Blood cardioplegia increases plasma iron overload and thiol levels during cardiopulmonary bypass

Cardiopulmonary bypass and crossclamping of the ascending aorta introduce two well-characterized phases of oxidative stress, namely, the extracorporeal circulation of blood and the reoxygenation of ischemic tissue. A feature of both forms of stress is the release of reactive and damaging oxygen species.

Forty-seven patients undergoing aortic valve replacement received either cold crystalloid, cold blood, or warm blood cardioplegia. Plasma thiol levels were measured in all groups before and during bypass. All cardiopulmonary bypass patients had, before going onto bypass, low plasma thiol levels (3.80 +/- 0.22 nmol/mg protein) compared with normal healthy controls (5.48 +/- 0.14 nmol/mg protein).

Thiol values remained low throughout bypass in patients receiving cold crystalloid cardioplegia, but rose in patients receiving cold blood cardioplegia, and rose even more in patients receiving warm blood cardioplegia to reach normal plasma values. During cardiopulmonary bypass it has previously been reported that plasma transferrin can become fully saturated with iron and cause transient iron overload. Two patients (13%) receiving cold crystalloid cardioplegia went into plasma iron overload, whereas 18% receiving cold blood and 27% receiving warm blood cardioplegia showed plasma iron overload.

We suggest that blood cardioplegia provides an additional source of thiols as well as a source of reactive iron. However, the reactive iron and thiol-containing molecules have the potential to interact and exacerbate oxidative stress, already a feature of bypass. Control of reactive iron by chelation may be strongly indicated when blood cardioplegia is used.