Ischemia-Reperfusion Injury in Stroke

Abstract

Despite ongoing advances in stroke imaging and treatment, ischemic and hemorrhagic stroke continue to debilitate patients with devastating outcomes at both the personal and societal levels. While the ultimate goal of therapy in ischemic stroke is geared towards restoration of blood flow, even when mitigation of initial tissue hypoxia is successful, exacerbation of tissue injury may occur in the form of cell death, or alternatively, hemorrhagic transformation of reperfused tissue. Animal models have extensively demonstrated the concept of reperfusion injury at the molecular and cellular levels, yet no study has quantified this effect in stroke patients. These preclinical models have also demonstrated the success of a wide array of neuroprotective strategies at lessening the deleterious effects of reperfusion injury. Serial multimodal imaging may provide a framework for developing therapies for reperfusion injury.

Clinical Impact of Ventilation Duration in Patients with Stroke Undergoing Interventional Treatment under General Anesthesia: The Shorter the Better?

“…7 After revascularization was achieved, normotension (systolic pressure, 110 -130 mm Hg) was restored to reduce the risk of reperfusion injury. 14 After the procedure, patients were extubated in the angiography suite or after postinterventional CT whenever possible. Postacute work-up and treatment were performed in a certified stroke unit or neurologic intensive care unit.…”

Guanosine and its role in neuropathologies

“…Additionally, its therapeutic potential was also observed in response to reperfusion injury in rat models of middle cerebral artery occlusion [102]. Despite the fact that reperfusion is necessary after stroke to restore blood flow, this may also cause further injury in the brain as a result of a complex series of events including glutamate release and excessive ROS generation [150]. Importantly, the mechanisms underlying the neuroprotective activity of guanosine in in vivo models of cerebral ischemia are in agreement with those observed in vitro, involving the modulation of glutamatergic transmission, attenuation of inflammatory parameters, and the induction of an antioxidant response [93,101,151].…”

Hypothermia in Stroke Therapy: Systemic versus Local Application

“…Reperfusion often initiates a detrimental cascade, collectively termed ischemia/reperfusion injury, which can be disastrous; in some animal models, reperfusion after an extended period of ischemia caused larger infarct volumes than if the occlusion had been left permanently [45]. Reperfusion injury is a complex, multifaceted injury cascade initiated by sterile inlammation from anoxic tissue damage, and propagated by both the innate and adaptive immune systems and complement system [75,76].…”