2005
A pilot study indicating that bradykinin B2 receptor antagonism attenuates protamine‐related hypotension after cardiopulmonary bypass
Pretorius M, Scholl FG, McFarlane JA, Murphey LJ, Brown NJ. A pilot study indicating that bradykinin B2 receptor antagonism attenuates protamine‐related hypotension after cardiopulmonary bypass. Clinical Pharmacology & Therapeutics 2005, 78: 477-485. PMID: 16321614, DOI: 10.1016/j.clpt.2005.08.010.Peer-Reviewed Original ResearchConceptsMean arterial pressureSaline solution groupT-PA activityAdministration of protamineCardiopulmonary bypassProtamine administrationHoe 140Receptor antagonismBradykinin concentrationsSolution groupTissue-type plasminogen activator releaseACE inhibitor-treated patientsBradykinin B2 receptor antagonismReceptor antagonist HOE 140Angiotensin-converting enzyme inhibitorB2 receptor antagonismInhibitor-treated patientsElective cardiac surgeryAdult male patientsBradykinin receptor antagonismDegradation of bradykininPlasminogen activator releaseSaline solutionProtamine infusionArterial pressure
2002
Randomized trial of normal saline solution injection versus bipolar electrocoagulation for treatment of patients with high-risk bleeding ulcers: Is local tamponade enough?
Laine L, Estrada R. Randomized trial of normal saline solution injection versus bipolar electrocoagulation for treatment of patients with high-risk bleeding ulcers: Is local tamponade enough? Gastrointestinal Endoscopy 2002, 55: 6-10. PMID: 11756906, DOI: 10.1067/mge.2002.120390.Peer-Reviewed Original ResearchConceptsSaline solution injectionSaline solution groupNormal saline solutionBipolar electrocoagulationLocal tamponadeNonbleeding visible vesselIndependent risk factorSolution injectionSolution groupTreatment of patientsSaline solutionMajor bleedingActive bleedingEndoscopic injectionHospital daysStandard therapyUlcer sizeLack of injuryClinical evidenceVisible vesselRisk factorsEffective treatmentPatientsBleedingUlcers
1998
Anti-C5a monoclonal antibody reduces cardiopulmonary bypass and cardioplegia-induced coronary endothelial dysfunction
Tofukuji M, Stahl G, Agah A, Metais C, Simons M, Sellke F, This study was supported by National Institutes of Health grants HL46716 H. Anti-C5a monoclonal antibody reduces cardiopulmonary bypass and cardioplegia-induced coronary endothelial dysfunction. Journal Of Thoracic And Cardiovascular Surgery 1998, 116: 1060-1068. PMID: 9832699, DOI: 10.1016/s0022-5223(98)70059-5.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalCardiopulmonary BypassChemotaxis, LeukocyteComplement C5aCoronary VesselsEndothelium, VascularFemaleHeart Arrest, InducedHemodynamicsMaleMiceMice, Inbred BALB CMyocardial Reperfusion InjuryNeutrophilsNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIPeroxidaseSwineConceptsEndothelium-dependent relaxationSaline solution groupCardiopulmonary bypassMonoclonal antibodiesCardioplegic reperfusionSolution groupImpaired endothelium-dependent relaxationAnti-C5a monoclonal antibodyCoronary endothelial dysfunctionPolymorphonuclear leukocyte infiltrationLeft ventricular pressureSaline solution vehiclePercent segmental shorteningMonoclonal antibody groupC5a inhibitionEndothelial dysfunctionMyeloperoxidase activityCoronary arteriolesLeukocyte infiltrationSegmental shorteningCoronary arteryHyperkalemic cardioplegiaFunctional preservationVentricular pressureVascular studies
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