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T Ohhashi

Publications and source records attributed to T Ohhashi.

At least 37 records · Page 2Linked to original sources
PubMed1997

[A new helical CT approach with ECG gated reconstruction].

We proposed a new helical CT approach with ECG-gated reconstruction for obtaining high quality 2D, 3D, and 4D images. Original helical images were acquired with a single helical scan with overlapping reconstruction and ECG information. Post-processing to improve temporal resolution and 4D volume set reconstruction were performed, and 2D, 3D and 4D displays were obtained. Using this new method, 2D and 3D images without cardiac motion artifacts were obtained by selecting images in diastolic phase. 2D images with cardiac motion were obtained using images of the same position and different cardiac phases. Finally, 4D images (3D images with phase information) were obtained.

Artifacts↗
PubMed1997

5-Hydroxytryptamine-induced endothelium-dependent and -independent relaxations in isolated dog anterior spinal small arteries.

The mode of action of 5-hydroxytryptamine (5HT) was investigated in isolated dog anterior spinal small arteries. Lower concentrations of 5HT (10(-9)-10(-7) M) caused a dose-dependent contraction and higher concentrations (10(-6)-10(-3) M) produced a dose-dependent relaxation of the arteries precontracted by 10(-7) M U 46619. The 5HT-induced relaxation was significantly antagonized by methiothepin (10(-9)-10(-6) M). Ketanserin (10(-6) M) and ICS 205-930 (3 x 10(-6) M) did not affect the 5HT-induced relaxation of the arteries. The relaxant response to 5HT was reduced significantly by mechanical rubbing of the endothelial cells. The 5HT-induced endothelium-independent relaxation was also antagonized significantly by methiothepin (10(-6) M). Aspirin (5 x 10(-5) M) or N omega-nitro-L-arginine methyl ester (L-NAME) (10(-6) M) significantly suppressed the 5HT-induced endothelium-dependent relaxation. L-Arginine (10(-3) M) also significantly reversed the L-NAME induced reduction of the 5HT-induced endothelium-dependent relaxation. Treatment with L-NAME in the presence of aspirin also produced much greater reduction of the 5HT-induced endothelium-dependent relaxation. Isocarbacyclin (10(-9)-10(-5) M) induced a concentration-dependent relaxation of the isolated spinal small arteries precontracted by 10(-7) M U 46619. These results suggest that 5HT induces endothelium-dependent and -independent relaxations of the isolated anterior spinal small arteries mainly via activation of 5HT1-like receptor and that endogenous nitric oxide and vasodilative prostaglandins may contribute to the 5HT-induced endothelium-dependent relaxation of the arteries.

Animals↗
PubMed1997

Macrophage-induced nitric oxide and prostanoid dependent relaxation of arterial smooth muscles.

We have studied mechanisms of vasodilation induced by supernatant fluid of rat macrophages (Mø), using an arterial bioassay preparation. The cells emigrated by an intraperitoneal injection of thioglycollate were isolated and cultured for 12 h in RPMI 1640 medium with and without 2.0 mM L-arginine. More than 98% of the isolated cells clearly demonstrated Wright's esterase staining and phagocytosis of acetylated low-density lipoprotein. The bioassay preparation was made of dog isolated femoral arteries with and without the endothelium. The supernatant of macrophages cultured in the L-arginine-free RPMI 1640 caused a significant reduction of the precontraction in the bioassay rings, being approximately 51.6-66.7% of sodium nitroprusside (SNP) induced maximum vasodilation in each ring. The supernatant of macrophages cultured in the RPMI 1640 containing 2.0 mM L-arginine produced a significantly smaller relaxation (approximately 32.3-33.3%). The Mø-induced vasodilation was significantly inhibited by the coculture of the macrophages with 1 microM dexamethasone, 10 microM cycloheximide, 50 microM N omega-nitro-L-arginine methyl ester (L-NAME), 10 microM indomethacin, or 10 microM aspirin. The L-NAME-induced inhibition was significantly reversed by an additional treatment with 100 microM L-arginine. The coculture with both L-NAME and indomethacin caused a reduction of the Mø-induced vasodilation (approximately 12.5-13.4%) similar to reductions produced by dexamethasone (approximately 10.8-12.1%) and cycloheximide (approximately 11.4-12.4%). Coculture with 10 micrograms/mL bacterial lipopolysaccharide caused a slight facilitation of the Mø-induced vasodilation (approximately 78.2-79.6%). These findings suggest that supernatant fluid of rat exuded macrophages cultured with low concentrations of L-arginine causes an endogenous nitric oxide (NO) and vasodilative prostaglandin dependent relaxation of arterial smooth muscles.

Animals↗
PubMed1996

Acetylcholine- and flow-induced production and release of nitric oxide in arterial and venous endothelial cells.

To study flow-mediated responses in a conduit vein, we investigated the physiological characteristics of endothelium-dependent acetylcholine (ACh)- and flow-induced relaxations using a conventional bioassay cascade. Cylindrical segments isolated from canine common carotid arteries and external jugular veins were perfused at a constant mean flow rate ranging from 1 to 8 ml/min. Endothelium-derived nitric oxide (NO) activity in perfusion effluent through the arterial and venous segments was measured by relaxation of endothelium-denuded arterial rings and arterial and/or venous rings precontracted by prostaglandin F2 alpha, respectively. Stimulation by a flow rate of 8 ml/min on the arterial and venous endothelial cells produced approximately 60 and 20% of the maximum relaxation in the arterial and venous rings, respectively. ACh (10(-6) and 10(-5) M) perfused through the arterial and venous segments with endothelium caused dose-related relaxations of both bioassay rings. The ACh- and flow-induced relaxations were completely reduced by mechanical removal of the endothelial cells. Pretreatment with 5 x 10(-5) M NG-nitro-L-arginine methyl ester (L-NAME) produced a significant reduction of the ACh- and flow-induced vasodilation. Additional treatment with 10(-4) M L-arginine significantly reversed the L-NAME-induced inhibition of ACh-induced relaxation but had no effect on flow-induced relaxation. When the flow rate was increased from 2 to 4 ml/min, the same concentrations of ACh produced larger dose-related relaxations than those obtained at a flow rate of 2 ml/min. Pretreatment with 25 U/ml superoxide dismutase caused no significant effect on the flow-mediated potentiation of ACh-induced relaxation. These findings suggest that venous endothelial cells of canine large vein are able to produce and release NO by stimulation of increased flow or ACh to a significantly lesser extent compared with the artery and that ACh-induced vasodilation is potentiated by an increase in shear stress up to approximately 4 dyn/cm2 loaded on the endothelial cells.

Acetylcholine↗
PubMed1995

5-Hydroxytryptamine-induced NO-dependent relaxation in isolated strips of monkey popliteal lymph nodes.

5-Hydroxytryptamine (5-HT, 0.01-100 microM) and 5-carboxamidotryptamine (5-CT, 0.001-10 microM) produced dose-related relaxations in strips cut from monkey popliteal lymph nodes precontracted with a perfusion of Krebs bicarbonate solution containing 80 mM KCl. These 5-HT agonists caused no significant effect on the basal tone of the lymph node strips. The 5-HT-induced relaxation is competitively antagonized by pretreatment with a selective 5-HT1-like receptor antagonist, methiothepin (0.01-0.1 microM). Schild plot analysis showed that the pA2 value and slope of methiothepin against 5-HT were 8.80 +/- 0.11 and 0.99 +/- 0.07 (n = 6), respectively. Pretreatment with methysergide (0.01-0.1 microM) significantly attenuated the 5-HT-induced relaxation of the strips. On the other hand, treatment with ketanserin (0.01-0.1 microM) and ICS-205-930 (0.01-0.1 microM) caused no significant effect on the 5-HT-or the 5-CT-induced relaxation. The 5-HT-induced relaxation was significantly reduced by 10 microM NG-monomethyl-L-arginine, which was reversed by 1 mM L-arginine. The relaxation in the lymph node strips was also significantly reduced by treatment with 10 microM methylene blue but not with 30 microM aspirin. These results suggest that 5-HT1-like receptors exist in the monkey popliteal lymph nodes. Stimulation of these receptors produces an endogenous nitric oxide (NO)-dependent relaxation in lymph node smooth muscle through an activation of cytosolic guanylate cyclase in the cells.

Animals↗
PubMed1995

Histopathological features of atrophic thyroiditis with blocking type-TSH binding inhibitor immunoglobulins.

To investigate the histopathological features of atrophic thyroiditis (AT) with blocking type-TSH binding inhibitor immunoglobulins (TBII), the present morphological observations were carried out employing additional immunohistochemical procedures. Moreover, these were compared with examples of goitrous Hashimoto's thyroiditis showing negative TBII (HT). There exist apparent differences between AT and HT. In particular, significant follicular atrophy with epithelial flattening including decreased positive staining of the follicular epithelial cells for thyroglobulin in AT was characteristically observed. These results suggest that the mechanism for the development of hypothyroidism in AT with blocking type-TBII might be due to suppression of thyroid cell function through the inhibition of endogenous TSH stimulation by the blocking antibody with subsequent epithelial degenerative destruction.

Adult↗
PubMed1995

Histamine H2 receptor-mediated endothelium-dependent relaxation in canine spinal artery.

The mechanisms of histamine-induced relaxation were investigated in isolated canine spinal branches of intercostal artery (SBICA). Histamine (10(-7) to 10(-4)M) and dimaprit (3 x 10(-6) to 3 x 10(-4)M) produced concentration-dependent relaxation in the SBICA which had been contracted by 5 x 10(-6)M norepinephrine, whereas 2-pyridylethylamine caused only a very small relaxation. The histamine- and dimaprit-induced relaxation were inhibited by famotidine but not by diphenhydramine. In the SBICA without endothelium, histamine elicited very little relaxation. Aspirin (5 x 10(-5)M) and AA 861 (10(-5)M) did not affect the histamine-induced relaxation. Treatment with L-NMMA (3 x 10(-5)M) or methylene blue (10(-5)M) significantly suppressed the acetylcholine-induced relaxation of the SBICA but not the histamine-induced one. These results suggest that histamine produces relaxation in the isolated canine SBICA through stimulation of H2-receptors on the endothelium. The relaxing mediator(s) released by histamine seems to be neither endogenous prostaglandins, lipoxygenase products, nor nitric oxide.

Animals↗
PubMed1994

Effects of isocarbacyclin, a stable prostacyclin analogue, on monkey isolated cerebral and peripheral arteries.

1. The effects of isocarbacyclin (TEI 7165), a stable prostacyclin analogue, were examined in monkey isolated cerebral and peripheral arteries. 2. Addition of TEI 7165 (0.1 nM-10 microM) produced a dose-dependent relaxation in cerebral arteries pre-contracted with 1 microM 5-hydroxytryptamine (5-HT). High concentrations (more than 1 microM) of TEI 7165 elicited a transient contraction followed by a sustained relaxation. 3. TEI 7165 also elicited a dose-dependent relaxation in the peripheral (except popliteal) arteries. The maximum relaxation induced by 10 microM TEI 7165 was greater (P < 0.05) in the mesenteric artery than in the cerebral artery. The negative logarithm of the EC50 value for the mesenteric, 7.6 +/- 0.3, was greater (P < 0.05) than that for the cerebral artery, 6.4 +/- 0.3. The decreasing order of potency for the TEI 7165-induced relaxation was as follows: mesenteric > renal > cerebral > coronary > popliteal. 4. Removal of the endothelium did not significantly affect TEI 7165-induced relaxations. 5. The transient contraction produced by high concentrations of TEI 7165 was not observed in cerebral arteries precontracted with 1 nM U46619, a stable analogue of thromboxane A2 (TXA2). Furthermore, the TEI 7165-induced contraction was markedly suppressed (P < 0.05) by treatment with 10 nM S1452, a TXA2 blocking agent. 6. These results suggest that TEI 7165 causes an endothelium-independent relaxation in monkey cerebral and peripheral arteries, and that there is a marked regional difference in the TEI 7165-induced relaxations. A high concentration of TEI 7165 also produces a transient contraction which is probably through activation of TXA2 (TP-) receptors.

Animals↗
PubMed1994

Purification and characterization of a membrane-bound ATPase from Acetabularia cliftonii that corresponds to a Cl(-)-translocating ATPase in Acetabularia acetabulum.

A Mg(2+)-ATPase was solubilized from membranes of Acetabularia cliftonii using nonanoyl-N-methylgluconamide and purified by ion-exchange and gel permeation chromatography. One active ATPase fraction after Mono Q chromatography had a specific activity of 10 units/mg of protein. Judged from subunit composition [54 (a), 50 (b) with a fainter band around 40 kDa], catalytic properties, and N-terminal amino acid sequence of the b subunit, the isolated enzyme was comparable to the Cl(-)-ATPase of Acetabularia acetabulum. Immunological characterization of both subunits showed significant similarity to the F type of ATPase. Cl(-)-transport activity was observed by reconstitution studies into liposomes.

Acetabularia↗
PubMed1994

Chloroplast ATPase in Acetabularia acetabulum: purification and characterization of chloroplast F1-ATPase.

ATPases were isolated from chloroplasts of the unicellular marine alga Acetabularia acetabulum. Two preparations of ATPase, a chloroplast-enriched fraction and an alpha beta gamma-complex were compared. The alpha beta gamma-complex was released into an EDTA solution and purified by anion-exchange chromatography, hydrophobic chromatography, and gel permeation chromatography. The subunit composition of this enzyme appeared to be 52-53 (alpha), 51 (beta), and 40 (gamma) kDa from SDS-PAGE. ATPase activity was enriched about 260-fold to a specific activity of approximate 4.1 U.mg protein-1. The catalytic properties of the alpha beta gamma-complex were as follows: pH optimum at 7.5; substrate specificity, ATP > ITP, GTP > UTP = CTP (Km for ATP 0.2 mM); divalent cation requirement, Mg2+ = Mn2+ = Co2+ > Zn2+ > Ni2+ > Ca2+; ATPase activity was inhibited by monovalent anions (NO3-, SCN-), while monovalent cations had neither inhibitory nor stimulatory effect. Orthovanadate had no inhibitory effect on the enzyme activity of alpha beta gamma-complex. Azide was the most effective inhibitor of the alpha beta gamma-complex. N-Terminal amino acid sequences of the alpha and beta subunits were not obtained and appeared to be blocked. The gamma subunit gave a sequence of AGLKEMKD-XIGSVXNTKKI, which showed 60% similarity to the gamma subunits of spinach and Chlamydomonas reinhardtii CF1-ATPase and EF1-ATPase.

Acetabularia↗
PubMed1994

5-Hydroxytryptamine-2 and -4 receptors located on bovine isolated mesenteric lymphatics.

Effects of 5-hydroxytryptamine (5-HT) agonists were investigated in the bovine isolated mesenteric lymphatics, and then the 5-HT receptor subtypes in the responses were pharmacologically classified by use of several 5-HT antagonists. Addition of 5-HT and that of alpha-methyl-5-hydroxytryptamine (alpha-methyl-5-HT) both produced concentration-dependent contractions in the presence of 3 x 10(-6) M [(1 alpha H, 5 alpha H)-8-methyl-8-azabicyclo(3.2.1)oct-3 alpha-yl]1H-indole-3-carboxylate hydrochloride, whereas 5-carboxamidotryptamine (5-CT) and 2-methyl-5-hydroxytryptamine (2-methyl-5-HT) caused no, or only slight, contraction in the lymphatics. Pretreatment with ketanserin caused a significant shift to the right in the concentration-response curve for 5-HT or alpha-methyl-5-hydroxytryptamine. Schild plot analyses showed that the pA2 values for ketanserin against 5-HT and alpha-methyl-5-hydroxytryptamine were 8.75 and 8.68, respectively. In contrast, 5-CT, 5-HT and metoclopramide caused concentration-dependent relaxations in the presence of 10(-6) M ketanserin in the lymph vessels after contraction with prostaglandin F2 alpha. 2-Methyl-5-HT up to 10(-4) M did not produce any relaxation. High concentrations of [(1 alpha H, 5 alpha H)-8-methyl-8-azabicyclo(3.2.1)oct-3 alpha-y1]1H-indole-3-carboxylate hydrochloride induced a significant inhibition of the 5-CT- and 5-HT-induced relaxation, but methiothepin and methysergide up to 10(-6) M and mechanical rubbing of the endothelium had no significant effect on the relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Effects of vasoactive substances on the pig isolated hepatic lymph vessels.

The present study examined the responses of isolated pig hepatic lymph vessels to vasoactive substances, the classification of alpha adrenoceptors and the mode of action of acetylcholine (ACh) with special reference to the lymphatic endothelial cells. Contractions of the hepatic lymph vessels were induced by norepinephrine (NE), epinephrine, prostaglandin F2 alpha, histamine and 5-hydroxytryptamine in a dose-dependent manner. NE was the most potent vasoconstrictor agent. 5-bromo-6[2-imidazolin-2-ylamino]-quinoxaline, xylazine and clonidine also produced dose-dependent contractions. NE-induced contractions were inhibited significantly by yohimbine (10(-8)-10(-6) M) but not by prazosin (10(-8)-10(-6) M). Pretreatment with yohimbine (10(-8)-10(-7) M) or rauwolscine (10(-8)-10(-7) M) caused a parallel shift to the right of the dose-response curve for 5-bromo-6[2-imidazolin-2-ylamino]-quinoxaline. These results suggest that the NE-induced contraction in pig hepatic lymph vessels seems to be mediated mainly through stimulation of alpha-2 adrenoceptors. ACh, isoproterenol, histamine, 5-hydroxytryptamine, ATP and adenosine caused dose-dependent relaxations in the hepatic lymph vessels precontracted by 5 x 10(-6) M prostaglandin F2 alpha. ACh was the most potent vasorelaxant agent. Pretreatment with atropine (10(-9)-10(-7) M) inhibited the ACh-induced relaxation in a competitive manner. Removal of endothelium caused a significant reduction of the ACh-induced relaxation. The ACh-induced relaxation was suppressed by pretreatment with N omega-nitro-L-arginine methyl ester (3 x 10(-5) M) and methylene blue (10(-5) M) but was unaffected by aspirin (10(-5) M).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1993

Acetylcholine-induced endothelium-independent relaxations in monkey isolated superior and inferior caval veins.

1. We examined the effects of acetylcholine (ACh), isoprenaline (Isop) and Ca-ionophore, A23187 on monkey isolated superior (SCV) and inferior caval veins (ICV) with and without intact endothelium, which had been partially contracted by 2 x 10(-6)-5 x 10(-6) M prostaglandin F2 alpha (PGF2 alpha). 2. Low concentrations of ACh (10(-10)-10(-9) M) produced a dose-dependent relaxation in the precontracted venous segments with endothelium. ACh at concentrations more than 10(-7) M elicited a transient contraction followed by a relaxation in these segments. 3. An addition of 5 x 10(-7) M A 23187 induced about 60% of maximum relaxation produced by 10(-5) M sodium nitroprusside (SNP) in each venous segment with endothelium. 4. Isop (10(-10)-10(-5) M) caused a dose-related relaxation in the precontracted caval veins with intact endothelium. 5. Removal of endothelium caused no significant effect on the ACh-induced dual responses but a significant inhibition of the A23187-induced relaxation. 6. Pretreatment with atropine antagonized competitively the ACh-induced relaxations in the endothelium-intact and endothelium-denuded caval veins. The Schild plot analysis showed that the pA2 values of the segments with and without endothelium were 9.72 +/- 0.14 (n = 5) and 10.01 +/- 0.23 (n = 6) in the ICV; and 9.95 +/- 0.20 (n = 5) and 9.70 +/- 0.10 (n = 5) in the SCV, respectively. 7. Pretreatment with 5 x 10-5M aspirin, 3 x 10-5M N0-nitro-L-arginine methylester, 1 mM tetraethylammonium,or 3 x 10-6 M glibenclamide caused no significant effect on the basal tone, ACh induced transient contraction, and ACh;.induced relaxation in the precontracted venous segments with and without endothelium.8. Pretreatment with 10-5 M methylene blue produced a significant reduction of the ACh- and SNP induced relaxations in the precontracted venous segments with and without endothelium. The pretreatment with the same concentration of methylene blue, however, caused no significant effect on the Isop-induced relaxation in venous segments with endothelium.9. The results suggest that ACh acts directly on the venous smooth muscle cells via a high-affinity muscarinic receptor subtype to accumulate cellular cyclic GMP producing endothelium-independent relaxation in the monkey caval veins.

Acetylcholine↗
PubMed1993

Effects of acetylcholine on spontaneous contractions in isolated bovine mesenteric lymphatics.

The effects of acetylcholine (ACh) on spontaneous contractions in isolated bovine mesenteric lymph vessels were investigated. ACh ranging from 3 x 10(-8) M to 10(-5) M produced dose-dependent negative chronotropic and inotropic effects on the spontaneous contractions. In the lymph vessels without endothelium, ACh at the same concentration range had no significant effect on the spontaneous contractions. Atropine (10(-9) and 10(-8) M) caused a parallel shift to the right of the dose-chronotropic response curve for ACh. The pA2 value of atropine to ACh in the negative chronotropic effect was 8.90 +/- 0.20 (n = 6). Aspirin (10(-5) M) produced no significant inhibition of the ACh-induced negative chronotropic and inotropic effects. NG-monomethyl-L-arginine (L-NMMA; 3 x 10(-5) M) significantly suppressed the ACh-induced negative responses on spontaneous contractions. In the same lymphatic segments, L-arginine (10(-4) M) reversed completely the inhibition by L-NMMA of the ACh-induced responses. These results suggest that low concentrations of ACh produce negative chronotropic and inotropic effects on spontaneous contractions in bovine mesenteric lymphatics and that the responses may be mediated by nitric oxide or its related compound released from the endothelial cells through activation of low-affinity muscarinic receptors.

Acetylcholine↗
PubMed1993

Effects of collagenase, elastase, and hyaluronidase on mechanical properties of isolated dog jugular veins.

To study the contribution of tissue components to the mechanical properties of veins, pressure-volume relationships were obtained with the cylindrical segments of isolated dog external jugular veins at several levels of longitudinal extension. At each length, the transmural pressure of the segment was raised up to 20 cmH2O and then reduced to 0 cmH2O by increasing and decreasing the intraluminal volume at a constant rate. The longitudinal extension of the venous segments caused a significant reduction in the incremental volume elasticity within the pressure range of 0-2 cmH2O (E0-2) as well as a significant increase of the incremental volume elasticity within 10-20 cmH2O (E10-20). The pressure-volume relationships of venous segments were also constructed in the same way after treatment with 1 mg/ml collagenase for 30 min, 0.1 mg/ml elastase for 5 min, or 1 mg/ml hyaluronidase for 60 min. Treatment with collagenase or elastase produced a significant increase of the E0-2. The treatment, however, caused no effect on E10-20. Treatment with hyaluronidase induced no effect on these mechanical parameters but produced a significant attenuation of the extension-induced decrease in E0-2. Activation of the venous smooth muscles induced by norepinephrine (10(-4) M) or high-potassium Krebs solution caused a significant decrease of E0-2 as well as a significant increase of E10-20. A complete relaxation of the smooth muscles elicited by Ca(2+)-free Krebs solution containing ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (2 mM) caused an increase of E0-2. Mechanical rubbing of the endothelium caused no significant effect on E0-2 and E10-20.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗