The pathogenesis of fulminant pulmonary edema in EV71 infection may involve sympathetic overactivation due to medullary destruction, as well as iNOS and nitric oxide.
May implicate autonomic dysregulation and iNOS in EV71 edema pathogenesis; hypothesis-generating, requires prospective validation before clinical consideration.
Pulmonary edema (PE) may occur with enterovirus 71 (EV71) infection. We monitored arterial pressure (AP) and heart rate (HR) in patients with EV71 infection and analyzed the variability of AP and HR. Sympathetic activity, AP, and HR increased with respiratory stress. Thereafter, parasympathetic activity increased with decreases in AP and HR. The lungs showed edema with inducible nitric oxide synthase (iNOS) expression. Destruction of the medial, ventral, and caudal medulla may lead to sympathetic overactivation, causing blood to shift to the lungs. The pathogenesis of PE may also involve iNOS and nitric oxide.
No takes yet. Share an insight, caveat, or question.
Kao et al. (2004) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: