Ischaemic preconditioning is not dependent on neutrophils or glycolytic substrate at reperfusion in rabbit heart

The aim was to determine whether reperfusion with either neutrophil free reperfusate or perfusate containing only pyruvate as the metabolic substrate would alter the protection against infarction afforded by preconditioning.

Rabbit hearts (n = 4-14 per group) underwent 30 minutes of regional ischaemia followed by 120 minutes of reperfusion. Blood reperfused groups experienced both ischaemia and reperfusion in situ while Krebs reperfused groups experienced regional ischaemia in situ but were reperfused with Krebs buffer in vitro. In another group, glucose in Krebs buffer was replaced by pyruvate.

Preconditioning with 5 minutes regional ischaemia caused smaller infarct size in the blood reperfused hearts: 43.0(SEM 5.4)% v 8.8(4.2)%. In Krebs reperfused hearts, preconditioning caused a similar reduction of infarct size [49.9(2.5)% v 22.9(4.3)%] which was not different from that seen in the blood reperfused hearts. Replacing the glucose in the Krebs buffer by pyruvate also had no effect on infarct size in either the control or the preconditioned hearts [40.9(6.1)% v 11.8(5.2)%]. Histology of the ischaemic zones revealed 59.6(15.0) neutrophils per 10 high power fields in hearts reperfused in situ but only 2.6(0.6) in Krebs reperfused hearts, equal to the numbers in nonischemic blood perfused myocardium [2.8(0.9)].

The mechanism of preconditioning is not due to attenuation of neutrophil function during reperfusion. Furthermore, substituting pyruvate for glucose in the reperfusate did not prevent the protection against infarction afforded by ischaemic preconditioning.