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Biomedical subjects

M Fujiwara

Publications and source records attributed to M Fujiwara.

At least 523 records · Page 29Linked to original sources
PubMed1988

GABAA-receptor-mediated inhibition of the delayed increase in intragastric pressure to stimulation of vagal afferent fibres in cats.

1. The possible involvement of gamma-aminobutyric acidA (GABAA)- and GABAB-receptors in the inhibitory effects of GABA on the delayed increase in intragastric pressure of the stomach to stimulation of vagal afferent fibres in cats was studied. 2. Cats were anaesthetized with pentobarbitone-gallamine and pretreated with hexamethonium. GABA inhibited the hexamethonium-resistant delayed contraction of the stomach in a dose-dependent manner. Such effects of GABA were antagonized by both bicuculline and picrotoxin. 3. Muscimol, a GABAA-receptor agonist, mimicked the inhibitory effects of GABA and the effects of muscimol were antagonized by bicuculline and picrotoxin. The ID50 of muscimol was 10 times less than that of GABA. 4. In contrast to muscimol, baclofen, a GABAB-receptor agonist did not mimic the inhibitory effects of GABA. 5. The present experiments demonstrate that GABAA-receptors are involved in the inhibitory action of GABA on the delayed contraction of the stomach to vagal afferent stimulation.

Animals↗
PubMed1988

Physiological effects of portal ligation on the longitudinal and circular muscles of the dog portal tree.

We studied physiological effects of portal vein ligation on the longitudinal and circular muscles of the dog portal tree. Portal venous blood pressure after portal ligation was higher in dogs that died than in those that survived. The portal veins isolated from dogs that died after portal ligation exhibited both lower rate of onset and decreased intensity of spontaneous activity, compared with those from dogs that survived. Responsiveness of longitudinal muscles of each of the four portal segments to noradrenaline, acetylcholine, histamine and KCl was markedly reduced in dogs that died, compared with those that survived, although the responsiveness of circular muscle was nearly equal in both groups of dogs. The longitudinal muscle of the truncal portal vein from dogs that died responded less strongly to electrical transmural stimulation than that from surviving dogs. The nonadrenergic, noncholinergic response was almost abolished in dogs that died rapidly. The degree of spontaneous activity or responsiveness to various stimulations in smooth muscles of the portal tree is considered to reflect muscular development. The degree of development of the longitudinal muscle of the portal tree may determine the survival of dogs after portal ligation.

Acetylcholine↗
PubMed1988

Presynaptic and postsynaptic alpha 2-adrenergic receptors in human cerebral arteries and their alteration after subarachnoid hemorrhage.

The nature of alpha-adrenergic receptors in human cerebral arteries was characterized, and alteration of these receptors after subarachnoid hemorrhage was examined using a radioligand binding assay. Norepinephrine content of control arteries was also analyzed and compared with that of arteries after subarachnoid hemorrhage. Norepinephrine content in human cerebral arteries in cases of subarachnoid hemorrhage was about 5% of the control group. Specific binding of [3H]yohimbine, a selective alpha 2-antagonist, to cerebral arteries of the control group indicated two classes of binding sites: high-affinity sites with KD of 0.5 nM and Bmax of 18 fmol/mg protein and low-affinity sites with KD of 29 nM and Bmax of 248 fmol/mg protein. In cerebral arteries obtained from the subarachnoid hemorrhage group, [3H]yohimbine binding sites were of a single class with KD of 53 nM and Bmax of 456 fmol/mg protein. These results suggest that sympathetic denervation and subsequent alterations in alpha 2-adrenergic receptors occurred after subarachnoid hemorrhage in human cerebral arteries. These changes in sympathetic innervation to cerebral arteries were considered to be one of the antecedents of delayed vasospasm after subarachnoid hemorrhage.

Adult↗
PubMed1988

Effect of alismol on adrenergic mechanism in isolated rabbit ear artery.

Effects of alismol, a sesquiterpenoid isolated from the rhyzome of Alisma orientale, on adrenergic mechanisms were examined in the isolated rabbit ear artery. Alismol (10(-6) to 10(-4) M) inhibited the contraction of isolated rabbit ear artery by electrical stimulation of the perivascular nerves. The inhibition was concentration-dependent; at a concentration of 10(-4) M, the inhibition was 90% (n = 8). Treatment with 10(-4) M alismol inhibited the increase in 3H-noradrenaline (3H-NAd) release induced by electrical stimulation by 63 +/- 6%. Alismol at 10(-4) M did not affect the neuronal uptake of 3H-NAd in the artery. Alismol at 10(-4) M slightly inhibited contractions induced by exogenously administered NAd. These results demonstrate that alismol inhibits the adrenergic neuro-effector mechanisms in rabbit ear artery, and they suggest that alismol acts primarily on nerve terminals and inhibits their responses to electrical stimulation by interfering with NAd release.

Animals↗
PubMed1988

Involvement of uptake2 mechanism in inactivation of noradrenaline released by tyramine under anoxic conditions in perfused rat heart.

Effects of uptake2 inhibition by corticosterone on tyramine-induced noradrenaline (NA) overflow under control, glucose-deprivation, anoxia and anoxia with glucose-deprivation were examined in perfused rat heart. Uptake2 inhibition by corticosterone (100 microM) had no effect on the NA overflow under control and glucose-deprivation, but significantly augmented the NA overflow by about 40% and 25% under anoxia and anoxia with glucose-deprivation, respectively. These results indicate that the uptake mechanism is at least in part responsible for the inactivation of NA under anoxic conditions in the perfused rat heart.

Animals↗
PubMed1988

Two types of gastric excitatory responses to stimulation of the vagal trunk in cats: efferent and afferent responses.

Experiments were performed on cats anesthetized with pentobarbital sodium and gallamine triethiodide. Gastric motility was recorded by a balloon method. The excitatory response to electrical stimulation of the vagal trunk was composed of an initial response during the stimulation period and a late response following stimulation. The maximal excitation of the initial response was elicited by a short pulse duration and that of the late response by a long pulse duration. The initial response was inhibited by treatment with hexamethonium or atropine. The late response was hexamethonium-resistant. This hexamethonium-resistant response was inhibited by atropine, hemicholinium and morphine, and enhanced by physostigmine. Treatment with (D-Pro2, D-Trp7,9)-substance P did not affect the hexamethonium-resistant response. Treatment with morphine inhibited the late response without affecting the initial response. From these results, it was suggested that the initial excitatory response was probably due to the activation of the parasympathetic cholinergic fibers. The late response might be due to the activation of the vagal afferent cholinergic fibers, since the pharmacological nature of the late response was similar to that in the cat with supranodose vagotomy (surviving afferent fibers) in our previous reports.

Afferent Pathways↗
PubMed1988

An endothelium-dependent contraction induced by A-23187, a Ca++ ionophore in canine basilar artery.

In most isolated canine basilar arteries tested, Ca++ ionophore A-23187 induced a small relaxation followed by a transient contraction. Both contraction and relaxation were abolished by removal of endothelium. The endothelium-dependent contraction induced by A-23187 was attenuated by a phospholipase A2 inhibitor (quinacrine), cyclooxygenase inhibitors (aspirin and indomethacin), a thromboxane A2 (TXA2) synthetase inhibitor (OKY-046) and a TXA2 antagonist (ONO-3708). The A-23187-induced contraction was abolished by lowering the Ca++ concentration of medium to 10%, whereas the contraction induced by 9,11-epithio-11,12-methano-TXA2 (STA2) was attenuated slightly by lowering [Ca++]. The A-23187-induced contraction was reduced markedly by nifedipine (10(-9) to 10(-7) M), but the STA2-induced contraction was only attenuated slightly by nifedipine. Bay K 8644 did not affect the A-23187- and STA2-induced contractions. The present experiments demonstrate that A-23187 induced an endothelium-dependent contraction in canine basilar artery, and suggest that Ca++ might play a key role in production of an endothelium-derived contracting factor (probably TXA2).

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

Hemorrhagic autoimmune encephalomyelitis induced by adoptive transfer of activated semiallogeneic spleen cells into irradiated rats.

Using lethal irradiation of recipients, adoptive transfer of experimental allergic encephalomyelitis (EAE) into Lewis (LEW) rats using (LEW x PVG/c)F1 (LPVGF1) spleen cells was successfully achieved. Recipient rats usually developed clinical signs of EAE 5 or 6 days after transfer. The EAE was characterized by the presence of a number of petechiae over the spinal cord. Immunohistochemical examination using OX27, a monoclonal antibody specific for RT1.Ac, revealed the localization of transferred F1 (RT1(1/c] cells in the LEW recipients (RT1(1]. Most of the inflammatory cells in the spinal cord lesions were stained positively for OX27, indicating that they were transferred cells. In mild EAE, more W3/25+ cells were found than OX8+ cells. OX8+ cells were predominant in severe EAE, however. Examination of the spleens of rats that developed EAE by OX27 staining revealed that transferred F1 cells gradually increased in number and reached a maximal level on days 5 and 6. In the spleens of rats that received irradiation and transfer but did not develop EAE, few transferred F1 cells were observed. In addition, bromodeoxyuridine (BrdU)-anti-BrdU immunohistochemistry was employed to demonstrate that cell proliferation really takes place in the spleen. It was revealed that the spleens of the recipients of lethal irradiation and F1 cells contained many BrdU+ cells. Because rats given lethal irradiation alone had extremely few BrdU-positive cells in their spleens, labeled cells in the recipients of radiation and transfer originated from transferred F1 cells. Collectively, these findings strongly suggest that transferred cells previously activated in vitro undergo further proliferation in the lymphoid organs of recipients to bring about the development of EAE.

Animals↗
PubMed1988

Cholinergic transmission in the superior cervical ganglion reinnervated by peripheral vagal stump cut below the nodose ganglion in cats.

In cats, the peripheral stump of the vagus nerve cut below the nodose ganglion was sutured with preganglionically denervated superior cervical ganglion (SCG). Cross-anastomosis were performed in a total of 23 cats, of which 21 survived. In 20 cats, after 9 to 13 weeks of surgery, functional reinnervation of SCG by the vagus was established by contraction of the nictitating membrane in response to stimulation of the vagal preganglionic trunk. This contraction was reduced by the treatment with hexamethonium and atropine. Stimulation of the vagal preganglionic trunk caused release of acetylcholine into perfusate through the anastomosed SCG perfused with Kreb's solution. It is concluded that the vagal afferent fibers do reinnervate the preganglionically denervated SCG and the pharmacological nature of this reinnervated SCG is, at least in part, cholinergic.

Acetylcholine↗
PubMed1988

Generation of self-macrophage-toxic non-T cells in the MHC-homozygous F1 spleen cells co-cultured with parental cells: possible involvements of host cells in impaired immunity in GVH disease.

Simplified-in vitro system was developed to examine the contribution of host's cells in graft-versus-host (GVH)-disease-associated immunodeficiencies. In analogy with major histocompatibility complex (MHC)-matched GVH-reaction, (BALB/c x DBA/2)F1 (H-2d) hybrid spleen cells were co-cultured with irradiated BALB/c (H-2d) spleen cells, so that cellular activities to be generated are ascribable to F1 cells. In vitro development of anti-allo-specific cytotoxic T cells of the F1 origin was dramatically suppressed by coexistence of the irradiated parental cells and by the addition of F1 cells precultured once with the parental cells, suggesting the generation of suppressor cells in the F1 (host) cells activated by the parental cells. Thus generated suppressor cells are Thy.1-, weakly or nonadherent and radiosensitive. Interestingly, in the same reactions there also developed Thy.1- cytotoxic cells for autologous macrophage targets. An involvement in immunodeficiencies in GVH disease of the host-derived cytotoxic and/or immunosuppressive, non-T cells was discussed.

Animals↗
PubMed1988

Adoptively transferred experimental allergic encephalomyelitis in chimeric rats: identification of transferred cells in the lesions of the central nervous system.

Experimental allergic encephalomyelitis (EAE) was induced by adoptive transfer of myelin basic protein (MBP)-activated LEW spleen cells into (LEW x PVG/c) F1----LEW chimeras. By double-immunofluorescent staining using OX27, which is specific for RT1c, and monoclonal antibodies (mAb) against various T-cell antigens (TAg), inflammatory cells in the lesions of the central nervous system (CNS) were categorized into MBP-activated and transferred LEW T cells (TAg+ OX27-), accompanying T cells (TAg+ OX27+) of chimera origin and non-T cells (TAg- OX27+). Examination of the lesions at various stages of EAE revealed that transferred OX19 (CD5)+ T cells accounted for 46% of the total number of inflammatory cells at the preclinical stage, became reduced to 23% at the clinical stage and recovered to a level between those of the preclinical and clinical stages at the recovery stage. In parenchymal infiltrates, 93% of the total T cells were transferred cells at the preclinical stage, whereas 66% were present in perivascular aggregates. At the clinical stage, the proportion of transferred T cells in the parenchyma was not different from that in the perivascular cuffs. At the recovery stage, the proportion of transferred T cells in the parenchyma was increased. Collectively, MBP-activated and transferred T cells first appeared in the CNS parenchyma followed by infiltration of T and non-T cells of recipient (chimera) origin. All these inflammatory cells formed the lesions of full-blown EAE. At the recovery stage, inflammatory cells decreased in number in all the compartments of the CNS. Transferred T cells formed the major proportion of parenchymal infiltrates at this stage. These findings strongly suggest that transferred T cells remain in the CNS parenchyma longer than cells of chimera origin and that antigen-activated T cells have well-expressed CNS-homing activity.

Animals↗
PubMed1988

Endothelium-dependent contraction and -independent relaxation induced by adenine nucleotides and nucleoside in the canine basilar artery.

ATP, ADP, AMP and adenosine at 10(-8) induced a slight relaxation, and at concentrations greater than 10(-7) M caused a biphasic response consisting of an initial relaxation followed, after a brief period, by a transient contraction in canine basilar artery. ATP (10(-6) and 10(-5) M) caused a triphasic response consisting of a rapid, small contraction, a relaxation and then a second, transient contraction. The order of agonist potency for contraction was ATP greater than ADP much greater than AMP = adenosine, but for producing relaxation the agonists were equipotent. Removal of the endothelium abolished the contraction after the relaxation, but had virtually no effect on the relaxation and the rapid contraction induced by ATP (10(-6) and 10(-5) M). Only the relaxation in response to ATP (10(-6) M) was attenuated by removal of the endothelium. Aspirin (a cyclooxygenase inhibitor) (5 X 10(-5) M), OKY-046 (a thromboxane A2 synthetase inhibitor) (10(-5) M) and ONO-3708 (a thromboxane A2 antagonist) (5 X 10(-9) M) attenuated markedly the endothelium-dependent contraction induced by ATP (10(-5) M) and ADP (10(-5) M), but did not affect the relaxation. Phentolamine (10(-6) M) and atropine (10(-6) M) did not affect either the contraction or the relaxation. The relaxations induced by both ATP and adenosine in both endothelium-intact preparations and endothelium-removed preparations were attenuated by 8-phenyltheophylline (P1 antagonist) (10(-6) M).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗
PubMed1988

Studies on the mechanisms of the development of lupus nephritis in BXSB mice. II. Comparative studies between male BXSB and MRL/lpr mice at the onset period.

In order to analyze relation of immunological abnormalities to the development of lupus glomerulonephritis (LGN) at an early stage, various immunological parameters were examined in BXSB and MRL/lpr mice at 8 and 13 weeks of age. The following results were obtained. (a) Male BXSB mice showed slight LGN already at 8 weeks of age and the disease became obvious at 13 weeks of age. On the other hand, glomerular change of MRL/lpr mice became apparent at 13 weeks. (b) Immunofluorescent studies to semiquantify degree of the deposition of immune complexes (IC) at glomeruli revealed that there were no difference in fluorescence intensities among BXSB mice at 8 and 13 weeks and 13-week-old MRL/lpr mice. (c) MRL/lpr mice had much higher level of serum IC than male BXSB mice at 13 weeks as assessed by fluid- and solid-phase C1q-binding assays. Both strains showed almost the same level of Raji cell-binding IC which might be related to glomerular depositing ones. (d) Spleen of 13-week-old MRL/lpr mice contained extraordinary number of IgG-producing cells in spleen as compared with 8-week-old mice or male BXSB mice at 8 or 13 weeks. There were no differences in IgM-producing cell numbers among the strains and ages of mice. These results indicate that MRL/lpr and male BXSB mice have different immunological backgrounds for the development of LGN. It was noticeable that male BXSB mice showed some degree of LGN already at 8 weeks of age, without apparent polyclonal B cell activation and enhanced serum level of IC, as compared with MRL/lpr mice of the same age.

Age Factors↗