Synaptosomal susceptibility on global ischaemia caused by cardiac arrest correlated with early and late times after recirculation in rats

The aim of the study was to assess the sensitivity of brain synaptosomes and their mitochondria to the effects of global cerebral ischaemia caused by temporary cardiac arrest and the early and late consequences. The effects of 10 min of global ischaemia were measured immediately and after 1 h, 24 h and 7 days post-resuscitation. Ischaemia caused a reduction in oxygen consumption by synaptosomes of about 20%, a drop in ATP/ADP ratio of about 40%, a decrease in CrP/Cr ratio at about 45% and a reduction of synaptic vesicles and disturbances in the mitochondrial structure in isolated synaptosomes and in nerve endings of brain specimens. Morphometric analysis showed that ischaemic conditions caused a decrease in synaptic vesicles by about 61% and an increase of mitochondrial damage to 58 and 50% after 1 and 24 h postreperfusion time, respectively. Seven days postresuscitation, all the observed changes returned to normal but small numbers (about 2%) of neutrones which were destroyed neurons appeared at that time. It is concluded that global ischaemia with early resuscitation after cardiac arrest may lead to damage of synaptosomes and synaptic mitochondria. This, in turn, modifies substrate oxidation, synthesis of energy variables and affects neurotransmitter function. The observed disturbances return to normal later after resuscitation but the ischaemic events and reoxygenation caused selective morphological injury of certain neurones and this may form the basis for irreversible brain damage.