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    CMUR > China Medical University Hospital > Jurnal articles >  Item 310903500/29513
    Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/29513


    Title: Unilateral ventilation-perfusion mismatch on pulmonary scintigraphy caused by anomalous origin of a pulmonary artery from the innominate artery
    Authors: Hung, GU;Tsai, SC;Fu, YC;Kao, CH
    Contributors: 附設醫院核子醫學部;Kao, CH, China Med Coll Hosp, Dept Nucl Med, 2 Yuh Der Rd, Taichung 404, Taiwan
    Date: 2001
    Issue Date: 2010-09-24 14:36:38 (UTC+8)
    Publisher: LIPPINCOTT WILLIAMS & WILKINS
    Abstract: The effects of,a soluble guanylyl cyclase (sGC) activator, 3-(5 ' -hydroxymethyl-2 ' -furyl)-1-benzyl indazole (YC-1), on formylmethionyl-leucyl-phenylalanine (fMLP)-stimulated [Ca2+](i) elevation in rat neutrophils were examined. YC-1 produced a concentration-dependent inhibition of [Ca2+](i) elevation. Pretreatment of neutrophils with YC-1 did not enhance its inhibitory effect. YC-1 also inhibited the [Ca2+](i) changes caused by ionomycin. In a biphasic model, measuring the [Ca2+](i) stimulation by fMLP in a Ca2+-free medium followed by reintroduction of Ca2+, YC-1. mainly affected Ca2+ influx. YC-1 also inhibited active and passive Mn2+ influx, and this inhibitory effect was not attenuated by the sGC inhibitor 6-anilino-5,8-quinolinequinone (LY83583). Sodium nitroprusside did not affect the fMLP-stimulated [Ca2+](i) changes. Pretreatment of neutrophils with the cyclic GMP-dependent protein kinase inhibitor 8-(4-chlorophenylthio) guanosine-3 ' ,5 ' -monophosphorothioate, Rp-isomer (Rp-8-pCPT-cGMPS), LY83583, the protein phosphatase 2B inhibitor cyclosporin A, or the protein kinase inhibitor staurosporine did not attenuate the inhibition of [Ca2+](i) by YC-1. YC-1 inhibited the fMLP-stimulated protein tyrosine phosphorylation. These results indicate that cyclic GMP does not play an important role in the regulation of (Ca2+]i in rat neutrophils. Inhibition of fMLP-stimulated [Ca2+](i) changes by YC-1 is mainly via the blockade of Ca2+ entry through the inhibition of tyrosine kinase activity, but not the stimulation of protein kinase C and protein phosphatase 2B. (C) 2001 Elsevier Science Inc. All rights reserved.
    Relation: CLINICAL NUCLEAR MEDICINE 26(8):719-720
    Appears in Collections:[China Medical University Hospital] Jurnal articles

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