Aims: Numerous studies suggested that cardiopulmonary bypass (CPB) induces a systemic inflammatory
response and subsequent myocardial and vascular dysfunction. However, it remains unclear
how far CPB itself or subsequent cardioplegic arrest (CA) and reperfusion are responsible
for these changes.
Methods: Three groups of dogs (n=12/each) were studied: group 1 underwent 90 minutes CPB with
60 minutes of crystalloid CA, group 2 underwent 90 minutes CPB without CA and group
3 served as control without CPB. The slope (Ees) of the end-systolic pressure-volume
relationship was determined before and 60 minutes after CPB. Relaxation response of
the coronaries isolated at the end of the experiments was examined. Plasma myeloperoxydase
and malonaldehyde as indices of neutrophil activation and free radical generation
were measured.
Results: While Ees decreased significantly in group 1 (58±8% of baseline, p<0.05) it remained
unchanged in group 2 and 3 (96±8% and 101±11%). Response to acethylcholne was attenuated
in group 1 in comparison to group 2 and 3 (70±7% vs. 86±2% vs. 83±4%, p<0.05). Both
myeloperoxydase and malonaldehyde showed an approximately 3-fold increase in group
1 and 2 during CPB which however did not reach the level of significance. In group
1 a further doubling of myeloperoxidase and malonadehyde could be observed (p<0.05),
while the values resolved at baseline level in group 2.
Conclusions: CPB alone leads to a transient and spontaneously reversible inflammatory response
which however does not impair myocardial and vascular function. Concomitant CA and
reperfusion are mainly responsible for declined cardiovascular function and prolonged
systemic inflammation.
