Fumito IchinoseDepartment of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA, USA F1000 Faculty Member (since 19 April 2010)
Associate Professor, Harvard Medical School
The broad long-term goal of my research program is to elucidate the role of NO-cGMP signaling in cardiovascular injury associated with systemic inflammation and ischemia-reperfusion.
While NOS3 is widely expressed in the cardiovascular system and importantly contributes to its homeostasis, the role of NOS3 in myocardial dysfunction of sepsis is incompletely understood. Understanding how NO modulates LV function, particularly the role of NOS3, may elucidate novel targets for the prevention and treatment of inflammatory LV dysfunction.
In the past several years, studying NOS2 (inducible NO synthase) deficiency and a highly selective inhibitor of NOS2 dimerization, we reported NOS2 deficiency protected against endotoxin-induced myocardial dysfunction.
Along these lines, we have recently found a previously unrecognized protective role of NOS3 (endothelial NOS) in the sepsis-induced myocardial dysfunction while studying cardiac myocyte-specific overexpression of NOS3.
One of the most extreme examples of ischemia and reperfusion injury is that associated with cardiac arrest and subsequent cardiopulmonary resuscitation (CPR). It is estimated that 335,000 people die suddenly each year due to a cardiac arrhythmia (most often ventricular fibrillation).
Despite advances in resuscitation methods, including therapeutic hypothermia, CPR is frequently unsuccessful, at least in part, due to cardiovascular dysfunction. Recently, we initiated a research program to evaluate the role of NO/NOS3 in cardiac arrest/CPR-induced cardiac dysfunction. We are examining the protective role of NOS3 and NO on cardiac and neurological function after cardiac arrest and CPR.
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