Brief exposure to exogenous testosterone increases death signaling and adversely affects myocardial function after ischemia

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Publisher: American Physiological Society
Document Type: Author abstract
Length: 230 words
Lexile Measure: 60L

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Abstract :

Chronic endogenous testosterone exposure adversely affects proinflammatory and proapoptotic signaling after ischemia/reperfusion; however, it remains unknown whether a single acute testosterone exposure is equally detrimental. We hypothesized that acute exogenous testosterone infusion before ischemia would worsen myocardial functional recovery, increase the activation of MAPKs and caspase-3, and increase myocardial proinflammatory cytokine production. To study this, isolated-perfused rat hearts (Langendorff) from adult females and castrated males were subjected to 25-min ischemia and 40-min reperfusion with and without acute testosterone infusion (17[beta]-hydroxy-4-androstenone, 10 ng*[ml.sup.-1]*[min.sup.-1]) before ischemia. Myocardial contractile function was continuously recorded. After ischemia/reperfusion, hearts were assessed for levels of testosterone (ELISA), expression of proinflammatory cytokines (ELISA), and activation of MAPKs and caspase-3 (Western blot analysis). Data were analyzed with two-way ANOVA or Student's t-test; P myocardial infarction; sex hormones; inflammation

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Gale Document Number: GALE|A146383241