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J Tamaoki

Publications and source records attributed to J Tamaoki.

At least 181 records · Page 10Linked to original sources
PubMed1990

[Case report and literature analysis of the clinical factors relating to the development of fibrotic changes in gold lung].

A 26-year-old female with gold lung induced by Shiosol (gold thiomalate) administered for her rheumatoid arthritis is presented. Chest X-ray films after treatment with prednisolone hardly improved and showed diffuse fibrotic shadow. We reviewed previously reported cases of gold lung and tried to determine the clinical factors which might affect the development of pulmonary fibrotic changes in gold lung. The cases reported in Japan were classified into two groups according to the improvement of X-ray films after steroid therapy: group A in which the chest X-ray film returned to almost normal, group B these with diffuse fibrotic shadow. No significant difference was observed in the values of %VC and PaO2 admission between the two groups. The total dose of gold received was greater (p less than 0.05) and the duration of gold received was longer (p less than 0.01) in group B than in group A. These findings suggest that the development of pulmonary fibrosis does not depend on the severity of the injury indicated by pulmonary function, but in part on the amount of gold which has been stored in pulmonary macrophages. No statistical difference was shown in the initial dose of steroids between these groups. The duration between the onset of gold lung and the start of steroid therapy were longer in group B than than group A (p less than 0.05). Thus, early diagnosis and treatment with steroids are highly recommended in the clinical management of patients with gold lung.

Adult↗
PubMed1990

[Possible contribution of lung macrophage to airway hyperreactivity].

To elucidate the possible contribution of lung macrophage to airway hyperreactivity, we studied the effect of canine pulmonary alveolar macrophages (PAM) stimulated with anti-dinitrophenyl (DNP) IgE antibody and DNP-human serum albumin on airway smooth muscle and epithelial functions in vitro. IgE-stimulated PAM increased the contractile responses of bronchial segments to electrical field stimulation and the short-circuit current of cultured tracheal epithelium, the former effect being abolished in the presence of the thromboxane A2 receptor antagonist and the latter inhibited by the leukotriene antagonist and the Cl transport blocker. These results suggest that PAM may increase the parasympathetic contraction and Cl secretion in the airway through IgE-dependent release of thromboxane A2 and leukotriene, respectively.

Animals↗
PubMed1989

Inhibition of ciliary activity by phorbol esters in rabbit tracheal epithelial cells.

To study the effect of protein kinase C activation on respiratory ciliary activity, we measured ciliary beat frequency (CBF) by a photoelectric technique in response to phorbol esters and cell-permeable diglyceride in cultured tracheal epithelial cells from rabbits. Phorbol 12-myristate 13-acetate (PMA) resulted in a concentration- and time-dependent inhibition of CBF (half maximum inhibitory concentration (IC50) = 3 x 10(-10) M) with the maximal decrease being 21.0 +/- 1.4% (mean +/- SE, p less than 0.001) observed at 10(-6) M. L-alpha-dioctanoylglycerol (DiC8), another known activator of protein kinase C, likewise reduced CBF in a dose-dependent fashion. In contrast, phorbol 12,13-didecanoate, a non-tumor-promoting phorbol ester that does not stimulate protein kinase C, produced no significant changes in CBF. The decrease in CBF induced by PMA was not affected by blockade of arachidonic acid metabolism with indomethacin and nordihydroguaiaretic acid, but was antagonized by pretreatment with H-7, a specific inhibitor of protein kinase C (p less than 0.01). Maximal ciliary inhibition with either PMA or DiC8 was not accompanied by a decrease in intracellular concentration of cyclic AMP. These results indicate that activation of protein kinase C has a significant depressive effect on ciliary activity, and hence the airway mucociliary transport function, presumably through a regulatory pathway that is not dependent on cyclic AMP or arachidonic acid metabolites.

Animals↗
PubMed1989

Corticotropin-releasing factor and adrenocorticotropin stimulate ciliary motility in rabbit tracheal epithelium.

To assess the effects of corticotropin-releasing factor (CRF) and adrenocorticotropin (ACTH) on airway ciliary activity, we measured ciliary beat frequency (CBF) by a photoelectric method in response to these peptides in cultured rabbit tracheal explants. When cumulatively added, both CRF and ACTH increased CBF in a dose-dependent fashion. Treatment of tissues with Ca2+-free medium or nifedipine abolished the effect of CRF but not of ACTH. The CRF- and ACTH-induced ciliostimulations were not affected by indomethacin or autonomic antagonists, but were attenuated by nordihydroguaiaretic acid and by their receptor antagonists, alpha-helical CRF (9-41) and ACTH (7-38). Intracellular cyclic AMP levels were significantly increased by CRF and ACTH. These results suggest that CRF and ACTH stimulate airway ciliary motility through the activation of adenylate cyclase and lipoxygenase by binding to their specific receptors, where the effect of CRF may be triggered by Ca2+ influx.

Adrenocorticotropic Hormone↗
PubMed1989

Effect of cAMP on ciliary function in rabbit tracheal epithelial cells.

To study the effect of adenosine 3',5'-cyclic monophosphate (cAMP) on respiratory ciliary activity, we measured ciliary beat frequency (CBF) of rabbit tracheal epithelium by a photoelectric method in response to cAMP analogues and agents that can increase endogenous cAMP production. Addition of 8-bromo-cAMP dose dependently enhanced CBF, with the maximal increase and the concentration necessary to produce a half-maximal response (KD) being 31.0 +/- 3.4% (SE) (P less than 0.001) and 3.2 +/- 1.5 x 10(-7) M, respectively. Other structurally dissimilar cAMP analogues dibutyryl cAMP and chlorophenylthio-cAMP likewise caused increases in CBF. The phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine and the adenylate cyclase stimulator forskolin also augmented CBF in a dose-dependent fashion and were accompanied by the increases in intracellular concentrations of cAMP. Ciliary discoordination was not observed in any of the experiments. These results suggest that cAMP may accelerate mucociliary clearance through the activation of ciliary motility and that intracellular cAMP levels appear to be an important determinant for the lung mucociliary transport functions.

1-Methyl-3-isobutylxanthine↗
PubMed1989

Adenosine potentiates neurally- and histamine-induced contraction of canine airway smooth muscle.

We studied the effect of adenosine on airway reactivity of isolated canine bronchial smooth muscle under isometric conditions in vitro. Administration of adenosine and its analogs increased the contractile responses of bronchial segments to electrical field stimulation in a dose-dependent fashion, where the rank order potency was N-ethylcarboxamideadenosine greater than adenosine greater than N-cyclohexyladenosine, but had no effect on those to exogenous acetylcholine. This potentiation was more pronounced at relatively low than at high stimulus frequencies, the maximal increase from the baseline responses being 56.3 +/- 9.6% at 1 Hz (mean +/- SE, p less than 0.01). Adenosine also increased the histamine-induced contraction causing a leftward shift of the histamine dose-response curves, an effect that was abolished in the presence of atropine. These results suggest that adenosine potentiates airway responsiveness to vagal stimulation and to histamine through the activation of prejunctional A2 receptor, probably involving the accelerated release of acetylcholine from the cholinergic nerve terminals.

Acetylcholine↗
PubMed1989

Adenosine-mediated cyclic AMP-dependent inhibition of ciliary activity in rabbit tracheal epithelium.

We wished to determine whether adenosine, a purine nucleotide, modulates activity of respiratory cilia and, to this end, we studied cultured rabbit tracheal epithelium in response to adenosine and related substances in vitro. Ciliary beat frequency (CBF) as determined by a photoelectric method was depressed by adenosine (10(-3) M), the maximal decrease from the baseline value (965 +/- 29 beats/min, mean +/- SE) being 31.6 +/- 5.0% (p less than 0.001). The adenosine A2-receptor agonist N-ethylcarboxamide adenosine had only a small effect on ciliary activity, whereas other adenosine analogs elicited decreases in CBF in a dose-dependent fashion. The order of potency of cilia-inhibitory action was N-cyclohexyladenosine (an agonist for adenosine A1-receptor) greater than phenylisopropyladenosine greater than adenosine greater than N-ethylcarboxamide adenosine. Intracellular cyclic AMP (cAMP) levels were decreased by 10(-3) M adenosine from 39.2 +/- 6.5 to 25.3 +/- 4.8 pM/mg protein (p less than 0.05). The effect of adenosine on CBF was enhanced by dipyridamole, an adenosine uptake inhibitor, and by deoxycoformycin, an adenosine deaminase inhibitor. The adenosine-induced decreases in CBF and cAMP content were reversed by 8-phenyltheophylline, an adenosine receptor antagonist. These results suggest that there is an adenosine A1-receptor on rabbit tracheal epithelium that inhibits adenylate cyclase, which may result in the impairment of respiratory ciliary activity, and that adenosine-induced ciliary inhibition may be modulated by adenosine uptake and its catabolism by airway epithelial cells.

Adenosine↗
PubMed1989

Effect of bradykinin on airway ciliary motility and its modulation by neutral endopeptidase.

We studied the effect of bradykinin on ciliary activity and its modulation by peptidases in cultured rabbit tracheal epithelium in vitro. Bradykinin (10(-7) M) elicited a rapid, transient increase in ciliary beat frequency (CBF) from the baseline values of 1,031 +/- 25 to 1,388 +/- 38 beats/min (mean +/- SE, p less than 0.001), followed by a decline to a steady-state value of 1,180 +/- 30 beats/min, which was still greater than the baseline CBF. This ciliostimulation was dose-dependently inhibited by the B2-receptor antagonist (D-Arg,Hyp3,Thi5.8,D-Phe7)-bradykinin but not by the B1-receptor antagonist (Des-Arg9,Leu8)-bradykinin. Nifedipine, Ca2+-free medium, indomethacin, the phospholipase A2 inhibitor mepacrine, and the methyltransferase inhibitor 3-deazaadenosine reduced the change in CBF. Involvement of tachykinins, leukotrienes, prostaglandin D2, or thromboxane A2 was ruled out because bradykinin's action was not affected by (D-Pro2,D-Trp7.9)-substance P, nordihydroguaiaretic acid, or SQ29548, an antagonist for prostaglandin D2 and thromboxane A2. Bradykinin also increased prostaglandin E2 release (p less than 0.01), an effect that was abolished by indomethacin and Ca2+ deficiency. The CBF dose-response curve for bradykinin was shifted to lower concentrations by 1 log U by the neutral endopeptidase inhibitor phosphoramidon (p less than 0.01), whereas the angiotensin-converting enzyme inhibitor captopril was without effect. These results suggest that bradykinin interacts with B2-type receptors and stimulates ciliary activity through Ca2+-dependent prostaglandin E2 release, and that neutral endopeptidase may play a role in modulating the effect of bradykinin on airway mucociliary transport.

Animals↗
PubMed1989

Corticotropin-releasing factor potentiates the contractile response of rabbit airway smooth muscle to electrical field stimulation but not to acetylcholine.

We studied the effect of corticotropin-releasing factor (CRF) on airway smooth muscle functions in isolated rabbit tracheal segments under isometric conditions in vitro. The addition of ovine CRF synthesized by solid-phase methods did not cause muscle contraction, but it potentiated the contractile response to electrical field stimulation (EFS) at 5 Hz in a dose-dependent fashion, the maximal increase from the baseline response being 43.9 +/- 6.1% (mean +/- SE, p less than 0.001). This effect was not influenced by propranolol, phentolamine, indomethacin, pyrilamine, or (D-Pro2,D-Trp7.9)-substance P, but was completely inhibited by alpha-helical CRF, a CRF receptor antagonist. CRF (10(-7) M) also increased the responses to EFS at all frequencies of stimulation (1 to 40 Hz), so that the stimulus frequency required to produce a half-maximal contraction (ES50) decreased from 7.7 +/- 1.0 to 3.8 +/- 0.6 Hz (p less than 0.01). In contrast, contractile response to administered acetylcholine was not affected by CRF. CRF-induced potentiation of the response to EFS (5 Hz) was further increased from 44.5 +/- 5.4 to 144.6 +/- 11.1% in the presence of physostigmine and was abolished by atropine. These results suggest that CRF prejunctionally potentiates the vagally mediated contraction of airway smooth muscle through activation of CRF receptors on the cholinergic nerve terminals, likely involving the accelerated release of acetylcholine.

Acetylcholine↗
PubMed1989

[Indomethacin inhalation therapy for patients with excessive sputum].

We studied the effect of indomethacin (INDO) inhalation therapy on patients with excessive sputum due to chronic respiratory infection. INDO (3.5 x 10(-2) M) reduced sputum production from 211 +/- 43 to 106 +/- 22 ml/day (p less than 0.05, n = 7), the effect that was more remarkable in patients with diffuse panbronchiolitis (DPB). The prostaglandin E2 (PGE2) levels in sputum were also decreased significantly. In addition, to elucidate the mechanism of action of INDO on epithelial ion transport, we measured short-circuit current (Isc) of canine tracheal epithelium in response to 3 x 10(-6) M INDO under short-circuit conditions in vitro. Addition of INDO to mucosal medium decreased Isc from 42.8 +/- 6.0 to 8.2 +/- 3.5 microA/cm2 (p less than 0.01, n = 6). The increases in Isc produced by PGE2 and PGF2 alpha were abolished by furosemide, a Cl-transport blocker. These results suggest that INDO inhalation is a promising therapy in improving excessive sputum production, and that this effect may be attributed to inhibition of PGE2-dependent Cl-secretion into the airway lumen.

Administration, Inhalation↗
PubMed1988

Modulation of cholinergic neurotransmission by vasoactive intestinal peptide in ferret trachea.

We studied the effect of vasoactive intestinal peptide (VIP) on the contractile responses to electrical field stimulation (EFS) in isolated ferret tracheal segments. VIP did not change resting tension up to 2 X 10(-7) M, but it showed a biphasic effect on the responses to EFS. In concentrations up to 10(-9) M, VIP potentiated the response; at higher concentrations VIP reduced responses. Thus, at a concentration of 10(-9) M, VIP decreased the mean (+/- SE) log EFS frequency, producing 50% of maximum contraction significantly from a control value of 0.476 +/- 0.062 to 0.214 +/- 0.057 Hz (P less than 0.01); at a concentration of 2 X 10(-7) M VIP increased the half-maximal frequency from a control value of 0.513 +/- 0.086 to 0.752 +/- 0.053 Hz (P less than 0.05). The potentiating effect of VIP (10(-9) M) was not inhibited by hexamethonium, indomethacin, pyrilamine, methysergide, or [D-Pro2,D-Trp7,9] substance P. The inhibitory effect of VIP (2 X 10(-7) M) was also not inhibited by hexamethonium, indomethacin, or naloxone. In contrast to EFS-induced contraction, contractions produced by acetylcholine (10(-9) to 10(-3) M) were not affected by VIP at concentrations of 10(-9) and 2 X 10(-7) M. These results suggest that VIP modulates contractions produced by EFS via presynaptic cholinergic mechanisms and probably through a specific VIP receptor.

Acetylcholine↗
PubMed1988

Influenza infection causes airway hyperresponsiveness by decreasing enkephalinase.

Ferret tracheal segments were infected with human influenza virus A/Taiwan/86 (H1N1) in vitro. After 4 days, the smooth muscle contractile responses to acetylcholine and to substance P were measured. The response to substance P was markedly accentuated, with a threefold increase in force of contraction at a substance P concentration of 10(-5) M, the highest concentration tested. In contrast, the response to acetylcholine was not affected by viral infection. Histological examination of tissues revealed extensive epithelial desquamation. Activity of enkephalinase (neutral metallo-endopeptidase, EC.3.4.24.11), an enzyme that degrades substance P, was decreased by 50% in infected tissues. Inhibiting enkephalinase activity by pretreating with thiorphan (10(-5) M) increased the response to substance P to the same final level in both infected and control tissues. Inhibiting other substance P-degrading enzymes including kininase II (angiotensin-converting enzyme), serine proteases, and aminopeptidases did not affect the response to substance P. Inhibiting cyclooxygenase and lipoxygenase activity using indomethacin and BW 755c did not affect hyperresponsiveness to substance P. Pretreating tissues with antagonists of alpha-adrenoceptors, beta-adrenoceptors, and H1 histamine receptors (phentolamine 10(-5) M, propranolol 5 X 10(-6) M, and pyrilamine 10(-5) M, respectively) had no effect on substance P-induced contraction. These results demonstrate that infection of ferret airway tissues with influenza virus increases the contractile response of airway smooth muscle to substance P. This effect is caused by decreased enkephalinase activity in infected tissues.

Animals↗
PubMed1988

Effects of elastase-induced emphysema on histochemical properties of guinea pig diaphragm.

We studied the changes of histochemical properties of diaphragm in guinea pigs with elastase-induced emphysema. Using myofibrillar ATPase staining, three types of diaphragmatic muscle fibers were classified as slow-twitch, oxidative (SO), fast-twitch, oxidative, glycolytic (FOG), and fast-twitch, glycolytic (FG). Capillaries adjacent to individual fibers were also demonstrated by ATPase reaction. After 24 weeks of tracheal instillation of elastase, both the size and number of SO and FOG fibers were increased, thereby indicating the increase in relative areas occupied by these oxidative fibers in the diaphragm (p less than 0.01 in each case). Moreover, these changes were accompanied by the increased capillary density (p less than 0.01). These results suggest that chronic respiratory load with emphysema may establish the diaphragm more resistant to fatigue by increasing oxidative capacity of the diaphragmatic muscle fibers.

Animals↗
PubMed1988

Stimulation of ciliary activity by indomethacin in rabbit tracheal epithelial organ culture.

Inflammatory mediators influence mucociliary transport function in the lung, which may be dependent on the beating of the underlying cilia. To determine whether a nonsteroidal anti-inflammatory drug affects this function, and, if so, what is the mechanism action, we examined the effect of indomethacin on ciliary beat frequency (CBF) of cultured rabbit tracheal epithelial cells by a photoelectric technique. Addition of indomethacin dose-dependently enhanced CBF without any ciliary discoordination, the maximal increase and Km being 26.5 +/- 4.8% (mean +/- SE, p less than 0.001) and 6.8 X 10(-7) M, respectively. Pretreatment of tissues with nordihydroguaretic acid (10(-5) M), an inhibitor of the lipoxygenase pathway, did not change the baseline CBF, but inhibited the response of CBF to 3 X 10(-6) M indomethacin (p less than 0.01). These results suggest that indomethacin may accelerate mucociliary clearance through the augmentation of ciliary motility and that this ciliostimulation may be mediated by leukotrienes produced by activation of the lipoxygenase pathway of arachidonic acid metabolism.

Animals↗
PubMed1988

Stimulation of Cl secretion by neurokinin A and neurokinin B in canine tracheal epithelium.

We studied the effects of neurokinin A (NKA) and neurokinin B (NKB), the mammalian-derived tachykinins, on the electrical and ion transport properties of canine tracheal epithelium. Both tachykinins dose-dependently increased short-circuit current (Isc) when added to the mucosal (NKA: delta Isc(max) = 24.2 +/- 2.4 microA/cm2, KD = 9 nM; NKB: delta Isc(max) = 1.42 +/- 2.2 microA/cm2, KD = 32 nM) or submucosal (NKA: delta Isc(max) = 10.5 +/- 1.2 microA/cm2, KD = 45 nM; NKB: delta Isc(max) = 2.2 +/- 1.4 microA/cm2, KD = 80 nM) bath. Isc responses to mucosal addition of tachykinins consisted of transient and subsequent steady-state components, whereas submucosal addition elicited only steady-state responses. Inhibition of Cl transport with bumetanide or substitution of Cl reduced the maximal changes in Isc. In paired tissues, NKA increased net 36Cl flux toward the mucosa from 1.83 +/- 0.49 to 2.71 +/- 0.46 mu eq.cm-2.h-1 (p less than 0.05), without affecting net 22Na flux toward the submucosa. The increases in Isc induced by tachykinins were not modified by prior tissue incubation with phentolamine, propranolol, atropine, tetrodotoxin, or indomethacin, but were effectively inhibited by (D-Pro2, D-Trp7,9)substance P. The cyclic AMP (cAMP) levels in the surface epithelium were increased by the addition of NKA and NKB. These findings suggest that NKA and NKB selectively stimulate the secretion of Cl across canine tracheal epithelium, probably by acting directly on the tachykinin receptors, and that these effects are associated with the increased production of intracellular cAMP.

Animals↗
PubMed1987

Effect of macrophage stimulation on parasympathetic airway contraction in dogs.

The effect of lung macrophages stimulated with calcium ionophore on parasympathetic contractile response of canine bronchial rings was studied. Macrophages augmented the contraction induced by electrical field stimulation, an effect that was inhibited by indomethacin and by SQ29548, a thromboxane A2 receptor antagonist, but had no effect on the contractile response to exogenous acetylcholine. These results suggest that macrophage-derived thromboxane A2 facilitates cholinergic neurotransmission prejunctionally in airway smooth muscle.

Animals↗
PubMed1987

Platelet aggregation increases cholinergic neurotransmission in canine airway.

To determine whether thromboxane A2 released from aggregating platelets increases the contractile response of airway smooth muscle to cholinergic nerve stimulation and, if so, what the mechanism of action is, we studied in vitro bronchial segments from dogs under isometric conditions. The contractile responses to electrical field stimulation at 30 s and 1 min after the addition of autologous platelets were increased by 11.1 +/- 3.2 (SD) and 20.7 +/- 5.4%, respectively, and were accompanied by the release of thromboxane A2. These effects were inhibited either by pretreatment of platelets with indomethacin or by addition of the thromboxane A2 receptor antagonist SQ 29548. Likewise, the thromboxane A2 mimetic U 46619, in subthreshold doses (i.e., insufficient to increase base-line tension), increased electrical field stimulation-induced contraction by 18.7 +/- 4.8%. The increase was greater in the presence of a concentration of physostigmine that did not cause spontaneous contraction and was blocked by SQ 29548 but not by hexamethonium or by phentolamine. Methacholine-induced contractions were unaffected by U 46619. These results indicate that aggregating platelets, by releasing thromboxane A2, increase the airway contractile response to neural stimulation probably by the accelerated release of acetylcholine.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗