Ischaemia/reperfusion and permanent ischaemia differentially affect haemoglobin properties – Possible influence of oxidative stress and adaptation to acute hypoxia

Le résumé fourni par la source

Cerebral ischaemia is an acute state characterised by a severe decrease in the supply of oxygen (O 2 ) to the brain, resulting in the death of neurons and glial cells. Despite multiple studies investigating the processes that lead to cell damage under ischaemic stroke, there is still a lack of information about the changes in blood properties under various phases of transient ischaemia with restoration of blood flow or under prolonged ischaemia. Blood, as a source of O 2 , might either contribute to the brain damage owing to the development of oxidative stress, or might prevent cell death by the modulation of O 2 bioavailability to cells. Here, we studied hydrogen peroxide (H 2 O 2 ) generation in mitochondria of neurons in vivo using the H 2 O 2 ‐sensitive biosensor HyPer7, and blood properties [haemoglobin (Hb) oxygenation and Hb affinity to O 2 , estimated with Raman microspectroscopy (RS)] in two experimental rat models: transient 60‐min ischaemia induced by the occlusion of the middle cerebral artery (MCAO) followed by 48 h reperfusion, and permanent 48‐h MCAO‐induced ischaemia. We found that an increase in the amount of H 2 O 2 synthesised in neuronal mitochondria under the reperfusion period correlated with a decrease in blood oxygenation level, whereas permanent ischaemia did not affect the amount of oxyhaemoglobin but led to an increase in the affinity of Hb to O 2 . We hypothesise that H 2 O 2 may initiate processes that lead to increased O 2 penetration to the brain tissue under reperfusion, and that increased Hb affinity to O 2 may be an adaptive reaction of the blood system to acute prolonged ischaemia.

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