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Biomedical subjects

M Fujiwara

Publications and source records attributed to M Fujiwara.

At least 559 records · Page 31Linked to original sources
PubMed1987

Absence of donor-type major histocompatibility complex class I antigen-bearing microglia in the rat central nervous system of radiation bone marrow chimeras.

Localization of bone marrow-originated cells in the central nervous system (CNS) of the rat was investigated by using bone marrow chimeras. In order to do this, Lewis rats which carry major histocompatibility complex (MHC) class I antigens haplotype 1 (RT1.Al) were reconstituted with (Lew X PVG)F1 (RT1.Al/c) bone marrow cells after lethal irradiation. Transferred bone marrow cells were detected by immunohistochemical staining using a monoclonal antibody, OX27, specific for haplotype c of rat MHC class I antigens (RT1.Ac). The spleen and thymus of chimeric rats were fully reconstituted with transferred F1 cells 4 weeks after bone marrow transplantation. At this stage, mononuclear cells in the subarachnoid space of the CNS expressed OX27 antigen indicating that they were of bone marrow origin. A few OX27-positive blood cells were scattered in the CNS parenchyma 4-12 weeks after reconstitution. Ramified microglia, however, remained OX27-negative. Bone marrow-derived microglia were not observed throughout the period of examination until 24 weeks. In addition, experimental allergic encephalomyelitis (EAE) was induced in chimeric rats in order to augment the expression of MHC class I antigens on microglia. Even under this condition, no OX27-positive microglia were observed. Taken together, ramified microglia might be of neuroectodermal origin and there is little possibility that the microglia are derived from the bone marrow. However, if the ramified microglia are derived from blood cells, the microglia may be expected to have characteristic cell kinetics from the following points: (1) the precursor cells of the microglia may enter the CNS only at the perinatal stage; and (2) even under the condition in which lymphocytes and macrophages enter the CNS as observed in EAE, the precursor cells of the microglia are not supplied from the blood.

Animals↗
PubMed1987

Simultaneous pleomorphic adenomas of the right parotid and ipsilateral submandibular glands.

A case of simultaneous pleomorphic adenomas of the right parotid and ipsilateral submandibular glands was reported. The patient was a 68-year-old woman who had a ten-year history of an otherwise asymptomatic non-enlarging mass in the parotid gland and a slowly enlarging mass in the submandibular gland. Microscopically, the parotid tumor consisted of predominant spindle-shaped cell proliferations with myxoid stroma in places. The submandibular gland tumor showed tubular and trabecular formations with stroma consisting of hyalinized fibrous connective tissues. Simultaneous pleomorphic adenomas in the salivary glands are so rare that only 23 cases can be found in the literature. Additionally, only five tumors occurring simultaneously in the parotid and submandibular glands are reported in the literature. Our case seems to be the sixth of simultaneous pleomorphic adenomas of the parotid and submandibular glands.

Adenoma↗
PubMed1987

A single fatal penetrating chest wound caused by a dagger-shaped fragment of broken door glass.

A 19-year-old woman ran against a glass door, and, breaking it, was struck in the left anterior chest by a single dagger-like fragment of broken door glass. This fragment deeply penetrated her chest and wounded the anterior wall of the left ventricle of her heart. She rapidly died from loss of blood. The majority of single fatal penetrating chest wounds seen at postmortem examinations are caused by firearms and bladed weapons. While penetrating chest wounds occasionally result from fragments of glass, most severe and fatal wounds from glass result from one's falling into or through plate glass and sustaining wounds of the head, face, abdomen, or extremities. A single fatal wound from a dagger-shaped piece of glass is distinctly uncommon. To prevent such an accident from occurring, safety glass must be used in front doors of public institutions.

Adult↗
PubMed1987

Possible role of endothelial thromboxane A2 in the resting tone and contractile responses to acetylcholine and arachidonic acid in canine cerebral arteries.

The amount of immunoreactive thromboxane B2 (iTXB2) released from isolated canine arteries was determined by radioimmunoassay. The amount of iTXB2 released from the cerebral, coronary, mesenteric, and saphenous arteries was 47.0 +/- 7.2, 4.0 +/- 0.6, 4.9 +/- 0.5, and 2.7 +/- 0.4 pg/mg wet weight tissue/30 min, respectively. The release of iTXB2 from the cerebral artery was decreased to less than 50% by the administration of indomethacin (10(-5) M) or OKY-046 (10(-4) M), and by intimal rubbing. The release of iTXB2 was enhanced nearly twofold by the addition of arachidonic acid (AA) (10(-5) M) to the medium, but not by the addition of acetylcholine (ACh) (10(-6) M). The cerebral arterial strips maintained the resting tone, which was reduced maximally by papaverine (10(-4) M). The resting tone was also reduced dose dependently by a cyclooxygenase inhibitor (indomethacin), a thromboxane A2 (TXA2) synthetase inhibitor (OKY-046), and a TXA2 antagonist (ONO-3708). The resting tone of rubbed strips was about half that of intact strips. ACh and AA induced similar transient contractions in the cerebral artery. Contractions produced by these agents were attenuated by indomethacin (10(-7) M), aspirin (5 X 10(-5) M), OKY-046 (10(-6) M), and ONO-3708 (10(-8) M), and abolished by intimal rubbing. From these results, it is concluded that TXA2 is produced in the endothelial cells and may be involved in maintaining the resting tone and contractile response to AA in the canine cerebral artery.

Acetylcholine↗
PubMed1987

Changes in beta-adrenergic receptor subtypes in Alzheimer-type dementia.

Using ligand binding techniques, we studied beta-adrenergic receptor subtypes in brains obtained at autopsy from seven histologically normal controls and seven histopathologically verified cases with Alzheimer-type dementia (ATD). Inhibition of [3H]dihydroalprenolol [( 3H]DHA) binding by the selective beta 1 antagonist, metoprolol, results in nonlinear Hofstee plots, suggesting the presence of the two receptor subtypes in the human brain. The calculated ratios of beta 1/beta 2-adrenergic receptors in control brains are as follows: frontal cortex, 49:51; temporal cortex, 31:69; hippocampus, 66:34; thalamus, 23:77; putamen, 70:30; caudate, 48:52; nucleus basalis of Meynert (NbM), 43:57; cerebellar hemisphere, 25:75. Compared with the controls, total concentrations of beta-adrenergic receptors were significantly reduced only in the thalamus of the ATD brains. beta 1-Adrenergic receptor concentrations were significantly reduced in the hippocampus and increased in the NbM and cerebellar hemisphere, whereas beta 2-adrenergic receptor concentrations were significantly reduced in the thalamus, NbM, and cerebellar hemisphere and increased in the hippocampus and putamen of the ATD brains. These results suggest that beta 1- and beta 2-adrenergic receptors are present in the human brain and that there are significant changes in both receptor subtypes in selected brain regions in patients with ATD.

Aged↗
PubMed1987

Determination of serotonin turnover in the rat brain using 6-fluorotryptophan.

After intraperitoneal injection of rats with 6-fluorotryptophan (6-FT), brain 5-hydroxytryptamine (5-HT) levels decreased exponentially over 1 h. Depletion was dose-dependent and maximum depletion was observed at 200 mg/kg. 6-FT (200 mg/kg) did not significantly alter the content of 5-hydroxyindoleacetic acid. Turnover rates of 5-HT obtained by the 6-FT and other methods were fairly consistent. 6-FT had little effect on the content of noradrenaline and dopamine. These data suggest that 6-FT completely inhibits tryptophan hydroxylase, in vivo, without affecting the release of 5-HT from 5-HT neurons and with little effect on the activities of tyrosine hydroxylase. Therefore, 6-FT is a good pharmacological tool for studying the turnover rate of 5-HT in the brain.

Animals↗
PubMed1987

Regional differences of reactivity to stimulants in the dog portal tree.

We studied the regional differences both of reactivity to various stimulants and of neurogenic responses elicited by transmural stimulation in the longitudinal and circular muscles of the truncal portal vein, mesenteric vein, splenic vein and gastric vein of the dog portal tree. Strong spontaneous activity appeared in the longitudinal muscle of the truncal portal vein (96% of preparations tested). Weak spontaneous activity sometimes appeared in the circular muscle of the truncal portal vein (41%) and rarely in the longitudinal muscle of the mesenteric vein (12%). It did not appear in other segments. The splenic vein and the gastric vein showed similar patterns in the relationship between resting tension and response to noradrenaline; that is, the responsiveness of either longitudinal or circular muscle of these two veins increased and then decreased almost parallel as resting tension increased and reached a maximum under the same resting tension. The longitudinal muscle of both the truncal portal vein and the mesenteric vein was more responsive to noradrenaline, acetylcholine, histamine and KCl than the circular muscle; for example 2.02 and 1.44 times more responsive to noradrenaline, respectively. On the other hand, the longitudinal muscle of the splenic vein and the gastric vein responded less well than the circular muscle; for example 0.36 and 0.16 times as responsive to noradrenaline, respectively. Acetylcholine and histamine caused marked contractions which were comparable to those elicited by noradrenaline in the longitudinal muscle of the truncal portal vein. Acetylcholine also elicited similar contractions in the longitudinal muscle of the mesenteric vein but the responses induced in preparations of other segments were small. 6 The longitudinal muscle of the truncal portal vein responded well even to low-frequency stimulation of 2 Hz, while the circular muscles of the truncal portal and splenic veins gave marked responses only to high-frequency stimulation of 10 or 20 Hz or more. These contractile responses were attenuated by phentolamine (10-6 M) or atropine (10-6 M). The longitudinal muscle of the splenic vein showed no significant response to stimuli of any frequency. 7 It seems that the portal tree receives not only adrenergic but also cholinergic innervation. In addition, the longitudinal muscle of the truncal portal vein may receive non-adrenergic, noncholinergic innervation as well. 8 The longitudinal muscle of the portal vein may be crucial to venous return in assisting movement of the blood it contains. If this is the case in man, then the regional differences in the portal tree demonstrated in this study may explain why varicose changes during portal hypertension occur preferentially in the oesophagogastric region and rarely in other regions, as blood stasis may occur more readily in the regions of the gastric and splenic veins where the longitudinal muscle is not very active.

Acetylcholine↗
PubMed1987

A possible role of thromboxane A2 in endothelium in maintaining resting tone and producing contractile response to acetylcholine and arachidonic acid in canine cerebral arteries.

Endothelial thromboxane A2 (TXA2) in maintaining the resting tone and producing the contractile response to acetylcholine (ACh) and arachidonic acid was studied in canine cerebral artery. The spontaneous release of TXB2 from cerebral artery was about tenfold higher than that of coronary, mesenteric and saphenous arteries. The resting tone, the release of TXB2 and the contraction produced by arachidonic acid were decreased by the presence of cyclooxygenase inhibitor, TXA2 synthetase inhibitor, TXA2 antagonist and rubbing of the luminal side of preparations. The contraction produced by ACh was inhibited by the presence of the above inhibitors and rubbing of the preparations without decreasing the release of TXB2. These results suggest that the resting tone of canine cerebral artery and the contractile response to arachidonic acid are related to activation of TXA2 synthesis in the endothelium.

Acetylcholine↗
PubMed1987

Lack of effects of carbachol on the Na-Ca exchange mechanism in frog atrial muscle treated with goniopora toxin.

Carbachol (CCh) at a concentration of 10(-7) M completely inhibited the twitch contraction of frog atrial muscle. However, when the preparation was treated with goniopora toxin (GPT), a selective inhibitor of Na channel inactivation, and the twitch contraction was augmented through the activation of Na-Ca exchange by this toxin, the reduction in contractile amplitude by CCh was only about 30% even at higher concentrations. The maximum rate of rise of the twitch contraction was not affected by CCh in GPT-treated preparations. The time course of configuration change of the twitch contraction after application of CCh in GPT-treated muscle indicated that the attenuation of amplitude preceded the shortening of duration. The residual contraction under the combined treatments with GPT and CCh was abolished by removal of external Ca++ or addition of TTX. CCh only moderately shortened the action potential which was prolonged by GPT, and further addition of TTX abolished the action potential. From these results, we suggest that CCh does not influence the twitch contraction which is augmented via the activation of the Na-Ca exchange mechanism in frog atrial muscle.

Action Potentials↗
PubMed1987

Endothelium-dependent vasocontraction in response to noradrenaline in the canine cerebral artery.

In the canine basilar artery, noradrenaline-induced contraction was markedly decreased by intimal rubbing. Scanning electron microscopic studies showed that the rubbing procedure had scrapped away the endothelial cells from the intimal surface of the artery. Prazosin (10(-7) M) reduced the noradrenaline-induced contraction in intact arteries, but did not significantly affect the contraction in the scrapped arteries. Yohimbine (10(-7) M) strongly inhibited the contraction in both intact and scrapped arteries. The endothelium-dependent vasocontraction produced by noradrenaline was inhibited by aspirin (5 X 10(-5) M), OKY-046 (10(-5) M) and ONO-3708 (5 X 10(-9) M). The present experiments provided evidence for endothelium-dependence of the vasocontraction produced by noradrenaline in canine basilar arteries, and they suggested that the endothelium-derived contracting factors might be arachidonic acid metabolites such as TXA2; they also suggested that alpha 1 adrenoceptors might be preferentially distributed on the endothelium, while alpha 2 adrenoceptors are preferentially located in smooth muscle.

Animals↗
PubMed1987

Nitroglycerin-sensitive and -resistant contractions mediated by receptor-operated calcium channels in rabbit ear artery.

In isolated rabbit ear arteries incubated in a Ca2+-free medium with EGTA and nifedipine in the presence of norepinephrine, serotonin or histamine, an addition of Ca2+ induced a tonic contraction which is due to Ca2+ entry through receptor-operated Ca2+ channels (ROCs). Nitroglycerin (10(-4) M) significantly inhibited the ROCs-dependent contractions produced by serotonin or histamine, but failed to inhibit the ROCs-dependent contraction by norepinephrine. These results suggest the possible existence of two types of receptor-operated Ca2+ channels in rabbit ear artery.

Animals↗
PubMed1987

Comparison of the responses to the sensory neuropeptides, substance P, neurokinin A, neurokinin B and calcitonin gene-related peptide and to trigeminal nerve stimulation in the iris sphincter muscle of the rabbit.

Three mammalian tachykinins (substance P, neurokinin A and B) and two non-mammalian ones (eledoisin and physalaemin) produced potent contractions of the isolated rabbit iris sphincter muscle. The rank order of potencies was eledoisin greater than neurokinin B = physalaemin greater than substance P greater than neurokinin A. The maximum efficacy was much the same. The contractile responses to neurokinin A and eledoisin developed more rapidly than did those to the other tachykinins used and were selectively attenuated by [D-Arg1, D-Pro2, D-Trp7,9, Leu11]-SP. Electrical transmural stimulation produced a contraction consisting of cholinergic and tachykininergic components. The tachykininergic component was abolished by pretreatment with capsaicin or by trigeminal denervation (Fujiwara et al., 1984). [D-Arg1, D-Pro2, D-Trp7,9, Leu11]-SP attenuated the tachykininergic component, but not the cholinergic one. KCl and capsaicin also produced a tachykininergic contraction which was inhibited by [D-Arg1, D-Pro2, D-Trp7,9, Leu11]-SP. Calcitonin gene-related peptide affected neither the iris sphincter muscle nor the response to electrical transmural stimulation. These results suggest that the tachykininergic responses induced by electrical transmural stimulation, KCl and capsaicin are predominantly mediated by neurokinin A, probably released from the peripheral endings of trigeminal nerves.

Animals↗
PubMed1987

Inhibitory effect of somatostatin on gastric acid secretion in rats.

Effects of somatostatin on parasympathetically induced increases in gastric acid secretion and mucosal blood flow (MBF) were studied in anesthetized rats with a gastric fistula. Intravenous infusion of small doses of somatostatin (0.1-0.5 microgram/kg/min) dose-dependently inhibited the increases in the vagally stimulated gastric acid secretion. Larger doses of somatostatin (0.5-2.5 micrograms/kg/min) also dose-dependently inhibited the bethanechol-induced gastric acid secretion. The dose of somatostatin required to inhibit the gastric acid secretion by about 50% of the preinfused control values was 0.25 microgram/kg/min for vagally stimulated acid secretion and 2.5 micrograms/kg/min for bethanechol-induced acid secretion. Thus, the inhibitory potency of somatostatin on the vagally stimulated gastric acid secretion was about 10-fold higher than that on bethanechol-induced acid secretion. Somatostatin had no effect on the increase in gastric MBF during vagus nerve stimulation or bethanechol infusion. Pretreatment with indomethacin or phentolamine had no effect on the inhibitory effect of somatostatin on the increase in gastric acid secretion during vagus nerve stimulation or bethanechol infusion. These results suggest that somatostatin exerts an inhibitory effect on gastric acid secretion by acting on the parasympathetic neurons in the gastric wall more than on the structures peripheral to the parasympathetic nerve terminals, and it reduces parasympathetically stimulated gastric acid secretion in rats. This inhibitory effect of somatostatin on the gastric acid secretion is independent of the changes in the gastric MBF and probably not related to prostaglandin-involved or alpha adrenoceptor-mediated mechanisms.

Animals↗
PubMed1987

Gastric excitation by stimulation of the vagal trunk after chronic supranodose vagotomy in cats.

Experiments were performed on cats anesthetized with thiopental sodium and gallamine triethiodide and ventilated artificially. Gastric motility was recorded by a balloon method. Electrical stimulation of the vagal trunk in cats with chronic supranodose vagotomy for 11 to 32 days caused an excitatory response of the stomach. The pulse duration of electrical stimulation to obtain a maximal excitatory response of the stomach was 3 msec. Administration of hexamethonium (10 mg/kg i.v.) did not inhibit but enhanced the excitatory response of stomach. Atropine (3, 10 and 30 micrograms/kg i.v.), hemicholinium (10 mg/kg i.v.) and morphine (5 mg/kg i.v.) inhibited this hexamethonium-resistant excitatory response of the stomach, whereas treatment with physostigmine (300 mu/kg i.v.) augmented it. A substance P antagonist, (D-Pro2, D-Trp7.9)-substance P (250 and 500 micrograms/kg i.v.), did not affect the hexamethonium-resistant excitatory response. Acetylcholine content of the nodose ganglion 6 to 8 days after supranodose vagotomy was assayed using the radioenzymatic method, and the level was about 48% that of the intact ganglion. These results suggest that the gastric excitatory response to stimulation of the supranodose denervated vagal trunk is produced by activation of vagal afferent fibers probably originating from the nodose ganglion; the fibers involved are cholinergic.

Acetylcholine↗
PubMed1987

Mechanism of sodium channel block in crayfish giant axons by 711389-S, a new antiarrhythmic drug.

The effects of 711389-S, a new antiarrhythmic drug, on the sodium channel of crayfish giant axon were studied using micro-electrode and sucrose-gap voltage-clamp techniques. When applied externally, 711389-S suppressed the action potential and the rate of rise without affecting the resting membrane potential. Voltage-clamp experiments revealed that 711389-S inhibits the sodium current more selectively than the potassium current and that the inhibition is more evident with internal rather than external application. The inhibitory effect of internally applied 711389-S on sodium current was enhanced at less negative holding potentials. 711389-S also shifted the steady-state inactivation curve in the direction of hyperpolarization. Use-dependent block became evident in the 711389-S-treated axons; this block resulted from an increase in the slow inactivating state during repetitive depolarization and from a slow recovery from the inactivated state during the pulse interval. 711389-S produced an additional inhibition when sodium channels were open at large depolarizations. This additional inhibition could be reversed by small depolarizations that opened the sodium channels. These observations suggest that 711389-S binds the resting, inactivated and open states of the sodium channel, resulting in a reduction of sodium channel availability. 711389-S also shifted the voltage dependence of peak sodium conductance toward a less negative potential.

Action Potentials↗
PubMed1987

Catecholamine receptors involved in the inhibitory effects of dopamine on vagally stimulated gastric acid secretion and mucosal blood flow in rats.

The mechanisms of inhibitory effects of dopamine on the vagally stimulated gastric acid secretion and mucosal blood flow (MBF) were studied in anesthetized rats with a gastric fistula. Intravenous infusion of dopamine significantly reduced both gastric acid secretion and MBF. The inhibitory effect of dopamine on the vagally stimulated gastric acid secretion was not attenuated by sulpiride, metoclopramide or domperidone. Haloperidol abolished the inhibitory effect of dopamine on the acid secretion; it also abolished the inhibitory effect of norepinephrine on the vagally stimulated acid secretion. The inhibitory effect of dopamine on the acid secretion was abolished by phentolamine and yohimbine but not by propranolol or prazosin. Dopamine-induced reduction in the vagally stimulated gastric MBF was abolished by haloperidol and was partially antagonized by sulpiride or metoclopramide. In addition, the dopamine-induced reduction in the MBF was abolished by phentolamine and prazosin and was partially antagonized by yohimbine. These results indicate that the inhibitory effect of dopamine on the vagally stimulated gastric acid secretion is mediated by alpha-2 adrenoceptor mechanisms and that the inhibitory effect of dopamine on the MBF is, at least in part, mediated by alpha-1 adrenoceptor mechanisms. The authors did not obtain evidence for the existence of dopamine receptor-mediated mechanisms.

Animals↗