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Biomedical subjects

A Nishio

Publications and source records attributed to A Nishio.

At least 19 recordsLinked to original sources
PubMed1995

Mechanisms of the enhanced contractile response to a low concentration of phorbol 12,13-dibutyrate in thoracic aorta isolated from rats with dietary magnesium deficiency.

The mechanisms underlying the enhanced contractile response to phorbol 12,13-dibutyrate (PDBu) were examined in de-endothelialized thoracic aortas isolated from rats with dietary magnesium (Mg) deficiency. PDBu (1.0 nM)-induced contractions were significantly larger in Mg-deficient rats than in the controls. The contraction was completely inhibited by nifedipine, removal of external Ca2+ or by l-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7). PDBu (1.0 nM) and phorbol 12-myristate 13-acetate (1.0 microM) significantly decreased the KD value and increased the Bmax for the binding of [3H]PN200-110 to the aortas. The degree of the decrease in the KD value was significantly greater in Mg-deficient rats than in the controls. The PDBu-induced decrease in the KD value was abolished by H7. These results suggest that activation of protein kinase C by phorbol esters may participate in the activation of L-type Ca2+ channels, which increases both the affinity of [3H]PN200-110 binding and the magnitude of the external Ca(2+)-dependent contraction. Dietary Mg-deficiency may enhance these processes.

Animals↗
PubMed1995

Responsiveness of equine basilar artery to transmural nerve stimulation differs from that of porcine and bovine basilar arteries in vitro.

Transmural nerve stimulation (TNS) induced relaxations in porcine and bovine basilar arteries which were abolished by tetrodotoxin (TTX) and by L-nitro-arginine (LNAG). However, TNS induced contractions in equine basilar artery which were abolished by TTX and by guanethidine, but not by LNAG. These results suggest that the TNS-induced contractions of equine basilar arteries may be mediated by norepinephrine release.

Animals↗
PubMed1995

[The effect of local transient cooling on anodermal blood flow].

To clarify the regulatory mechanism of blood flow of anodermal mucosal layers responding to the localized and transient coolong stimulation (around -4 degrees C), we examined the change of anodermal blood flow with use of Laser Doppler Flowmeter (Periflux, Perimed). The cooling stimulation was applied to anoderm by the insertion of chilled cold stick (Poscool, Maruho) into the anus of 11 healthy male volunteer, aged 20-25 years. Experimental results obtained are as follow; 1) The anodermal blood flow of healthy subjects are variant in degree and widely distributed from 30 to 80 Perfusion Unit (PU). 2) After cooling for five minutes by the insertion of a frozen Poscool, anodermal blood flow were increased in 8 cases out of eleven (72.7%). The changes corresponds to be 1.4 to 5.2 times. 3) Eight cases are divided into two groups on the basis of the time course after cooling: the one is "delayed responding group" (there is a delay 10-40 minutes before the blood flow is increasing) and the other is "rapid responding group" (the blood flow is immediately increasing). These results indicate that the anodermal blood flow, which are exposed to cooling, of healthy subjects is regulated not only by nervous mechanism but by humoral mechanism. Then, based on the Lewis reaction (cold vasodilatation), it is suggested that the short time cooling of anoderm should be appreciated as a conservative therapy of hemorrhoids and anal fissures.

Adult↗
PubMed1995

Breakdown of self-tolerance by intrathymic injection of a T-cell line inducing autoimmune gastritis in mice.

Autoimmune gastritis (AIG) develops spontaneously in BALB/c mice thymectomized 3 days after birth (3d-Tx). We first confirmed our previous observations that CD4+ splenic T cells in AIG mice induced AIG in nu/nu mice, while those in normal mice suppressed the development of the disease. In addition, we found that a quantitative balance between these effector (Te) and suppressor (Ts) T cells determined either onset or prevention of the disease. Peripheralization of Ts seemed to begin around 3 days after birth, since the incidence of AIG in mice that underwent Tx 6 days after birth (6d-Tx) decreased markedly, compared with that of 3d-Tx mice; 12% in the former, while 79% in the latter. Notably, Ts existed in the 6d-Tx mice that escaped AIG. We next examined the target specificity of such Ts using syngeneic parietal cells known as autoantigens and two kinds of T-cell lines established from an AIG mouse; one is gastritis inducible in vivo, termed A-II, while another is not, named AC-II. Intrathymic injection of parietal cells into mice 3 days after birth followed by 6d-Tx completely prevented the development of AIG. In contrast, injection of irradiated A-II, but not AC-II cells resulted in AIG in 67% of the mice. No autoimmune oophoritis (AIO) was induced in female mice, implying that the breakdown of tolerance is organ specific. Taken together, peripheral tolerance for organ-specific autoantigens seems to be maintained by CD4+ Ts responding to Te, which induces the disease.

Animals↗
PubMed1994

Vasomotor effects of histamine on bovine and equine basilar arteries in vitro.

The vasomotor effects of histamine on isolated bovine and equine basilar arteries were examined. Histamine induced contractions in both these preparations. The maximal response to and pEC50 value for histamine of the equine artery were larger than those of bovine tissue. Similar results were obtained with endothelium-denuded basilar arteries. Diphenhydramine (H1-receptor antagonist) inhibited histamine-induced contractions of the basilar arteries from both species in a concentration-dependent manner and its pA2 values (with 95% confidence limits) were 7.61 (7.39-7.83) and 8.15 (8.01-8.29) for the bovine and equine preparations, respectively. Cimetidine (H2-receptor antagonist) slightly potentiated histamine-induced contractions of bovine, but not equine, basilar arteries. 2-Thiazolylethylamine (H1-receptor agonist) induced contractions in both preparations, whereas impromidine (H2-receptor agonist) induced weak relaxation of the bovine, but not the equine, tissue. These findings indicate that bovine basilar arterial smooth muscle cells possess H1- and H2-receptors. Stimulation of the former results in contraction, whereas stimulation of the latter results in weak relaxation. Equine basilar arterial smooth muscle cells possess H1-receptors, stimulation of which results in contraction.

Animals↗
PubMed1994

A conserved epitope on H+,K(+)-adenosine triphosphatase of parietal cells discerned by a murine gastritogenic T-cell clone.

BACKGROUND/AIMS: H+,K(+)-adenosine triphosphatase (H+,K(+)-ATPase) of parietal cells is an organ-specific enzyme recognized by autoantibodies found in human and murine autoimmune gastritis (AIG). Murine AIG can be induced in BALB/c mice by thymectomy 3 days after birth and is a T cell-mediated disease. This study examined the specificity of T cells that cause AIG and the role of H+,K(+)-ATPase in this disease. METHODS: From an AIG mouse, a gastritogenic T-cell clone (II-6) was established, and its reactivity to synthetic peptides of H+,K(+)-ATPase was tested. RESULTS: II-6 cells are CD4+, V beta 14+, and interferon gamma producers. Adoptive transfer of II-6 cells to syngeneic nude mice resulted in AIG without the production of autoantibodies to parietal cells. The II-6 cells were responsive not only to murine but also to human and porcine parietal cells. Their proliferation was also induced by amino acids 891-905 (alpha 891) and 892-906 (alpha 892) of the alpha subunit of porcine and human H+,K(+)-ATPase, respectively. CONCLUSIONS: The T-cell response to a single epitope of H+,K(+)-ATPase, the amino acid sequence of which is conserved among at least three mammals tested, is sufficient to cause AIG. Autoantibodies to parietal cells are not detected in these AIG mice.

Amino Acid Sequence↗
PubMed1994

Equine coronary artery responds to 5-hydroxytryptamine with relaxation in vitro.

Isolated equine coronary arteries responded to 5-hydroxytryptamine (5-HT) with relaxations in both endothelium-dependent and endothelium-independent mechanisms. Experiments were designed to characterize the 5-HT receptor subtype mediating these relaxations. Both 5-HT and alpha-methyl-5-HT (alpha-Me-5-HT; 5-HT2 agonist) produced concentration-dependent relaxations in equine coronary arteries precontracted with a thromboxane A2 derivative (ONO11113). The degree of the maximal relaxation induced by alpha-Me-5-HT was about one-half of that induced by 5-HT. In the coronary arteries without endothelium, alpha-Me-5-HT produced no relaxation, but 5-HT caused relaxation, which was inhibited by a 5-HT1 antagonist (methysergide, mianserin and methiothepin), but was inhibited neither by ketanserin (5-HT2 antagonist) nor by MDL72222 (5-HT3 antagonist). In the coronary arteries with endothelium, however, the relaxation induced by alpha-Me-5-HT was inhibited by ketanserin, L-nitro-arginine (NO synthase inhibitor) and methylene blue (soluble guanylate cyclase inhibitor). These results suggest that the relaxation induced by 5-HT in equine coronary arteries depends mainly on the stimulation of both 5-HT1 receptor subtype on smooth muscle cells directly, and 5-HT2 receptor subtype on endothelial cells indirectly by liberating endothelium-derived NO.

Animals↗
PubMed1994

Characterization of muscarinic receptor subtype mediating contraction and relaxation in equine coronary artery in vitro.

In coronary arterial rings isolated from horses, 10(-8)-10(-6) mol/l acetylcholine (ACh) induced concentration-dependent contractions which were potentiated by the removal of endothelium and by pretreatment with L-nitro-arginine (LNAG) or methylene blue (MB). Relatively lower concentrations of ACh (10(-14)-10(-8) mol/l) induced relaxation when the coronary rings were contracted by phenylephrine (PE). ACh-induced contractions in the coronary rings without endothelium were competitively inhibited by each muscarinic subtype selective antagonist in the following order of potency: 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) > pirenzepine > or = parafluoro-hexahydrosiladiphenidol (pFHHSiD) > methoctramine. ACh-induced relaxation in the rings with endothelium was inhibited by LNAG or MB, and by each selective antagonist in the following order of potency: 4-DAMP > pFHHSiD > pirenzepine > methoctramine. These results suggest that the ACh-induced contraction and relaxation in equine coronary arteries are mediated mainly by an M3-receptor located on the smooth muscle cells and endothelial cells, respectively, and that the stimulation of the M3-receptor on the endothelial cells liberates nitric oxide.

Acetylcholine↗
PubMed1994

Endovascular treatment of acute thrombotic occlusion of the cervical internal carotid artery associated with embolic occlusion of the middle cerebral artery: case report.

A 68-year-old man with acute, total thrombotic occlusion of the right cervical internal carotid artery, associated with embolic occlusion of the ipsilateral middle cerebral artery, was treated by the endovascular approach, i.e., intra-arterial fibrinolysis and balloon angioplasty. Endovascular treatment for a totally occluded internal carotid artery is indicated in the very early stage where there is no thrombus or a short thrombus that can be evacuated. Fibrinolysis of the associated embolus in the middle cerebral artery, if any, can be done in the same session, enabling an early restoration of the blood flow.

Aged↗
PubMed1994

Mechanisms of the enhanced contractile response to phenylephrine in thoracic aorta isolated from rats with dietary magnesium deficiency.

The mechanisms underlying the enhanced contractile response to phenylephrine (PE) and increased susceptibility to nifedipine of de-endothelialized thoracic aorta isolated from rats with dietary magnesium deficiency (Mg-deficient rats) were examined by functional and radioligand binding studies. Enhanced PE-induced contractions and increased susceptibility to nifedipine in Mg-deficient rats were not observed in the presence of 10 microM H7. PE significantly decreased the KD value without changing Bmax in the binding of [3H]PN200-110 to de-endothelialized aortic strips. The KD value obtained in the Mg-deficient rats was significantly smaller than that in the controls. Nifedipine displaced the binding of [3H]PN200-110 concentration-dependently, and the pKi value in Mg-deficient rats was significantly larger than that in the controls. A combination of PE and H7 abolished this difference. These results indicate that the modulation of L-type Ca2+ channels via the stimulation of alpha 1-adrenoceptors may be involved in the enhancement of vasoconstriction and increased susceptibility to nifedipine in aortas isolated from Mg-deficient rats. The H7-sensitive mechanisms may play an important role in these phenomena.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1994

Characterization of 5-hydroxytryptamine receptors on the isolated pig basilar artery by functional and radioligand binding studies.

5-Hydroxytryptamine (5-HT)-receptor subtypes on pig basilar arteries were investigated by measuring the contractile responses to 5-HT agonists, the effects of antagonists on the responses and by carrying out a radioligand binding assay with [3H]5-HT. The rank order of contractile agonist potency (according to the pEC50 values) was 5-carboxamidotryptamine > or = 5-HT > alpha-methyl-5-HT > (+/-)-8-hydroxy-dipropylaminotetralin. The contractile responses were not affected by endothelial denudation, and the 5-HT-induced contractions were antagonized competitively by ketanserin. Methiothepin shifted the 5-HT concentration-response curves to the right and downwards in a concentration-dependent manner. In the presence of ketanserin (10(-6) M), however, methiothepin antagonized the 5-HT-induced contractions competitively. Specific [3H]5-HT binding to 5-HT receptors was saturable, reversible and showed high (Kd, 2.5 nM) and low (Kd, 710 nM) affinities, with respective Bmax values of 29.5 and 1950 fmol/mg protein. These results indicate that both 5-HT1 and 5-HT2 receptors are present on pig basilar arterial smooth muscle cells, and their stimulation results in contraction.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1994

Participation of alpha 1- and beta 1-adrenoceptors in norepinephrine-induced contraction and relaxation of isolated equine coronary artery in vitro.

In coronary arterial rings isolated from horse, norepinephrine (NE)(10(-7) - 10(-5) M) induced concentration-dependent contractions which were not influenced by endothelial denudation. Prazosin (alpha 1-antagonist) inhibited the contraction, but yohimbine (alpha 2-antagonist) did not, and propranolol (beta-antagonist) enhanced the contraction. Pretreatment with phentolamine (10(-5) M) (alpha-antagonist) converted the contraction induced by NE to relaxation in coronary rings precontracted with ONO11113 (thromboxane A2 derivative). The relaxation was not influenced by removal of the endothelium, and was inhibited by propranolol and atenolol (beta 1-antagonist) but not by butoxamine (beta 2-antagonist). These results suggest that in equine coronary arteries, the contractile response to NE is mediated by stimulation of alpha 1-adrenoceptors on the smooth muscle, and that stimulation of beta 1-adrenoceptors on the smooth muscle modifies the contraction by inducing relaxation.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1994

Endothelial modulation of vascular tone in isolated porcine and bovine basilar arteries.

Endothelium-dependent modulation of vascular tone was investigated in isolated porcine and bovine basilar arteries. L-Nitro-arginine (NO synthase inhibitor) and methylene blue (soluble guanylate cyclase inhibitor) increased, but indomethacin (cyclooxygenase inhibitor) decreased the vascular tone in the basilar arteries from both species. Bradykinin evoked relaxation of precontracted porcine basilar artery, but not bovine basilar artery. Sodium fluoride (endothelial G-protein activator) produced relaxation of precontracted basilar arteries from both species. The effects of bradykinin and sodium fluoride were completely abolished by endothelial denudation and markedly inhibited by L-nitro-arginine and methylene blue, but not by indomethacin. Sodium nitroprusside (guanylate cyclase activator) evoked relaxation of precontracted endothelium-denuded basilar arteries from both species. These results suggest that there is species variation in endothelium-dependent modulation of vascular tone in the basilar artery.

Amino Acid Oxidoreductases↗
PubMed1994

Enhanced contractile response to phenylephrine and increased density of [3H]PN200-110 binding sites in thoracic aorta isolated from dietary magnesium-deficient rats.

The present study was undertaken to examine whether the enhanced contractile response to phenylephrine observed in thoracic aorta isolated from dietary magnesium-deficient rats depends on an increased density of alpha 1-adrenoceptor or calcium channels. Adult male Wistar rats were fed with a magnesium-deficient diet (0.001 per cent magnesium) for 30 days with control groups (0.07 per cent magnesium). The contractile response to phenylephrine was significantly inhibited by nifedipine in both aortas without endothelium, and the degree of the inhibition was significantly greater in magnesium-deficient rats than in controls. Membranes were isolated from both thoracic aortas without endothelium, and the binding of [3H]PN200-110 or [3H]prazosin to the membranes was studied. A single binding site for [3H]PN200-110 or [3H]prazosin was evident for both membranes with high affinity. Dietary magnesium-deficiency increased significantly the maximal number (Bmax) of [3H]PN200-110 binding sites, but not Bmax of [3H]prazosin, and did not alter the binding affinity of both ligands. These results suggest that increased density of calcium channels participates in the enhanced contractile response to phenylephrine in thoracic aortas isolated from dietary magnesium-deficient rats.

Animals↗
PubMed1993

Effects of intrathymic injection of organ-specific autoantigens, parietal cells, at the neonatal stage on autoreactive effector and suppressor T cell precursors.

Thymectomy on day 3 after birth (3d-Tx) induces autoimmune gastritis (AIG) in 81%, and oophoritis (AIO) in 25% of BALB/c mice at the age of 2 to 3 months. Intrathymic, but not intraperitoneal injection of syngeneic parietal cells into sex-matched BALB/c mice within 24 h of birth resulted in almost complete prevention of the development of AIG in these mice in which 3d-Tx was performed. The prevention induced was parietal cell specific, since the development of AIO was not inhibited in female mice. Moreover, the injection of BALB/c liver cells, Mls-matched (BALB/c) and -disparate (DBA/2) B blasts which resulted in V beta 6 T cell deletion, as well as the injection of staphylococcal enterotoxin B failed to prevent the diseases. These findings suggested that recognition of an autoantigen in the thymus is necessary for the induction of tolerance, and that involvement of Mls-1 antigens in the pathogenesis of AIG, as has been suggested previously (Schwartz, R. H., Cell 1989. 57: 1073), was unlikely. T cells that suppress the development of organ-specific autoimmune diseases in 3d-Tx mice seem to maintain the unresponsiveness of autoreactive T cells at the periphery in normal mice. In agreement with our previous observations, we found that intraperitoneal (i.p.) injection of spleen cells from 3-month-old normal mice into 3d-Tx mice on day 10 after birth prevented the development of AIG, whereas spleen cells from age-matched AIG+ (mice with AIG) or AIG- (mice without AIG) 3d-Tx mice failed to do this. This implies that the suppressor cells probably affect the differentiation of effector-precursor to effector. In fact, these suppressor cells did not inhibit the adoptive transfer of AIG to nu/nu BALB/c mice by spleen cells from 3d-Tx mice manifesting AIG. By negative selection using monoclonal antibody and complement, it was confirmed that the phenotype of the suppressor cell was CD4. In contrast to 3d-Tx, 10d-Tx did not induce AIG, indicating the peripheralization of the suppressor cell by that time. On the other hand, intrathymic injection of parietal cells immediately after birth did not affect suppressor cell generation, implying that some T cells, including suppressor cells, escape thymus selection. We postulate that these cells correspond to the precursors of the autoreactive effector T cells and suppressor T cells that are present in normal mice.

Animals↗
PubMed1993

Characterization of histamine receptors in isolated pig basilar artery by functional and radioligand binding studies.

Histamine receptors in pig basilar arteries were investigated in vitro by radioligand binding assays and by measuring the contractile and relaxant responses to histamine. Histamine and 2-pyridylethylamine (H1-agonist) induced concentration-dependent contractions, whereas impromidine (H2-agonist) induced concentration-dependent relaxations. These responses were independent of the presence of endothelial cells. Diphenhydramine (H1-antagonist) partially reversed the histamine-induced contractions to relaxations. Cimetidine (H2-antagonist) potentiated the contraction in a concentration-dependent manner. In the presence of cimetidine, the pEC50 value of histamine for the contraction was 6.30, and diphenhydramine competitively antagonized the histamine-induced contractions (pA2, 7.77). In the presence of diphenhydramine, the pEC50 value of histamine for the relaxation was 5.93, and cimetidine competitively antagonized the histamine-induced relaxations (pA2, 6.62). In the binding studies, the Kd value of [3H]mepyramine was 2.1 nM and the Bmax value was 95.6 fmol/mg protein. A competition experiment with diphenhydramine showed that the pKi value (7.51) was similar to the pA2 value. The Kd value for [3H]cimetidine was 126.0 nM and the Bmax value was 459.8 fmol/mg protein. The pKd (6.90) for [3H]cimetidine was similar to the pA2 for cimetidine. The Hill coefficients for these experiments were not significantly different from unity. The present findings indicate that the number of H1-receptors, in terms of the Bmax value for [3H]mepyramine, is smaller than that of H2-receptors, in terms of the Bmax value for [3H]cimetidine. However, the contractile response to histamine is predominantly mediated through stimulation of H1-receptors on vascular smooth muscle cells in pig basilar artery.

Animals↗
PubMed1993

Extravasation of contrast medium from the lenticulostriate artery following local intracarotid fibrinolysis.

Two patients with acute embolic occlusion of the intracranial internal carotid artery and the lenticulostriate arteries were treated by local intraarterial fibrinolysis using tissue plasminogen activator. Although fibrinolysis started within 2.5 hours from the ictus, extravasation of the contrast medium from the lenticulostriate arteries occurred in the region of the basal ganglia. Local intraarterial fibrinolysis for acute embolic occlusion of the internal carotid artery may be a high-risk therapeutic intervention even within the ultra-acute stage, especially when the lenticulostriate arteries are occluded by an embolus.

Aged↗