Does trypanosoma cruzi coax cardiac fibroblasts into preventing cardiomyocyte death by activating nerve growth factor receptor TrkA?
TrkA residing in CFs induces an exuberant NGF production in response to T. cruzi infection, enabling, in a paracrine fashion, myocytes to resist oxidative stress, a leading Chagas cardiomyopathy trigger. Thus, PDNF-TrkA interaction on CFs may be a mechanism orchestrated by T. cruzi to protect its heart habitat, in concert with the long-term (decades) asymptomatic heart parasitism that characterizes Chagas disease. Moreover, as a potent booster of cardioprotective NGF in vivo, PDNF may offer a novel therapeutic opportunity against cardiomyopathies.
Shocks with most current proportioned to the B-pathway had lower defibrillation currents than nonproportioned shocks using both pathways. Thus, defibrillation efficacy was changed by HF proportioning without changing the electrodes or shock waveform. These findings suggest that HF proportioning may be a method to improve defibrillation.