Hyperglycemia, diabetes and stroke: focus on the cerebrovasculature

Abstract

Acute ischemic stroke (AIS) results from the occlusion of an artery and causes vascular and neuronal damage, both of which affect the extent of ischemic injury and stroke outcome. Despite extensive efforts, there is only one effective treatment for AIS. Given that up to 40% of the AIS patients present with admission hyperglycemia either as a result of diabetes or acute stress response, targets for neuronal and vascular protection under hyperglycemic conditions need to be better defined. Here, we review the impact of diabetes and acute hyperglycemia on experimental stroke with an emphasis on cerebrovasculature structure and function. The relevance to clinical evidence is also discussed.

Figure. Consequences of chronic and acute hyperglycemia-mediated changes in cerebral resistance artery structure and function on ischemic brain injury

Moderate diabetes promotes neovascularization, remodeling and increases in vascular tone limiting cerebral perfusion. Resulting hypoxia and/or metabolic changes mediate ischemic tolerance via neuronal preconditioning but decreases vascular ischemic tolerance leading to increased and accelerated HT development and edema in the event of an ischemic event. Acute hyperglycemia also increases vascular tone and disrupts vascular integrity but in the absence of sufficient time to stimulate adaptive protective mechanisms, the magnitude of neuronal damage is greater.