The effects of hyperglycemia on brain physiology in a healthy and injured state: An experimental pig study with state-of-the-art multimodal neuromonitoring.

Although hyperglycemia is associated with worse outcome following acute brain injury, the pathomechanisms remain elusive. In this experimental pig study, we explored the effects of hyperglycemia on brain physiology. Six pigs were anesthetized and received multimodal neuromonitoring of intracranial pressure (ICP), cerebral perfusion pressure (CPP), cerebral autoregulatory metrics (PRx, CBFx, ORx, and with transfer function analysis), cerebral blood flow (CBF), partial brain tissue oxygenation (pbtO2), and cerebral microdialysis (MD). The effect of hyperglycemia was studied in the healthy brain after injection of intravenous glucose injections, which increased MD-glucose, while ICP, CPP, PRx, CBFx, ORx pbtO2, and cerebral energy metabolism remained unchanged. After normalization of arterial glucose, an intracranial balloon was inflated to increase ICP, followed by an intravenous glucose injection to study the effect of hyperglycemia in the injured brain. The latter induced a significant CBF elevation, but no changes in PRx, pbtO2, or cerebral energy metabolism (but a trend towards higher glucose). Hyperglycemia led to favorable short-term effects on cerebral physiology and the immediate increase in arterial glucose that usually follows acute brain injury may be physiologically neuroprotective and the detrimental role of hyperglycemia is more likely related to cellular and molecular pathophysiological mechanisms or merely a confounder.