Publications by authors named "Graham Slaughter"

Post-infarct remodeling is associated with the upregulation of the receptor for advanced glycation end products (RAGE), the induction of its ligand the calcium binding protein S100B and the release of the potent endothelial-cell specific mitogen vascular endothelial growth factor (VEGF). To determine a possible functional interaction between S100B, RAGE and VEGF we stimulated rat neonatal cardiac myocyte cultures transfected with either RAGE or a dominant-negative cytoplasmic deletion mutant of RAGE with S100B for 48 h. Under baseline conditions, cardiac myocytes express low levels of RAGE and VEGF and secrete VEGF in the medium as measured by ELISA.

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Hyaluronan (HA) degradation fragments have been linked to inflammation in a wide range of lung diseases. In idiopathic pulmonary arterial hypertension, HA accumulation has been associated with advanced disease. In this study, we investigated the potential role of HA degradation in the early stages of disease by examining HA distribution, molecular mass, synthesis, and enzymatic degradation at different stages of disease progression in a rat model of monocrotaline (MCT)-induced pulmonary hypertension (PH).

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Objectives: Current guidelines suggest that most patients who present to an emergency department (ED) with chest pain should be placed on a continuous electrocardiographic monitoring (CEM) device. We evaluated the utility of CEM in ED patients with chest pain.

Methods: We enrolled stable patients who presented to a single ED with chest pain suspected to be ischemic in origin and who were placed on CEM.

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Study Objective: We estimate the effect of emergency department (ED) crowding on door-to-needle time for patients given intravenous thrombolysis for suspected acute myocardial infarction.

Methods: This was a retrospective observational study of patients thrombolyzed in the ED for suspected acute myocardial infarction in 1998 to 2000 in 25 community and teaching hospital EDs in Ontario. EDs located close together and sharing a common ambulance diversion system were grouped into networks consisting of 2 to 5 hospitals each.

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Apoptosis is involved in ventricular remodeling after myocardial infarction (MI). We investigated the effects of the vasopeptidase inhibitor (VPI) omapatrilat on cardiomyocyte apoptosis and compared it to the angiotensin converting enzyme inhibitor (ACEI) captopril in the rat post-MI model and in cultured neonatal rat cardiomyocytes. Wistar males rats surviving 4 h post-MI were assigned to omapatrilat (40 or 80 mg/kg/day), captopril (160 mg/kg/day) or no treatment.

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