Nitrosative Stress as a Modulator of Inflammatory Change in a Model of Takotsubo Syndrome

Summary Previous studies have shown that patients with Takotsubo syndrome(TS) have supranormal nitric oxide signaling, and post-mortem studies of TS heart samples revealed nitrosativestress. Therefore, we first showed in a female rat model that isoproterenol induces TS-like echocardiographic changes, evidence of nitrosativestress, and consequent activation of the energy-depleting enzyme poly(ADP-ribose) polymerase-1. We subsequently showed that pre-treatment with an inhibitor of poly(ADP-ribose) polymerase-1 ameliorated contractile abnormalities. These findings thus add to previous reports of aberrant β-adrenoceptor signaling (coupled with nitric oxide synthaseactivation) to elucidate mechanisms of impaired cardiac function in TS and point to potential methodsof treatment.