Plasma hypoxanthine levels during crystalloid and blood cardioplegias: Warm blood cardioplegia increases hypoxanthine levels with a greater risk of oxidative stress
Gj. Quinlan et al., Plasma hypoxanthine levels during crystalloid and blood cardioplegias: Warm blood cardioplegia increases hypoxanthine levels with a greater risk of oxidative stress, J CARD SURG, 40(1), 1999, pp. 65-69
Background. Patients undergoing cardiopulmonary bypass (CPB) are subjected
to severe oxidative stress, and frequently show evidence of acute lung inju
ry post surgery. Associations between acute lung injury, oxidative stress,
and aberrant ATP catabolism have been made and prompted us to consider whet
her the purine metabolites xanthine and hypoxanthine alter significantly du
ring CPB when different types of cardioplegia are used.
Methods. Experimental design: retrospective follow up study on stored plasm
a samples from patients randomly selected to receive either warm blood, col
d blood, or crystalloid cardioplegia. Setting: adult intensive care unit of
post graduate teaching hospital. Patients: thirty-eight patients undergoin
g aortic valve replacement, with or without artery grafting. Operation was
carried out by a single surgeon. Interventions: all patients received eithe
r a homograft aortic valve or a stentless porcine valve.
Results. No significant differences in xanthine levels at any time points d
uring CPB, or between the different cardioplegic groups. Hypoxanthine level
s were, however, significantly higher in patients receiving warm blood card
ioplegia (74.84+/-16.715 mu M, p=0.0151), and was most marked at time point
3 when the aortic cross clamp was released. Patients receiving crystalloid
cardioplegia showed higher levels of hypoxanthine (44.56+/-10.16 mu M) tha
n those receiving cold blood cardioplegia (21.57+/-7.106 mu M).
Conclusions. Considering these data together, it suggests that aberrant ATP
catabolism, characteristic of ischaemia/reperfusion, is further disturbed
during warm blood cardioplegia leading to a marked increase in plasma hypox
anthine levels. This has the potential to further increase oxidative stress
during CPB.