that in AC untreated with DBcAMP. These results suggest that ET-1 potently induced a retraction of the differentiation state of AC from fully the specialized state and that the high responsiveness of differentiated AC to ET-1 was partly attributed to the high level expression of the ETB receptor.

Animals↗

Reversible stepwise mechanism involving a carbanion intermediate in the elimination of ammonia from L-histidine catalyzed by histidine ammonia-lyase.

L-Histidine labeled with deuterium at the C-5' position of the imidazole ring, L-[5'-2H]histidine (His-5'-D), was used as a probe for investigating a stepwise reversible mechanism via a carbanion intermediate in the elimination of ammonia catalyzed by histidine ammonia-lyase (EC 4.3.1.3). The labeled L-histidine (His-5'-D) (2.45 mM) was incubated with histidine ammonia-lyase (200 units) from Pseudomonas fluorescens at pH 7.0 or 9.0 at 25.0 degrees C for 24 h. The time course of the reaction was examined to determine the rates of enzyme-catalyzed hydrogen exchange at C-5' of L-histidine and urocanic acid. The finding of the enzyme-catalyzed hydrogen exchange at C-5' of both L-histidine and urocanic acid in the presence of L-histidine provided a rational explanation for a stepwise reversible mechanism via a carbanion intermediate in the elimination reaction. The rate of increase in the concentration of urocanic acid exchanged with hydrogen (UA-5'-H) did not depend on the formation rate of urocanic acid and UA-5'-H was continuously formed at a constant rate (25.6 microM/h) even after the completion of urocanic acid formation. These observations suggested the presence of the reversible reaction of urocanic acid and a carbanion intermediate. Since there was only a minor contribution for the formation of UA-5'-H from L-histidine exchanged with solvent hydrogen (His-5'-H), the main pathway in the enzymatic reaction of His-5'-D must be the formation of UA-5'-D via a carbanion intermediate (carbanion-D). Regeneration of the carbanion-D from UA-5'-D by its reverse reaction and subsequent hydrogen incorporation at C-5' would contribute to a large extent for the formation of UA-5'-H. The stability of carbanion was also demonstrated to be approximately three times higher at pH 7.0 than at pH 9.0.

Ammonia↗

Effects of diabetes on stress-induced analgesia in mice.

The present studies were designed to determine whether streptozotocin-induced (STZ-induced) diabetes in mice can attenuate the development of antinociception induced by exposure to both foot shock and forced swimming stress. Foot shock stress produced significant analgesia both in control and diabetic mice. However, the extent of foot shock stress-induced analgesia (FSSIA) in diabetic mice was significantly lower than that in control mice. Naloxone (2 mg/kg, i.p.) significantly attenuated FSSIA in control mice, but was without effect on FSSIA in diabetic mice. One-minute swimming stress had no significant effect on tail-pinch latency in control mice, whereas 3-min swimming stress produced significant analgesia in these mice. Diabetic mice exhibited robust swimming stress-induced analgesia (SSIA): one-min swimming stress produced significant analgesia in diabetic mice. These analgesic effects were blocked by naltrindole, a selective antagonist of delta-opioid receptors, but not by pretreatment with beta-funaltrexamine, an irreversible and selective antagonist of mu-opioid receptors. These results suggest that the deficiency in the functioning of mu-opioid receptors caused by diabetes results in significant activation of an endogenous analgesic system, which is mediated mainly by delta-opioid receptors.

Animals↗

Simultaneous determination of stable isotopically labelled L-histidine and urocanic acid in human plasma by stable isotope dilution mass spectrometry.

A capillary gas chromatographic-mass spectrometric method for the simultaneous determination of stable isotopically labelled L-histidine (L-[3,3-2H2,1',3'-15N2]histidine, L-His-[M + 4]) and urocanic acid ([3-2H,1',3'-15N2]urocanic acid, UA-[M + 3]) in human plasma was developed using DL-[2,3,3,5'-2H4,2'-13C,1',3'-15N2]histidine (DL-His-[M + 7]) and [2,3,5'-2H3,2'-13C,1',3'-15N2]urocanic acid (UA-[M + 6]) as internal standards. L-Histidine and urocanic acid were derivatized to alpha N-(trifluoroacetyl)-imN-(ethoxycarbonyl)-L-histidine n-butyl ester and imN-(ethoxycarbonyl)urocanic acid n-butyl ester. Quantification was carried out by selected ion monitoring of the molecular ions of the respective derivatives of L-His-[M + 4], DL-His-[M + 7], UA-[M + 3] and UA-[M + 6]. The sensitivity, specificity, precision and accuracy of the method were demonstrated to be satisfactory for measuring plasma concentrations of L-His-[M + 4] and UA-[M + 3] following administration of trace amounts of L-His-[M + 4] to humans.

Gas Chromatography-Mass Spectrometry↗

Simultaneous determination of cortisol and cortisone in human plasma by stable-isotope dilution mass spectrometry.

A method for the simultaneous determination of cortisol and cortisone in human plasma was developed using capillary gas chromatography-mass spectrometry-selected ion monitoring. [2H5]Cortisol and [2H5]cortisone were used as internal standards. Cortisol and cortisone in plasma were determined from the peak-height ratios of the [M-31] fragment ions of the methoxime-trimethylsilyl derivatives of cortisol and [2H5]cortisol (m/z 605 and 610) and of cortisone and [2H5]cortisone (m/z 531 and 536). Sensitivity, specificity, precision, accuracy and reproducibility of the method were demonstrated to be satisfactory for measuring the circulating concentrations of cortisol and cortisone.

Cortisone↗

Role of spleen or spleen products in the deficiency in morphine-induced analgesia in diabetic mice.

We examined the possibility that the spleen or factor(s) derived from spleen mononuclear cells are involved in the deficient mu-opioid receptor-mediated analgesia encountered in diabetic mice. Splenectomized diabetic mice had a significantly higher sensitivity to morphine analgesia than untreated or sham-operated diabetic mice. Naive recipient mice injected with mononuclear spleen cells from diabetic mice exhibited a lower sensitivity to morphine analgesia than vehicle-treated naive mice. These results suggest that some factor(s) derived from spleen mononuclear cells may play an important, direct or indirect role in the selective reduction in mu-agonist-mediated analgesia in diabetic mice.

Analgesia↗