Aims: 

Cerebral ischaemia/reperfusion (I/R) injury results in mitochondrial dysfunction, decreased ATP production, inflammation and increased production of reactive oxygen species. The aim of our study was to examine biochemical changes in brain and their effects on heart mitochondria in a rat model of I/R injury.

Methods: 

Transient cerebral ischaemia was induced by our minimally invasive transmanubrial approach for the occlusion of brachiocephalic trunk and left common carotid artery. After 8-days of reperfusion, brain and heart were removed for polarographic mitochondrial respiratory chain analyses. Endogenous antioxidants were determined by HPLC, markers of brain inflammation by ELISA. Immunophenotypic analysis of peripheral blood leukocytes and expression of adhesion molecules were examined by flow cytometry.

Results: 

After 20min of ischaemia and 8-days of reperfusion, there was decrease in the respiratory control ratio (RCR, P < 0.001), decrease in the oxygen uptake stimulated by ADP (QO2S3, P < 0.001) and decrease in the rate of ATP production (OPR, P < 0.001) of the brain and heart mitochondria. Concentration of the a-tocopherol decreased by 31% and concentration of proinflammatory cytokine TNF-a increased by 38% (P < 0.01) in brain mitochondria. Expression of adhesion molecule CD11b increased by 26% (P < 0.001) and expression of marker MHC II by 21% (P < 0.05) in peripheral blood lymphocytes.

Conclusion: 

The results demonstrated mitochondrial dysfunction and inflammatory reactions in rat brain after acute ischaemia and reperfusion. We suppose that inflammatory toxic products and immune response might contribute to the mitochondrial dysfunction detected in the heart as a secondary target organ. Supported by APVV-21-022004.