Inhibition of LTB4 biosynthesis in situ by CGS 23885, a potent 5-lipoxygenase inhibitor, correlates with its pleural fluid concentrations in an experimentally induced rat pleurisy model

1997 ◽  
Vol 355 (4) ◽  
pp. 470-474 ◽  
Author(s):  
A. Raychaudhuri ◽  
Herbert Chertock ◽  
James Chovan ◽  
Lisa S. Jones ◽  
Earl F. Kimble ◽  
...  
1988 ◽  
Vol 46 (4) ◽  
pp. 359-372
Author(s):  
Yoshihiro KADOWAKI ◽  
Tetsuro OHTA ◽  
Nobuo HOTOKEBUCHI ◽  
Sadatoshi KIMOTO ◽  
Masao HARUNA ◽  
...  

1990 ◽  
Vol 68 (6) ◽  
pp. 2597-2603 ◽  
Author(s):  
R. A. Bethel ◽  
C. L. McClure

To determine whether cyclooxygenase inhibitors alter parasympathetic control of airway smooth muscle in situ, we pretreated anesthetized dogs with intravenous indomethacin, meclofenamate, or normal saline and measured the isometric contraction of tracheal muscle in response to electrical stimulation of the vagus nerves. Indomethacin and meclofenamate increase the response of airway smooth muscle to parasympathetic stimulation. In subsequent experiments to determine the site of action of cyclooxygenase inhibitors, we found that indomethacin does not alter the response of tracheal muscle to intra-arterial acetylcholine (a muscarinic agonist) but does augment the response to intra-arterial dimethylpiperaziniumiodide (a nicotinic agonist). Moreover, the response to parasympathetic stimulation after pretreatment with a combination of indomethacin and BW755C (a combined cyclooxygenase-lipoxygenase inhibitor) does not differ significantly from the response after indomethacin or meclofenamate alone. We conclude that cyclooxygenase inhibitors increase the sensitivity of the contractile response of tracheal smooth muscle to parasympathetic stimulation, that they exert their effect on the postganglionic parasympathetic neuron, and that their effect is prejunctional. The effect appears secondary to a decrease in cyclooxygenase products rather than to an increase in lipoxygenase products. These findings suggest that endogenous cyclooxygenase products may modulate parasympathetic control of airway smooth muscle in vivo. They may relate to the mechanisms that underlie airway hyperresponsiveness, by which mediators of inflammation modulate airway responsiveness and by which nonsteroidal anti-inflammatory drugs induce severe bronchoconstrictor responses in some persons who have asthma.


1988 ◽  
Vol 46 (4) ◽  
pp. 359-372 ◽  
Author(s):  
Yoshihiro KADOWAKI ◽  
Tetsuro OHTA ◽  
Nobuo HOTOKEBUCHI ◽  
Sadatoshi KIMOTO ◽  
Masao HARUNA ◽  
...  

2010 ◽  
Vol 414 ◽  
pp. 195-208 ◽  
Author(s):  
A Haselmair ◽  
M Stachowitsch ◽  
M Zuschin ◽  
B Riedel

1993 ◽  
Vol 265 (3) ◽  
pp. L301-L307 ◽  
Author(s):  
K. J. Hamann ◽  
M. E. Strek ◽  
S. L. Baranowski ◽  
N. M. Munoz ◽  
F. S. Williams ◽  
...  

We studied the biochemical indexes and corresponding induction of airway smooth muscle contraction and hyperresponsiveness in guinea pig trachealis in situ caused by cultured eosinophils derived from mononuclear cell fractions of human umbilical cord blood. A method was developed that permitted isolation of large numbers of cells (approximately 2.6 x 10(6)/ml cord blood) having morphological and immunohistological characteristics of human peripheral blood eosinophils. After activation with 10(-6) M formyl-Met-Leu-Phe + 5 micrograms/ml cytochalasin B (fMLP + B), in situ application to the epithelial surface of 6 x 10(6) cord-derived eosinophils (CDE)/surface area (cm2) caused 1.46 +/- 0.24 g/cm maximal active tracheal tension in guinea pig tracheal smooth muscle (P < 0.005 vs. zero baseline). Muscarinic responsiveness also was augmented in situ in trachealis preparations treated with activated 3-wk CDE. Contraction caused by 3 x 10(-7) mol/kg iv methacholine (MCh) was 0.94 +/- 0.18 g/cm at baseline vs. 1.80 +/- 0.24 g/cm after activated CDE (P = 0.02). Control (sham-activated) 3-wk CDE caused neither significant contraction [0.41 +/- 0.16 g/cm active tension (AT); P < 0.05 vs. fMLP+B] nor augmented muscarinic responsiveness. Cells cultured for 5 wk contained fewer granules than 3-wk CDE and also caused less direct contraction of trachealis (0.73 +/- 0.14 g/cm AT) after activation (P < 0.01 vs. 3-wk CDE). Both contraction and muscarinic augmentation were blocked in 3-wk CDE after blockade of leukotriene C4 (LTC4) synthesis by pretreatment with the 5-lipoxygenase inhibitor, A63162 (50 microM). Treatment with A63162 had no effect on the stimulated release of eosinophil peroxidase.(ABSTRACT TRUNCATED AT 250 WORDS)


2013 ◽  
Vol 10 (11) ◽  
pp. 7463-7480 ◽  
Author(s):  
D. Langlet ◽  
E. Geslin ◽  
C. Baal ◽  
E. Metzger ◽  
F. Lejzerowicz ◽  
...  

Abstract. Anoxia was successfully induced in four benthic chambers installed at 24 m depth on the northern Adriatic seafloor from 9 days to 10 months. To accurately determine whether benthic foraminifera can survive experimentally induced prolonged anoxia, the CellTrackerTM Green method was applied and calcareous and agglutinated foraminifera were analyzed. Numerous individuals were found living at all sampling times and at all sampling depths (to 5 cm), supported by a ribosomal RNA analysis that revealed that certain benthic foraminifera were active after 10 months of anoxia. The results show that benthic foraminifera can survive up to 10 months of anoxia with co-occurring hydrogen sulfides. However, foraminiferal standing stocks decrease with sampling time in an irregular manner. A large difference in standing stock between two cores sampled under initial conditions indicates the presence of a large spatial heterogeneity of the foraminiferal faunas. An unexpected increase in standing stocks after one month is tentatively interpreted as a reaction to increased food availability due to the massive mortality of infaunal macrofaunal organisms. After this, standing stocks decrease again in cores sampled after 2 months of anoxia to then attain a minimum in the cores sampled after 10 months. We speculate that the trend of overall decrease of standing stocks is not due to the adverse effects of anoxia and hydrogen sulfides but rather due to a continuous diminution of labile organic matter.


Pituitary ◽  
2012 ◽  
Vol 16 (2) ◽  
pp. 275-286 ◽  
Author(s):  
Elizabeth O. Johnson ◽  
Aldo E. Calogero ◽  
Maria Konstandi ◽  
Themis C. Kamilaris ◽  
Sandro La Vignera ◽  
...  

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