12 research outputs found
How to give an impulse to women's health care seeking through popular theatre? Experience of Mopti health district on tuberculosis control in Mali
FLWINinfo:eu-repo/semantics/publishedSupplement ;Abstract-No: A-039-0078-00756The Abstracts of the 5th European Congress on Tropical Medicine and International Health 24–28 May 2007 Amsterdam, the Netherland
TCT-653 An Intracoronary Near-infrared Spectroscopy Signature of Culprit Lesions in Non-ST-Segment Elevation Myocardial Infarction
TCT-108 Initial Clinical Experience Performing Robotic Percutaneous Coronary Intervention from the Radial Approach
TCT-401 Detection by Intracoronary Near-infrared Spectroscopy of Lipid-rich Plaques within Remotely Implanted Stents
TCT-653 An Intracoronary Near-infrared Spectroscopy Signature of Culprit Lesions in Non-ST-Segment Elevation Myocardial Infarction
TCT-660 Multicenter Validation of a Near-infrared Spectroscopic Signature of Culprit Lesions Causing ST-segment Elevation Myocardial Infarction: The NIRSTEMI II Study
Addressing Darwin's dilemma: Can pseudo‐overdominance explain persistent inbreeding depression and load?
Expression of Fas Ligand and CTLA4 in Adenoids Has a Predictive Value for Allergic Rhinitis Development in Children
Involvement of Kallikrein-Kinin System on Cardiopulmonary Alterations and Inflammatory Response Induced by Purified Aah I Toxin from Scorpion Venom
International audienceBradykinins are released from kininogen by kallikrein. They increase capillary lung permeability after their binding to β1 and especially β2 receptors before being metabolized by kininase enzyme. This study was performed to evaluate cardiopulmonary damages and inflammatory response on injected rats with Aah I toxin of scorpion venom and the involvement of Kallikrein-Kinin system in this pathogenesis. Obtained results revealed that Aah I toxin induces inflammatory cell infiltration accompanied by cellular peroxidase activities, a release of cytokine levels, pulmonary and myocardial damage, with altered metabolic activities and imbalanced redox status. Administration of aprotinin (bradykinin inhibitor) and especially icatibant (bradykinin β2 receptor antagonist) seemed to be able to protect animals against the toxicity of Aah I; nevertheless, the use of captopril (kininase II inhibitor) reduced partially some cardiac disorders. These findings indicate that the kallikrein-kinin system may contribute to the physiopathological effect and lung edema formation induced by toxin, which suggests a potential use of drugs with significant anti-kinin properties