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  • 1
    Electronic Resource
    Electronic Resource
    Presence of C5a-potentiating activity in the plasma of a patient with Kimura's disease (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 49 (1994), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: To determine whether the response to the active complement fragment C5a in polymorphonuclear leukocytes (PMN) obtained from a patient with Kimura's disease is similar to that in normal subjects, we evaluated superoxide anion (O2-) generation after stimulation with C5a. The patient's PMN produced more O2- than did those from healthy controls after stimulation with human C5a in vitro. The response returned to normal with the improvement in clinical indicators after initiation of steroid administration. We conducted the following experiments with the plasma of this patient during the active disease stage to establish the presence of a humoral factor that potentiated the C5a-response of PMN. Incubation of PMN from normal controls having the same blood type as the patient at 37°C for 2 h with the patient's plasma at the active disease stage revealed that the cells generated abundant O2- after stimulation with C5a. Incubation of normal PMN with the patient's plasma during the inactive disease stage showed no potentiated response to C5a. This activity was lost after incubation at 56°C for 30 min. Coincubation of PMN with methylprednisolone up to 100 μg/ml did not suppress this activity. Although the plasma concentration of C5a at the active stage was mildly elevated (13 ng/ml), it was below the limit of detection (〈10 ng/ml) at the inactive stage. These results suggest the presence of a heat-labile, humoral factor in the patient's plasma that upregulated the response of PMN to C5a and that was not suppressed by in vitro treatment with a steroid. This factor may influence the acute inflammatory reaction in this disorder.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1398-9995.1994.tb02662.x
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  • 2
    Electronic Resource
    Electronic Resource
    VIP antagonists enhance excitatory cholinergic neurotransmission in the human airway (1994)
    Springer
    Lung 172 (1994), S. 159-167 
    Details
    ISSN: 1432-1750
    Keywords: VIP-VIP Antagonist ; Human bronchus ; Smooth muscle ; Vagus nerve
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It has been reported that a low concentration of exogenously applied vasoactive intestinal peptide (VIP) suppresses the release of acetylcholine (ACh) from vagus nerve terminals in the ferret and feline trachea. There has been, however, no documentation of the prejunctional action of VIP in the human airway. We observed the effects of VIP and VIP antagonists on cholinergic excitatory neuro-effector transmission in the human bronchus to study the possible role of endogenous VIP on excitatory neurotransmission. In the human bronchus, VIP (10−10 to 10−7 M) showed no effect on either the contractions evoked by electrical field stimulation (EPS) or those evoked by ACh. To investigate the possible role of endogenous VIP on the human bronchus, we observed the effects of the VIP antagonists [4-Cl-D-Phe6,Leu17]-VIP and [Ac-Tyr1,D-Phe2-]-GRF(1–29)-NH2 on excitatory neuroeffector transmission. Both VIP antagonists (10−8 M) significantly enhances the contractions evoked by EFS without affecting the ACh sensitivity of smooth muscle cells. These results indicate that VIP antagonists have a prejunctional action that enhances excitatory neurotransmission. This study suggests that endogenous VIP may suppresses ACh release from the vagus nerve terminals in the human airway. It is also suggested that exogenously applied VIP may be inactivated by some mechanism in the human airway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00175944
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  • 3
    Electronic Resource
    Electronic Resource
    Airway epithelial cells modulate cholinergic neurotransmission in dog trachea (1994)
    Springer
    Lung 172 (1994), S. 241-249 
    Details
    ISSN: 1432-1750
    Keywords: Airway epithelial cell ; Airway hyperresponsiveness ; Vagus nerve ; Smooth muscle ; Neurotransmission
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the effects of epithelial cells on excitatory cholinergic neurotransmission in dog trachea, to shed more light on the role of airway epithelial cells in regulating airway responsiveness. Airway epithelial cells were prepared by an enzymatic dissociation of the tracheal mucosa using protease-free collagenase. Tracheal smooth muscle contractions evoked by electrical field stimulation (EFS) or acetylcholine (ACh) were measured before and after the application of epithelial cells. Isolated and dispersed epithelial cells (3 × 105 cells/ml) suppressed the amplitude of the twitch-like contractions evoked by EFS in the combined presence of guanethidine sulfate (10−6 m) and indomethacin (10−5 m). In contrast, epithelial cells did not affect the contraction evoked by exogenously applied ACh. Atropine (10−6 m) or tetrodotoxin (10−7 m) abolished the contraction evoked by electrical field stimulation. These findings indicate that airway epithelial cells inhibit the excitatory neurotransmission of the vagus nerve, presumably by suppressing the release of ACh. Airway epithelial cells may therefore play an important role in regulating the response of smooth muscle.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00164441
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  • 4
    Electronic Resource
    Electronic Resource
    Ipratropium bromide protects against bronchoconstriction during bronchoscopy (1994)
    Springer
    Lung 172 (1994), S. 293-298 
    Details
    ISSN: 1432-1750
    Keywords: Bronchoscopy ; Bronchoconstriction ; Atropine ; Ipratropium bromide ; Lidocaine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Pulmonary function is reportedly impaired by fiberoptic bronchoscopy. We investigated the effect of two anticholinergic agents, intramuscular atropine and inhaled ipratropium bromide, on bronchoconstriction in 29 patients who were undergoing diagnostic bronchoscopy. The patients were divided into three groups; the first received 0.5 mg of atropine intramuscularly; the second took four puffs of 0.02 mg ipratropium bromide aerosolized by a metered-dose inhaler, and the third inhaled four puffs of a placebo. Fifteen minutes later a standardized topical anesthetic, lidocaine, was administered, and a bronchoscopic examination was performed. Pulmonary function was measured before and 15 minutes after each step. Pulmonary function was not affected by the treatment with anticholinergics or the placebo. In the placebo and the atropine groups, the topical anesthesia produced significant reductions in forced expiratory volume in 1 second (FEV,) and peak expiratory flow rate (PEFR); further reductions in these values were observed after bronchoscopy. In the group treated with ipratropium bromide there were no significant changes in FEV, and PEFR after topical anesthesia. Bronchoscopy induced significant reductions in FEV1 and PEFR, but the changes were significantly smaller than those seen in the placebo and atropine groups. The results suggest that the deleterious effect of bronchoscopy on pulmonary function is due to topical lidocaine anesthesia and to the bronchoscopic examination itself. Inhaled ipratropium bromide protects against these deleterious effects, whereas intramuscular atropine does not.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00164311
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  • 5
    Electronic Resource
    Electronic Resource
    Inositol 1,4,5-trisphosphate mediates adrenaline activation of K+ conductance in mouse peritoneal macrophages (1993)
    Springer
    Pflügers Archiv 423 (1993), S. 140-148 
    Details
    ISSN: 1432-2013
    Keywords: α1-Adrenoceptor ; Inositol 1,4,5-trisphosphate ; GTP-binding protein ; Ca2+ release ; Ca2+-dependent K+ conductance ; Mouse peritoneal macrophage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In mouse peritoneal macrophages, α1-adrenoceptor stimulation evokes a Ca2+-dependent K+ current [I 0(Adr)] [Hara et al. (1991) Pflügers Arch 419:371–379]. The roles of D-myo-inositol 1,4,5-trisphosphate (InsP 3) and a GTP-binding protein (G protein) in I 0(Adr) were investigated with tight-seal whole-cell recordings and fura-2 fluorescence measurements. Intracellular injection of lnsP 3 (5–50 μM) evoked transient outward currents [I 0(InsP 3)] with or without damped oscillations in membrane currents at -40 mV. Dialysis with 0.2 mM guanosine 5′-[3-thio]triphosphate (GTP[γS], a poorly hydrolysable GTP analogue) at -40 mV activated oscillatory outward currents or a slowly developing steady current on which such oscillations were superimposed after a delay of 10–90 s. I 0(InsP 3) and the GTP[γS]-induced current {I 0(GTP[γS])} were accompanied by an increase in conductance. Reversal potentials of both responses closely depended on the extracellular K+ concentration. Fura-2 measurements revealed that I 0(InsP 3) and I 0(GTP[γS]) result from a rise in intracellular free Ca2+ concentration ([Ca2+]i). Removal of extracellular Ca2+ did not abolish I 0(InsP 3) and I 0(GTP[γS]). Both were blocked by bath-applied charybdotoxin. Intracellular D- myo-inositol 1,3,4,5-tetrakisphosphate (InsP 4, 50 μM) did not evoke any responses, whereas D-myo-inositol 2,4,5-trisphosphate [InsP 3(2,4,5), 20 μM] elicited an outward current at -40 mV. I0(InsP 3) was completely blocked by prior dialysis with the InsP 3 receptor antagonist heparin (5 mg/ml). Inclusion of guanosine 5′-[2-thio] diphosphate (GDP[βS], 2 mM) or heparin (5 mg/ml) together with GTP[γS] in the patch pipette solution completely blocked I 0(GTP[γS]). These results indicate that intracellular injection of InsP 3 or GTP[γS] mimic I 0(Adr). Furthermore, intracellular dialysis with heparin (3 mg/ ml) or GDP[βS] (2 mM) greatly accelerated a run-down of I 0(Adr). On the other hand, I 0(Adr) was markedly prolonged in a cell dialysed with GTP[γS] (0.2 mM). Therefore, it is concluded that I 0(Adr) results from stimulation of α1-adrenoceptor and InsP 3 formation via a G protein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374971
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  • 6
    Electronic Resource
    Electronic Resource
    The activation of Ca2+-dependent K+ conductance by adrenaline in mouse peritoneal macrophages (1991)
    Springer
    Pflügers Archiv 419 (1991), S. 371-379 
    Details
    ISSN: 1432-2013
    Keywords: Adrenaline ; α 1-Adrenoceptor ; Ca2+ release ; Ca2+-dependent K+ conductance ; Patch clamp ; Mouse peritoneal macrophage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Responses to adrenaline in mouse peritoneal macrophages were investigated with perforated and cell-attached patch-clamp recording, and with a combination of the perforated-patch recording and fura-2 fluorescence measurements. Extracellularly applied adrenaline induced a transient outward current (4–10s in duration, 100–500 pA in amplitude) at −40 mV associated with a marked increase in conductance. The adrenaline-induced current [I o (Adr)] reversed polarity near −80 mV. The reversal potential depended distinctly on the external K+ concentration but not on external Cl− concentration. Removal of external Ca2+ did not affect I o(Adr) within 2–4 min but subsequent responses to adrenaline were progressively depressed. In contrast, treatment with an intracellular Ca2+ chelator, the acetoxymethyl ester of 1,2-bis-(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid completely abolished I o(Adr). Furthermore, I o(Adr) was blocked by bath-applied quinidine and charybdotoxin, but not by tetraethylammonium or apamin. Extracellular application of an α 1-adrenoceptor agonist phenylephrine and of noradrenaline mimicked I o(Adr). On the other hand, I o(Adr) was antagonized by a non-selective α-adrenoceptor antagonist phentolamine (0.2 μM) and an α 1-adrenoceptor antagonist prazosin (0.2 μM), but was not affected by an α2-adrenoceptor antagonist yohimbine (1 μM) or a β-adrenoceptor antagonist propranolol (1 μM). Cell-attached single-channel recordings with the pipette solution containing 145 mM KCl revealed the activation of single-channel currents with a conductance of 40 pS during application of adrenaline outside the patch. Parallel measurements of membrane current and fura-2 fluorescence in the same cell demonstrated a correlation between the rise in [Ca2+]i and an increase in K+ conductance. Therefore, it is concluded that adrenaline activates a Ca2+-dependent K+ conductance by release of Ca2+ from internal stores through an activation of an α 1-adrenoceptor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00371119
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