Table 1.
An overview of hypoxic-ischemic and ischemic models in immature rats.
| Model | Rat strain | Age | Experimental procedure | Histological changes and outcomes | References |
|---|---|---|---|---|---|
| Hypoxia-Ischemia (HI) | SD or Wistar | P6-P7 | CCAL (left or right) + hypoxia (FiO2 8%) | Damage in the IL hemisphere (cortex, WM, striatum, hippocampus, thalamus, basal ganglia)—Scoring of the lesion (MAP2 loss: 86% at 24 h) Columnar cell death in the cortex, necrosis and apoptosis—Sexual dimorphism Cystic cavitation at 2 weeks |
(1, 30–32) |
| Hypoxia-Ischemia (HI) | Wistar | P12 | Right CCAL + hypoxia (FiO2 8%) | Seizure occurrence—damage [48–80%] | (26) |
| Ischemia-reperfusion (IR) | Wistar | P7 | pMCAO + transient CCAo (left CCA or both CCA) |
Damage in the IL hemisphere (cortex, WM, head of the caudate putamen)—Lesion volume at 48 h of recovery: 17 ± 10% of the IL hemisphere. Mortality: between 5 and 10% Columnar cell death in the cortex and apoptosis—Sexual dimorphism Bursts and seizures occurrence Cystic cavitation at 1 month |
(12, 15, 19, 20, 22, 24) |
| Ischemia-reperfusion | SD | P12 | pMCAO + transient left CCAo | Damage in the IL hemisphere—both apoptosis and autophagy in different neurons | (62, 63) |
| Ischemia-reperfusion | SD | P7 P10 | Transient MCAo (tfMCAo) (endovascular model) |
Damage in the IL hemisphere (cortex and subcortical areas- caudate nucleus)—Lesion volume at 24 h of recovery: 34 ± 10% of the IL hemisphere. Mortality: <15% | (13, 14) |
SD, Sprague-Dawley; CCAL, common carotid artery ligation; CCAo, CCA occlusion; pMCAo, permanent middle cerebral artery occlusion; tfMCAo, transient filament MCAo; IL, ipsilateral; WM, white matter.