TABLE 2.

The pathophysiological characteristics of stroke models

Stroke models	Common processes	Special characteristics
Ischemic stroke
Global ischemic stroke
4‐VO model	Energy failure, elevated intracellular Ca2+ level, excitotoxicity, spreading depressions, generation of free radicals, destruction of the blood‐brain barrier, inflammation, glial cell contribution, apoptosis, and necrosis	Biphasic changes in the brain edema and scavenging activity of superoxide
2‐VO model		Permanent 2‐VO model shows three phases of CBF changes Permanent 2‐VO model does not show BBB destruction
Complete global brain ischemia
Aorta/vena cava occlusion models		Purkinje cells and the CA1 pyramidal cells induced by CGBI consists of two phases, and the reversible change in the early phase is related to the decrease of the synaptic vesicles
Ventricular fibrillation cardiac arrest		A VF of 5‐7 min could be easily recovered with resuscitation, while VF for 10 and 12 min often cannot be recovered Significant ischemic cell changes (eosinophilic cytoplasm, dark‐staining triangular shaped nuclei, and eosinophilic‐staining nucleolus) in CA1 hippocampus can be observed at seven days of resuscitation
Chemical and gas hypoxia
Focal ischemic stroke
Transcranial occlusion	Energy failure, elevated intracellular Ca2+ level, excitotoxicity, spreading depressions, generation of free radicals, destruction of the blood‐brain barrier (BBB), inflammation, glial cell contribution, apoptosis, necrosis	Leakage of cerebrospinal fluid; one‐sided blindness
Endovascular filament occlusion		Spontaneous hyperthermia; unavoidable harm to the endothelial lining could alter vascular reactivity and BBB permeability
Embolic occlusion
Thromboembolic occlusion		Unreliable infarctions and variable neurologic deficits; mainly to investigate thrombolytic processes Autologous blood clots of experimental animals are resistant to human rt‐PA
Artificial spheres occlusion		Microsphere embolization produces relatively variable infarcts Macrosphere embolization model provides focal cerebral infarcts similar to intraluminal suture occlusion but avoids hypothalamic injury and hyperthermia
Endothelin‐1 (ET‐1) occlusion		Vasoconstriction; ET‐1 plays a role not only in local control of cerebral vascular tone but also in neural transmission/modulation. endothelin‐converting enzymes and endothelin receptor B are expressed in neurons and astrocytes, and regulated by nerve injury
Photothrombosis model		Photooxygenation leads to endothelial damage and platelet adhesion, and aggregation to form thrombi to block cerebral vessels Classic photothrombotic stroke has poor responses to rt‐PA‐mediated thrombolysis
Intracerebral hemorrhage
Whole blood injection model	Hematoma enlargement, coagulation cascade activation and clot retraction, red blood cells lysis and infusion of hemoglobin, brain edema, necrosis and apoptosis, CBF reduction, inflammation	Mimics the hematoma mass effect and blood toxicity; involves no rupturing of cerebral vessels; no activation of bleeding and coagulation cascade
Collagenase model		Mimics bleeding; degrades collagen IV in the basal lamina of the blood‐brain barrier; rupture of small vessels and capillary beds around the injection site. Bacterial collagenase exacerbates the inflammatory response