Role of Microvascular Shunts in the Loss of Cerebral Blood Flow Autoregulation

Abstract

Historically, determination of the critical cerebral perfusion pressure (CPP) was done in animals by a progressive lowering of arterial pressure yielding a nominal critical CPP of 60 mmHg. Subsequently, it was shown that if the CPP was decreased by increasing intracranial pressure (ICP), critical CPP fell to 30 mmHg. This discrepancy was unexplained. We recently provided evidence that the decrease in critical CPP was due to microvascular shunting resulting in maintained cerebral blood flow (CBF) at a lower CPP. We demonstrated by a progressive increase in ICP in rats using two-photon laser scanning microscopy (2PLSM) that the transition from capillary to microvascular shunt flow is a pathological process. We surmise that the loss of CBF autoregulation revealed by decreasing arterial pressure occurs by dilation of normal cerebral blood vessels whereas that which occurs by increasing ICP is due to microvascular shunting. Our observations indicate that the loss of CBF autoregulation we observed in brain injured patients that changes on an hourly or daily basis reflects an important pathophysiological process impacting on outcome that remains to be determined.

Association between the variability of cerebral oxygen saturation during cardiopulmonary bypass and delayed postoperative neurocognitive recovery in cardiac valve surgical patients: A pilot study

“…Regional cerebral oxygen saturation (rSO 2 ) readings are thought to reflect the balance between regional oxygen supply and demand and thereby local cerebral metabolism, 1,2 which is increasingly used in cardiac surgery. rSO 2 reduction as a result of local or whole brain ischemia can be explained by insufficient oxygen supply that cannot meet metabolic requirements 3,4 . rSO 2 can reflect changes in blood supply to brain tissue in real time 5 and rapidly assesses tissue oxygenation, and also can be used as an early indicator of potential nerve injury 6 .…”