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Unlabelled: Ischaemic preconditioning, with brief periods of ischaemia separated by reperfusion, increases myocardial resistance to infarction. In addition, preconditioning leads to preservation of myocardial adenosine triphosphate (ATP) during ischaemia. We propose that ischaemic preconditioning may share fundamental similarities with intermittent aortic cross-clamping utilised during aorto-coronary bypass surgery. The aim of this study was to test the hypothesis that controlled aortic cross-clamping is a form of preconditioning using conservation of ATP as the end point. Patients randomised to the preconditioned group (preconditioned, n = 10 patients), received a preconditioning stimulus of two 3-min periods of cross-clamping separated by 2 min of reperfusion prior to an ischaemic insult of 10 min ischaemia and ventricular fibrillation. In the control group (control, n = 10 patients) hearts received 10 min cross-clamping with fibrillation without prior preconditioning. Myocardial ATP, creatine phosphate (CP), and lactate were determined from biopsy specimens taken at the onset of cardiopulmonary bypass (A), at the end of preconditioning (B), and at the end of 10 min of ischaemic insult (C)., Results: expressed as mean +/- SE (mumol/g dry weight). Preconditioning resulted in a significant depletion of the myocardial ATP content (preconditioned, B: 11.7 +/- 0.9 vs A: 19.8 +/- 1.4; P < 0.01). Furthermore 10 min of ischaemia resulted in a significant depletion of ATP in the control patients (control, C: 7.2 +/- 0.3 vs B: 19.5 +/- 1.2; P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Objective: One of the mechanisms by which ischaemic preconditioning is thought to protect against later prolonged ischaemia is via a reduction in ATP utilisation during ischaemia. The ATP "wastage" that occurs during ischaemia is thought to be due to mitochondrial ATPase activity, which may be prevented in ischaemic preconditioning by the binding of a specific inhibitor protein. As the rat is known to have less inhibitor protein than other species, this study was designed to determine whether the rat heart could be ischaemically preconditioned., Methods: Rats were anaesthetised with pentobarbitone, the chest opened and the hearts ischaemically preconditioned with a 5 min occlusion of the left main coronary artery followed by 10 min reperfusion. The hearts were then subjected to a 45 min occlusion followed by 3 h reperfusion. Control hearts were treated identically but without ischaemic preconditioning. Infarct size was measured using triphenyl tetrazolium and expressed as a percentage of the region at risk, measured with fluorescent particles., Results: Infarct size as a percent of the risk area in the ischaemically preconditioned group (n = 8) was 31.4(SEM 6.1)%, versus 61.0(4.8)% in control hearts (n = 8) (p < 0.005)., Conclusions: These results show that rat hearts can be ischaemically preconditioned and suggest that the protective mechanism involved in this phenomenon is not mediated through the endogenous inhibition of mitochondrial ATPase. An overall reduction in mitochondrial ATP "wastage" may not be the sole mechanism in the protection seen in ischaemic preconditioning.