Oxidative stress plays an important role in neuronal
injuries after
cardiac arrest. Increased production of
carbon monoxide (CO) by the
enzyme hemeoxygenase (HO) in the brain is induced by the oxidative stress. HO is present in the CNS in two
isoforms, namely the inducible HO-1 and the constitutive HO-2. Elevated levels of serum HO-1 occurs in
cardiac arrest patients and upregulation of HO-1 in
cardiac arrest is seen in the neurons. However, the role of HO-2 in
cardiac arrest is not well known. In this review involvement of HO-1 and HO-2
enzymes in the porcine brain following
cardiac arrest and
resuscitation is discussed based on our own observations. In addition, neuroprotective role of
methylene blue- an
antioxidant dye on alterations in HO under in
cardiac arrest is also presented. The biochemical findings of HO-1 and HO-2
enzymes using ELISA were further confirmed by immunocytochemical approach to localize selective regional alterations in
cardiac arrest. Our observations are the first to show that
cardiac arrest followed by successful
cardiopulmonary resuscitation results in significant alteration in cerebral concentrations of HO-1 and HO-2 levels indicating a prominent role of CO in brain pathology and
methylene blue during
CPR followed by
induced hypothermia leading to superior neuroprotection after return of spontaneous circulation (ROSC), not reported earlier.