Spontaneous hypothermia is not able to completely counteract cardiac arrest-induced mitochondrial impairment in the rat heart.

Vijlbrief et al. [Neonatology 2012;102:243-248] reported a beneficial effect of hypothermia on cardiac function after perinatal asphyxia indicated by low levels of B-type natriuretic peptide (BNP). Elevated troponin I plasma levels, however, reflects impairment of cardiomyocytes under hypothermic conditions. The importance of BNP and cardiac troponin I as biomarkers of cardiac dysfunction that may supplement or substitute Doppler echocardiography has been outlined. Using an asphyxia cardiac arrest (ACA) animal model under spontaneous hypothermia, we found a decrease in the activities of NADH-cytochrome c-oxidoreductase and succinate-cytochrome c-oxidoreductase in comparison to normothermic sham-operated controls. This observation indicates the impairment of the respiratory chain of heart mitochondria, which is accompanied by morphological changes in these mitochondria. Changed cardiac troponin I levels and respiratory chain complexes activity represent different but corresponding steps within the process of cardiomyocyte injury. Interestingly, liver and brain mitochondria remained unchanged under this condition. Patients could benefit from the control of mitochondrial function during hypothermic intervention. When indicated, substances could be supplemented that support mitochondrial function, e.g. antioxidative-acting vitamins and ubiquinone.