Temperature
March 30, 2016
Sandra L Hrometz, Jeremy A Ebert, Karen E Grice et al.
Fatal hyperthermia as a result of 3,4-methylenedioxymethamphetamine (MDMA) use involves non-esterified free fatty acids (NEFA) and the activation of mitochondrial uncoupling proteins (UCP). NEFA gain access into skeletal muscle via specific transport proteins, including fatty acid translocase (FAT/CD36). FAT/CD36 expression is known to increase following chronic exercise. Previous studies have...
Toxicology Letters
October 10, 2011
Sandra L Hrometz, Karen Thatcher, Jeremy A Ebert et al.
MDMA (3,4-methylenedioxymethamphetamine) induces thermogenesis in a mitochondrial uncoupling protein 3-dependent manner. There is evidence that this hyperthermia is mediated in part by the lipolytic release of free fatty acids, that subsequently activate uncoupling protein 3 in skeletal muscle mitochondria. We hypothesize that atrial natriuretic peptide (ANP), a strong lipolytic mediator, may...
Critical Care Medicine
June 1, 2005
Jon E. Sprague, Petra Moze, David Caden et al.
75 citations
These data show that alpha1 and beta3-adrenergic receptors may contribute to the mediation of MDMA-induced hyperthermia and that drugs targeting these receptors, such as carvedilol, warrant further investigation as novel therapies for the treatment of psychostimulant-induced hyperthermia and its sequelae.
British Journal of Pharmacology
June 1, 2004
Jon E. Sprague, Robert E. Brutcher, Edward Mills et al.
53 citations
Studies were designed to examine the effects of α 1 ( α 1 AR)‐ plus β 3 ‐adrenoreceptor ( β 3 AR) antagonists on 3,4‐methylenedioxymethamphetamine (MDMA, Ecstasy)‐induced hyperthermia and measures of rhabdomyolysis (creatine kinase (CK)) and renal function (blood urea nitrogen (BUN) and serum creatinine (sCr)) in male Sprague–Dawley rats. MDMA (40 mg kg −1 , s.c.) induced a rapid and robust...