Reperfusion injury from a haemodynamic standpoint and role of pressure-controlled reperfusion in avoiding reperfusion injury

Abstract

Currently, there is no established treatment for post-ischaemic reperfusion-related injury, namely reperfusion injury (RI), which paradoxically exacerbates microvascular and tissue damage in any reperfused ischaemic organ territory. During the ischaemic phase, the autoregulatory apparatus in a subtended organ region temporarily loses its pressure-regulating function because of the combined effects of drastically increased oxygen demand and ischaemic insult. Therefore, it cannot protect the hypoxically injured distal capillary bed from the detrimental effect of the sudden and uncontrolled pressure rise that occurs during the initial phase of reperfusion. This acute capillary barotrauma caused by abruptly initiated reperfusion at systemic pressure can be regarded as an iatrogenic trigger for subsequent damage in the reperfused organ territory. From this haemodynamic perspective, RI can be redefined as a ‘capillary hyperpressurization syndrome’, dictated by the ‘initial reperfusion pressure’. Accordingly, initiating reperfusion gently at lower pressures [pressure-controlled reperfusion (PCR)] and maintaining it at that level until protective autoregulatory myogenic control mechanisms recover may provide substantial benefit in limiting the progressive damage caused by post-ischaemic abrupt and full-pressure reperfusion. In this review, we revisit RI from this haemodynamic perspective and suggest that the same pathomechanism—namely, acute exposure of ischaemically injured microvascular endothelium to an uncontrolled pressure rise during the initial reperfusion phase—predominantly dictates post-reperfusion damage in the heart and in other organ ischaemia–reperfusion settings, where PCR techniques may help limit post-reperfusion damage.