Table 1

Overview of the compounds mentioned in the review representing the different principles and timings of cerebroprotective therapy in relation to endovascular approaches to improve patient outcomes after ischaemic stroke



Compound
Mechanism of actionStudy referenceTreatment time in relation to recanalisation
Intra-arterial hypothermiaMultifaceted; Suppression of apoptotic pathways and excitotoxicity; Regulation of inflammatory pathways, metabolism and CBF; Upregulation of cell survival pathways. Chamorro et al 20217,
Sahin et al 2010 29
Before
Remote ischaemic conditioningPoorly understood; Repeated, temporary cessation of blood flow to a limb to create ischaemia may trigger self-protective pathways with cerebroprotective effects.Chamorro et al 20217,
Hougaard et al 201420
NerinetideDisruption of postsynaptic density protein 95 protein-protein interactions that would normally lead to cell death caused by excitotoxicity.Hill et al 202021
VerapamilA calcium-channel blocker that perturbs the developing complication of post-ischaemic vasospasm and cell death.Chamorro et al 20217,
Fraser et al 201723
During
Uric acidAntioxidative properties by scavenging reactive oxygen species, reactive nitrogen species, and non-radicals.Chamorro et al 20217
Peritoneal haemodialysisReduction of blood glutamate levels to accelerate brain-to-blood glutamate clearance.Chamorro et al 20217 After
Activated
protein C
Acts on the protease-activated receptor 1 (found on neurons, endothelial cells, pericytes, and astrocytes), promoting anticoagulant and cell-signalling properties.Chamorro et al 20217, Lyden et al 202115
Intra-arterial alteplaseLocal injection of the thrombolytic agent alteplase following recanalisation using thrombectomy.RenĂº et al 202227
  • CBF, cerebral blood flow.