BIOHEART E-JOURNAL
BIOMOLECULAR AND BIOCHEMICAL RESPONSE OF MYOCARDIAL CELL TO ISCHEMIA AND
REPERFUSION IN COURSE OF HEART SURGERY
G.G.Corbucci
Inst. of Anaesthesia – Resuscitation University of Cagliari – Italy
Summary
Objective: Previous studies have
shown that biomolecular and biochemical adaptive changes antagonize oxidative damage due
to hypoxia and ischemia in myocardial cell. Aim of our study was to verify in human
ischemic and reperfused cardiac tissue the relationship between the mitochondrial enzyme
activities and the activation of HSP70 and c-fos synthesies in the context of a
cytoprotective mechanism. Nitric oxide (NO) modulating effects on mitochondrial
respiratory chain enzyme activities in ischemic and reperfused tissue were investigated
(preliminary report).
Methods: During elective coronary
artery bypass grafting, in 30 consecutive patients ventricle samples were taken one before
aortic clamping the second after 55± 8 min. ischemic period and the third 34± 5 after
final reperfusion. Coronary sinus blood samples were taken in parallel to assess free
radical release measured by malonaldehyde (MDA) levels. In a small number of patients
(N=5) nitric oxide tissue levels were analyzed.
Results: When compared with
normoxic tissue, a significant decrease in cytochrome coxidase (COX) and succinate Cyt-c
reductase (SCR) activities in ischemic and reperfused samples were observed. The
activation of HSP70-72 and c-fos transcription factor was evident in courses of ischemia
and reperfusion. Blood MDA levels undeline the concept that oxyradical generation
characterize the peroxidative damage in reoxygenated myocardial tissue while adaptive
changes which occur in ischemic cell seem antagonize the oxyradical injury.
Conclusions: In course of heart
surgery the myocardial cell seems to prevent the ischemic damage activating some peculiar
biomolecular and biochemical adaptive changes which permit the reversibility of the
oxidative injury. In contrast appears evident that massive and rapid reoxygenation of the
cardiac tissue leads to a peroxidative damage due to oxyradical generation. The nitric
oxide seems to play a crucial role in the cellular adaptation to ischemia even if further
studies will be needed to elucidate these findings.
From the data obtained in this work we
cannot draw certain conclusions in terms of human cardiac cell adaptation to ischemia
whereas it seems convincible that reoxygenation, as actually employed in clinical
practice, compromise the integrity of the cells.
KEY WORDS: [Ischemia/Reperfusion -
Mitochondria – Heat Shock Proteins - Nitric Oxide.]
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