Background Brief ischaemia of one organ protects the heart against a sustained ischaemia-reperfusion insult (Remote ischaemic preconditioning, RIPC). The nature of the signal released from the remote organ and the timing of the triggered changes in the target organs remain controversial. It is not known whether RIPC also alters blood flow in other organs. In this study we investigated the changes in microcirculatory blood flow (MBF) in both hind limbs during RIPC and measured myocardial metabolites (e.g. ATP, AMP and adenosine) after induction of RIPC.
Methods RIPC was induced in C57/Bl6 mice using four cycles of 5 min ischaemia and 5 min reperfusion of the hind limb (experimental limb) using blood pressure cuff. MBF in both RIPC mouse and in control mouse was measured using Laser Doppler Flowmetry throughout the procedure of 50 min. In separate experiment, hearts were excised from RIPC and control mice and extracted for measuring metabolites using HPLC.
Results In control mice (no RIPC application) there was no significant change in MBF in both hind limbs. Inflating blood pressure cuff for 5 min resulted in complete occlusion of MBF in the experimental hind limb. Reperfusion in each cycle of RIPC was associated with a hyperaemic response. In contrast, MBF in the un-cuffed hind limb was reduced during the RIPC cycles. Interestingly, HPLC analysis showed that RIPC causes ischaemic stress (increase AMP/ATP).
Conclusion Our mouse model of RIPC is associated with reduced MBF in the non-conditioned hind limb and metabolic stress in the myocardium. Supported by NIHR BRISTOL BIOMEDICAL RESEARCH UNIT IN CARDIOVASCULAR MEDICINE.
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