2,518 research outputs found

    Mortality From Postoperative Myocardial Infarction in Nonthoracic Surgical Patients at a Community Hospital

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    In a 20-month prospective study, 35 patients with postoperative myocardial infarction were identified. All patients referred to cardiologists by nonthoracic surgeons were evaluated for evidence of postoperative myocardial infarction as defined by symptoms, electrocardiographic changes, and cardiac enzyme elevation. Ten of the 35 patients (29%) subsequently died, seven (20%) from the myocardial infarction. Twenty-five of the 35 patients (71%) had preexisting coronary artery disease. Reported experience with patient mortality following postoperative myocardial infarction varies from 28% to 69%. Our patient mortality rate at 29%, though still substantial, is lower than many current reports. Despite close perioperative surveillance of patients with coronary artery disease, the morbidity and mortality remains unacceptably high. Physicians should routinely evaluate the surgical patient thoroughly for cardiac risk

    Time-Dependent Vascular Effects of Endocannabinoids Mediated by Peroxisome Proliferator-Activated Receptor Gamma (PPARγ)

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    The aim of the present study was to examine whether endocannabinoids cause PPARγ-mediated vascular actions. Functional vascular studies were carried out in rat aortae. Anandamide and N-arachidonoyl-dopamine (NADA), but not palmitoylethanolamide, caused significant vasorelaxation over time (2 hours). Vasorelaxation to NADA, but not anandamide, was inhibited by CB1 receptor antagonism (AM251, 1 μM), and vasorelaxation to both anandamide and NADA was inhibited by PPARγ antagonism (GW9662, 1 μM). Pharmacological inhibition of de novo protein synthesis, nitric oxide synthase, and super oxide dismutase abolished the responses to anandamide and NADA. Removal of the endothelium partly inhibited the vasorelaxant responses to anandamide and NADA. Inhibition of fatty acid amide hydrolase (URB597, 1 μM) inhibited the vasorelaxant response to NADA, but not anandamide. These data indicate that endocannabinoids cause time-dependent, PPARγ-mediated vasorelaxation. Activation of PPARγ in the vasculature may represent a novel mechanism by which endocannabinoids are involved in vascular regulation
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