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V Inhibitor (v + inhibitor)

Distribution by Scientific Domains
Medical Sciences91%

Kinds of V Inhibitor

  • factor v inhibitor
    		•

    Selected Abstracts

    B2 kinin receptors mediate the Indian red scorpion venom-induced augmentation of visceral reflexes via the nitric oxide cyclic guanosine monophosphate pathway

    ACTA PHYSIOLOGICA, Issue 4 2009
    S. Kanoo
    Abstract Aim:, This study was performed to delineate the kinin (receptor)-dependent pathways in the Indian red scorpion (Mesobuthus tamulus; MBT) venom-induced pulmonary oedema as well as the augmentation of cardio-pulmonary reflexes evoked by phenyldiguanide (PDG). Methods:, In urethane-anaesthetized adult rats, the effect of venom on the PDG reflex responses (blood pressure, heart rate and respiration rate) and the pulmonary water content was ascertained using various antagonists(des- Arg, B1 receptor antagonist; Hoe 140, B2 receptor antagonist; N, -nitro- l -arginine methyl ester (l -NAME), nitric oxide (NO) synthase inhibitor; methylene blue, soluble guanylate cyclase inhibitor; and glibenclamide, K+ATP channel blocker). The effect of phosphodiesterase V inhibitor (sildenafil citrate) on the reflex response and the pulmonary water content was also examined and compared with venom-induced responses. Results:, Intravenous injection of PDG (10 ,g kg,1) evoked apnoea, bradycardia and hypotension lasting >60 s. Exposure to MBT venom (100 ,g kg,1) for 30 min augmented the PDG reflex responses by two times and increased the pulmonary water content, significantly. Hoe 140 blocked the venom-induced responses (augmentation of PDG reflex and increased pulmonary water content) whereas des-Arg did not. l -NAME, methylene blue or glibenclamide also blocked the venom-induced responses. Furthermore, sildenafil citrate (that increases cGMP levels) produced augmentation of PDG reflex response and increased the pulmonary water content as seen with venom. Conclusion:, The results indicate that venom-induced responses involve B2 kinin receptors via the NO-dependent guanylate cyclase-cGMP pathway involving K+ATP channels. [source]

    Spontaneous resolution of acquired factor V inhibitor associated with ovarian carcinoma

    INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 4 2007
    E. O. MAUGHAN
    Summary A 74-year-old lady who presented initially with loin pain and haematuria, then melaena was found to have a prothrombin time ratio (PTR) > 10 and activated partial thromboplastin time ratio (APTTR) > 7. A factor V inhibitor was diagnosed. She was managed with supportive care and the FV inhibitor resolved. A few weeks later she developed abdominal swelling and ascites and was found to have an ovarian tumour. This is the first case, as far as we are aware, of a malignancy-associated FV antibody that has spontaneously remitted before overt presentation of the tumour and illustrates the value of adopting an expectant approach to the management of acquired FV inhibitors. [source]

    Severe Hemorrhagic Complication Due to Acquired Factor V Inhibitor After Single Exposure to Bovine Thrombin Product

    JOURNAL OF CARDIAC SURGERY, Issue 6 2000
    Michio Kajitani M.D., Ph.D.
    Our patient underwent emergency repair of acute aortic dissection and coronary artery bypass grafting. The patient developed leg wound infection at the saphenous vein harvest site, which was debrided and left open. Attempt to reclose the leg wound 1 month later was complicated by a life-threatening hemorrhage with markedly elevated activated partial thromboplatin time. There was no evidence of infection or disseminated intravascular coagulation, and further study identified low factor V level with positive factor V inhibitor. Treatment with plasmapheresis and steroid successfully reversed the coagulopathy. Detailed case review failed to reveal exposure to any thrombin products other than the one used for the aortic dissection repair. This case was unusual because only a single exposure to this product resulted in severe hemorrhagic complication 1 month after surgery. [source]

    An acquired factor V inhibitor associated with defective factor V function, storage and binding to multimerin 1

    JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 2 2008
    S. B. JEIMY
    [source]

    Acquired factor V inhibitor in a context of sepsis and disseminated intravascular coagulation,

    AMERICAN JOURNAL OF HEMATOLOGY, Issue 2 2010
    Anne Tessier-Marteau
    No abstract is available for this article. [source]

    Response of factor V inhibitor to rituximab in a patient who received liver transplantation for primary biliary cirrhosis

    AMERICAN JOURNAL OF HEMATOLOGY, Issue 4 2004
    Eric Chun-Yet Lian
    Abstract A 43-year-old patient developed factor V inhibitor 6 months after liver transplantation for primary biliary cirrhosis in association with Sjögren's syndrome/systemic lupus erythematosus. She suffered from ecchymoses in the lower extremities. The factor V inhibitor was eradicated after 10 weekly doses of 375,500 mg/m2 rituximab. Am. J. Hematol. 77:363,365, 2004. © 2004 Wiley-Liss, Inc. [source]

    Acquired factor V inhibitor in a critically ill patient

    ANAESTHESIA, Issue 9 2009
    C. J. Morris
    Summary Acquired inhibitor of factor V is a rare condition with a variety of clinical manifestations, from extremely mild to life threatening haemorrhage. We present a case from our intensive care unit as a reminder of the less common causes of elevated prothombin and activated partial thromboplastin times, and how knowledge of the variable presentation may aid management. [source]

    The effects of selective phosphodiesterase III and V inhibitors on adrenergic and non-adrenergic, non-cholinergic relaxation responses of guinea-pig pulmonary arteries

    AUTONOMIC & AUTACOID PHARMACOLOGY, Issue 2 2003
    A. Tasatargil
    Summary 1 The aim of the present study was to investigate the role of several possible neurotransmitters in mediating non-adrenergic, non-cholinergic (NANC) relaxation, and the effects of phosphodiesterase (PDE) III and V inhibitors on adrenergic and NANC relaxation in branch pulmonary artery (PA) of guinea-pig. 2 Under the NANC conditions, electrical field stimulation (EFS, 60 V, 0.2 ms, 20 Hz) induced a tetrodotoxin-sensitive relaxation of the histamine-precontracted PA rings. The nitric oxide (NO) synthase inhibitor NG -nitro- l -arginine methyl ester (l -NAME, 10,4 m) and the guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 10,5 m) partially inhibited the EFS-induced relaxation. The inhibitory effect of l -NAME was reversed completely by l -arginine (10,3 m), but not d -arginine (10,3 m). 3 This NANC relaxation was attenuated by 8-phenyltheophylline (10,5 m), a P1 -purinoceptor antagonist. 4 The NANC response was potentiated by 10,6 m zaprinast, a type V PDE inhibitor, but was unaffected by 3 × 10,6 m milrinone, a type III PDE inhibitor. 5 Sodium nitroprusside (SNP) caused a concentration-dependent vasodilator effect which was potentiated by zaprinast, but unaffected by milrinone. Moreover, the effect of combination of zaprinast with milrinone was not significantly different from that observed with zaprinast alone. 6 Isoprenaline produced a concentration-dependent vasodilatation in branch PA of guinea-pig which was potentiated by both zaprinast and milrinone, the efficacy of milrinone being greater than zaprinast. 7 These results suggest that both nitrergic and purinergic pathways are involved in mediating the NANC relaxation in branch PA of guinea-pig. The combination of PDE III or V inhibitors with vasorelaxant drugs may be a hopeful approach for the treatment of pulmonary hypertension. [source]

    Sildenafil reduces alcohol-induced gastric damage: just say ,NO'

    BRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2008
    R Duffin
    Although sildenafil (Viagra) and other phosphodiesterase V (PDE V) inhibitors are increasingly recognized for their use in the treatment of male erectile dysfunction and perhaps more recently pulmonary artery hypertension, less is known of their potential beneficial effects in other situations. Medeiros et al., in the current issue of the British Journal of Pharmacology, report that sildenafil dramatically reduces alcohol-induced gastric damage in rats. The authors provide convincing evidence that such protection not only occurs via the nitric oxide (NO)/cGMP pathway, but also involves regulation of ATP-sensitive potassium channels. Therefore, in addition to exerting anti-impotence efficacy, PDE V inhibitors may provide significant beneficial effects from mucosal injury induced by alcohol. British Journal of Pharmacology (2008) 153, 623,624; doi:10.1038/sj.bjp.0707642; published online 17 December 2007 [source]