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Biomedical subjects

K Konno

Publications and source records attributed to K Konno.

At least 127 records · Page 7Linked to original sources
PubMed1996

Cholinergic control of rabbit tracheal transepithelial potential difference in vivo.

The aim of the present study was to investigate the role of the autonomic nervous system in the regulation of airway epithelial ion transport in vivo. Rabbits were anaesthetized and mechanically-ventilated through a cannula inserted above the carina. The upper tracheal mucosa was exposed, and the electrical potential difference (PD) between the mucosal surface and the submucosal space was continuously measured by a high-impedance voltmeter under open-circuit conditions. Perfusion of the mucosa with atropine caused a rapid decline in PD from -20.1+/-2.0 to -15.2+/-0.9 mV (p<0.01), whereas phentolamine, propranolol, or the tachykinin antagonist, FK224, had no effect. Cutting both cervical vagus nerves decreased PD to the same degree as did atropine. Exogenously applied acetylcholine increased PD in a dose-dependent manner. Topical application of ipratropium bromide reduced the baseline value PD in a dose-dependent manner. The maximal decrease in PD was 43 +/- 0.3 mV (p<0.01), and the dose required to produce a half-maximal effect was 34 microg. Perfusion with either amiloride, a Na channel blocker, and diphenylamine-2-carboxylate, a Cl channel blocker, decreased the baseline PD, and the subsequent application of ipratropium bromide further decreased the PD in each case. We conclude that a cholinergic neural component may play a role in the generation of tracheal potential difference in vivo, probably involving stimulation by endogenously released acetylcholine of both Cl secretion and Na absorption across the airway epithelium.

Acetylcholine↗
PubMed1996

[T-kinin-induced increase in airway vascular permeability and its modulation by angiotensin-converting enzyme].

We studied the effect of T-kinin on airway vascular permeability and its modulation by endogenous peptidases in anesthetized rats in vivo, Vascular permeability was assessed by photometric measurement of extravasated Evans blue dye after formamide extraction. Intravenous injection of T-kinin increased dye extravasation in the trachea and main bronchi in a dose-dependent manner. Plasma extravasation evoked by T-kinin was inhibited by Hoe 140, a B2 receptor but-not by des Arg9-Leu8-bradykinin, a B1 receptor antagonist. Treatment with captopril, an angiotensin-converting enzyme inhibitor, potentiated the T-kinin-induced plasma extravasation, whereas phosphoramidon, a neutral endopeptidase inhibitor, had no effect. These results suggest that T-kinin increases airway vascular permeability via stimulation of B2 receptors, and that this effect is modulated by endogenous angiotensin-converting enzyme.

Animals↗
PubMed1996

[Regulation of cyclooxygenase activity in airway epithelium by endogenous nitric oxide].

The role of nitric oxide (NO) in the activity of cyclooxygenase (COX) in cultured canine tracheal epithelium was studied. Tracheal epithelium spontaneously released prostaglandin E2 (PGE2), which is a product of COX. The release of PGE2 was increased by bradykinin and was decreased by two NO synthase inhibitors: NG-nitro-L-arginine methyl ester and NG-monomethyl-L-arginine. That decrease was reversed in the presence of L-arginine. Chrolpromadin, but not aminoguanidine, inhibited PGE2 production, which suggests that constitutive NO synthase is involved. Two stable NO donors, sodium nitroprusside and S-nitroso-N-acetyl DL-penicillamine, also increased the production of PGE2. These effects were abolished by coincubation with hemoglobin, which binds and inactivates NO, but not by methylene blue, an inhibitor of soluble guanylate cyclase. NADPH diaphorase histochemistry of cultured tracheal cells revealed activity in the periphery of the cytoplasm. These results suggest that, in cultured canine tracheal epithelium, NO directly interacts with COX to regulate PGE2 production.

Animals↗
PubMed1996

[Pleural fibroma with a cavity-like air space].

A 45-year-old man was admitted to the hospital because of an increase in the size of an abnormal shadow on chest X-ray films over the preceding 5 years. A chest X-ray film on admission revealed a round air space in a mass-like shadow in the right upper lung field. Results of physical examination, sputum cytologic examination, and Ziehl-Neelsen staining were negative. Histopathological examination of a percutaneous lung biopsy specimen revealed a benign fibrous tumor of the pleura. Thoracotomy revealed a pedunculated tumor arising from the visceral pleura at the apical segment of the right upper lobe. A wedge resection was done. Histological examination revealed that the tumor consisted of regularly-shaped spindle cells with densely collagenous tissue. Normal lung tissue was found to be invaginated into the tumor tissue. These findings are consistent with the radiologic findings.

Fibroma↗
PubMed1996

Effect of 5-hydroxytryptamine on bioelectric properties of airway epithelial cells in culture.

To elucidate whether 5-hydroxytryptamine (5-HT) affects airway epithelial electrolyte transport and, if so, what the mechanism of action is, we studied the bioelectric properties of canine cultured tracheal epithelium under short-circuit conditions in vitro. Mucosal addition of 5-HT dose-dependently increased short-circuit current (Isc), which was accompanied by increases in transepithelial potential difference and cell conductance. In contrast, 5-HT had no effect on bioelectric properties when it was added to the submucosal side. Pretreatment of cells with amiloride potentiated the increase in Isc produced by 5-HT. In the presence of diphenylamine-2-carboxylate or Cl-free medium, 5-HT decreased Isc from the baseline level. Incubation with BAPTA-AM but not dibutyryl cAMP greatly attenuated the 5-HT-induced increase in amiloride-insensitive portion of Isc. These results suggest that 5-HT inhibits Na absorption and stimulates Cl secretion across canine tracheal epithelium and that the Cl secretion may be associated with elevation of intracellular Ca2+ contents.

Amiloride↗
PubMed1996

[Methicillin-resistant Staphylococcus aureus infection in the Akita University Hospital: surveillance and microbiology data].

In order to control the nosocomial infections by methicillin-resistant Staphylococcus aureus (MRSA) in the Akita University Hospital, the systematic surveillance for MRSA-infection has been done since October in 1991. We reviewed MRSA-isolation numbers, MRSA-detected patient numbers, risk factors of nosocomial infection and patient's basic diseases with the data of a total 336 cases, and then examined the microbiological characteristics of MRSA strains which had been isolated in our hospital in 1986 approximately 1994. The results obtained are as follows; 1) MRSAs were isolated at 13 per month on the average and the detection rate was 0.81 to 1,000 inpatients per day. 2) MRSAs were isolated more in the surgical ward. 3) Patients with 0 year old and more than 60 years old were more infected. 4) MRSA was isolated more from the immunocompromised patients with underlying diseases such as malignant tumors but half of the diseases were not affected by MRSA. 5) Seventy percent of patients had the risk factors of MRSA-transmission such as surgical operation and IVH-cathetering. 6) All isolates of MRSA strains in our hospital showed type II in coagulase type analysis and resistance to minocycline and ofloxacin. 7) It was suggested that one strain expanded throughout the hospital by several DNA analysis with the mecA gene in MRSA. These surveillance and microbiology data will be useful for our nosocomial mecA gene in MRSA. These surveillance and microbiology data will be useful for our nosocomial infection control.

Adolescent↗
PubMed1996

[Effect of sodium cromoglycate on airway vascular leakage caused by hypertonic saline in the rat trachea].

The action of the anti-asthmatic drug sodium cromoglycate (SCG) on airway inflammation remains uncertain. Using Evans blue dye as a maker of plasma leakage, we studied the effect of SCG on neurogenic vascular extravasation evoked by hypertonic saline (HTS) in the rat trachea. Inhalation of HTS (5-15%) caused a concentration-dependent increase in plasma leakage, but inhaled 0.9% NaCl had no effect. Inhalation of SCG did not affect the baseline level of vascular permeability, but it inhibited the effect of HTS in a dose-dependent manner: plasma extravasation induced by 10% NaCl was significantly reduced by 2 minutes of inhalation of SCG at concentrations of 10 and 50 mg/ml (p < 0.05 and p < 0.01, respectively). SCG (10 mg/ml), also inhibited the changes in microvascular permeability caused by aerosols of substance P (10(-4) M), whereas it did not affect the responses to aerosols of platelet-activating factor (3 x 10(-4) M). A similar dose of SCG did not significantly alter microvascular leakage caused by 5% NaCl. However, phosphoramidon, a selective inhibitor of neutral endopeptidase, potentiated the response to 5% NaCl, an effect that was inhibited by SCG (p < 0.05). These results suggest that SCG inhibits HTS-induced airway vascular permeability, presumably through a tachykinin-antagonist-like property, and that this inhibition is exaggerated when the activity of endogenous neutral endopeptidase is low.

Animals↗
PubMed1996

Effects of K(+)-channel blockers on epithelium-derived relaxing factor (EpDRF)-mediated modulation of airway smooth muscle contractility.

Airway epithelium plays a role in the regulation of bronchial smooth muscle tone releasing cyclooxygenase products and epithelium-derived relaxing factor (EpDRF). To test possible involvement of K+ channels in the action of EpDRF, we studied rabbit tracheal segments in the presence of indomethacin under isometric conditions in vitro. Mechanical removal of the epithelium increased the contractile responses to acetylcholine, so that negative logarithm of the concentration required to produce 50% of maximal effect (pD2) increased from 5.0 +/- 0.4 to 5.7 +/- 0.3 (P < 0.01). Addition of charybdotoxin per se caused a leftward shift of acetylcholine concentration-response curves in epithelium-intact tissues, but the subsequent removal of the epithelium did not further potentiated the contractile responses. In contrast, apamin or glibenclamide had no effect on the epithelium-removal-induced potentiation of the contraction. The responses to electrical field stimulation were likewise potentiated by epithelial removal, an effect that was abolished by charybdotoxin. These results suggest that Ca(2+)-activated K+ channels are involved in the EpDRF modulation of airway smooth muscle responsiveness.

Acetylcholine↗
PubMed1996

[Six patients with pneumonitis related to blended Chinese traditional medicines].

We encountered six patients with pneumonitis related to blended chinese traditional medicine (Kampo). The duration of treatment with kampo ranged from 14 to 110 days (mean: 38 days). The most common complaints were dyspnea, fever, and dry coughing. Fine crackles were heard at the bases of both lungs. Abnormal laboratory findings included high values of C-reactive protein and glutamic-oxaloacetic transaminase in all patients, lactate dehydrogenase in 5 patients, and eosinophil count in 1 patient. Chest X-ray films and CT films revealed diffuse reticulo-nodular interstitial shadows with consolidation in both lung fields in 3 patients and pleural effusion in 1 patient. Bronchoalveolar lavage was done in 4 patients; examination of the lavage fluid showed lymphocyte alveolitis, either pure or associated with neutrophilia and eosinophilia in 3 patients. Inverted CD4/CD8 lymphocyte ratios were found in 3 patients. Transbronchial lung biopsy was done in 4 patients and specimens from 3 of those 4 showed organizing pneumonitis with thickening of alveolar septa. Lymphocyte stimulation tests were positive in 4 patients. Discontinuation of the drug (2 patients) or administration of corticosteroids (4 patients) was followed by rapid improvement. Patients being treated with kampo preparations should be observed for signs and symptoms of drug-induced pneumonitis.

Aged↗
PubMed1995

Lipoxin A4 inhibits cholinergic neurotransmission through nitric oxide generation in the rabbit trachea.

The effect of lipoxin A4 and lipoxin B4 on cholinergic neurotransmission in rabbit tracheal segments was studied under isometric conditions in vitro. Lipoxin A4 attenuated the contractile responses to electrical field stimulation and caused a rightward shift of the frequency-response curves, so that the stimulus frequency required to produce a half-maximal effect (ES50) increased from 8.1 +/- 0.8 to 25.7 +/- 1.9 Hz (P < 0.001), whereas lipoxin B4 had no effect. In contrast, lipoxin A4 did not alter the contractile responses to acetylcholine. Pretreatment of tissues with NG-nitro-L-arginine methylester inhibited the effect of lipoxin A4 on electrical field stimulation, but NG-nitro-D-arginine methylester did not. This inhibition by NG-nitro-L-arginine methylester was reversed by L-arginine but not by D-arginine. These results suggest that lipoxin A4 prejunctionally reduces the vagal nerve-mediated contraction of airway smooth muscle, probably by inhibiting the release of acetylcholine, and that this effect may be exerted through stimulation of nitric oxide generation.

Acetylcholine↗
PubMed1995

Tachykinins stimulate nitric oxide generation by canine cultured tracheal epithelium.

We studied the effects of tachykinins on the generation of nitric oxide (NO) from canine cultured tracheal epithelial cells using a specific amperometric sensor for this molecule. Immersion of the NO-selective electrode in the medium bathing the cells detected the baseline current of 30.5-61.7 pA, which corresponded to NO concentration ([NO]) at 44.0 +/- 7.6 nM (mean +/- S.E.M.). Substance P (SP, 10(-6) M) increased the current from 51.3 +/- 9.8 to 73.6 +/- 11.4 pA (P < 0.001), an effect that was not affected by NG-nitro-D-arginine methylester, but inhibited by NG-nitro-L-arginine methylester by 83 +/- 9% (P < 0.001), and this inhibition was restored by the subsequent addition of L-arginine, but not by D-arginine. SP and neurokinin A (NKA) increased [NO] in a dose-dependent manner, the maximal increases from the baseline level being 71.0 +/- 14.9 and 33.4 +/- 8.5 nM, respectively (P < 0.001 for each), whereas neurokinin B (NKB) had no effect. In the presence of phosphoramidon, the response of each tachykinin was augmented, but the rank order of potency was still NKA > SP >> NKB. These results suggest that NO is spontaneously released from airway epithelium and that tachykinins stimulate epithelial NO generation via NK2 receptors.

Animals↗
PubMed1995

Nitric oxide modulation of Ca2+ responses in cow tracheal epithelium.

Nitric oxide (NO) plays an important role in the regulation of Ca2+ -dependent airway epithelial function such as ciliary motility. In this experiment, the effect of NO on intracellular Ca2+ ([Ca2+]1) was studied in cultured cow tracheal epithelium by the fura-2 method. L-NG-nitroarginine methyl ester, an NO synthase inhibitor, per se did not significantly alter baseline [Ca2-]i, but bradykinin- and ATP-induced increases in [Ca2+]i were significantly reduced in the presence of L-NG-nitroarginine methyl ester. This inhibitory effect disappeared by a simultaneous addition of L-arginine. Sodium nitroprusside or dibutyryl cyclic GMP potentiated bradykinin- and ATP-induced increases in [Ca2+]i. Cytochemistry for NADPH diaphorase activity revealed the presence of NO synthase in the cultured epithelium. These results suggest that NO produced by NO synthase in airway epithelium modulates bradykinin- and ATP-induced [Ca2+]i responses, which may be dependent on cyclic GMP.

Adenosine Triphosphate↗
PubMed1995

Role of nitric oxide in tachykinin-induced increase in potential difference of rabbit tracheal mucosa.

1. The effect of tachykinins on transepithelial potential difference (PD) of rabbit trachea and possible involvement of nitric oxide (NO) generation in vivo were investigated. 2. Perfusion of tracheal mucosa with neurokinin A (NKA) or substance P (SP) dose dependently increased PD in the presence of amiloride, with the potency being NKA > SP, but neurokinin B (NKB) had no effect. 3. Application of NG-nitro-L-arginine methylester (L-NAME, 10(-3) M) attenuated the NKA-induced increase in the amiloride-sensitive PD, causing a rightward displacement of the dose-response curve by approximately 1.0 log U, whereas NG-nitro-D-arginine methylester (D-NAME, 10(-3) M) did not. 4. The inhibitory effect of L-NAME was reversed by L-arginine (10(-2) M) but not by D-arginine (10(-2) M). 5. The release of NO was determined by a real-time measurement of NO concentration ([NO]) in the perfusate using specific amperometric sensors for this molecule. 6. NKA and SP increased [NO] in a dose-dependent manner, the maximal increase from the baseline value being 114 +/- 11 nM (mean +/- S.E.M., P < 0.001) and 54 +/- 6 nM (P < 0.01), respectively. 7. Histochemistry for NADPH diaphorase activity showed a strong staining within the epithelial cells. 8. We conclude firstly that tachykinins increase amiloride-sensitive PD in vivo, which probably reflects Cl- movement from the submucosa toward the respiratory lumen in tracheal mucosa, and secondly that NO generation by epithelial cells may be involved in this process.

Amiloride↗
PubMed1995

Effect of azelastine on airway hyperresponsiveness mediated by stimulated macrophages.

The effect of the anti-allergic drug azelastine, 4-(p-chlorobenzyl)-2-(hexahydro-1-methyl-1H-azepine-4-yl)-1-(2H)-phth alazione), on airway hyperresponsiveness induced by immunologically stimulated pulmonary alveolar macrophages was investigated in canine bronchial segments under isometric conditions in vitro. Macrophages stimulated with anti-dinitrophenyl immunoglobulin E (IgE) antibody and dinitrophenyl-human serum albumin potentiated the contractile responses to electrical field stimulation at all frequencies, an effect that was abolished by azelastine (3 x 10(-5) M). In contrast, azelastine had no effect on the potentiation of the contractile responses to electrical stimulation by U46619, a thromboxane A2 mimetic. The IgE-mediated release of thromboxane A2 from macrophages was inhibited by azelastine in a concentration-dependent fashion, the maximal decrease and the concentration required to produce a half-maximal effect being 84 +/- 6% (P < 0.001) and 16 microM, respectively. These results suggest that azelastine may attenuate macrophage-induced parasympathetic airway hyperresponsiveness through an inhibition of the release of thromboxane A2.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1995

Use of lactate dehydrogenase to evaluate the anti-viral activity against influenza A virus.

The detection of lactate dehydrogenase (LDH) can be used to evaluate efficiently anti-influenza A virus agents. LDH levels in the virus-infected Madin-Darby canine kidney cell cultures were significantly higher than in controls, were in proportion to the degree of virus infection, and corresponded to a decrease in mitochondrial dehydrogenase activity as assayed using a tetrazolium colorimetric assay (MTT method). The EC50 value and cytotoxicity of ribavirin, 3-deazaguanine, pyrazofurin, and carbodine against influenza A virus as measured by the LDH detection method was equivalent to that derived by the MTT method.

Amides↗