Table 2.

An overview of inflammatory responses in ischemic and hypoxic-ischemic models in the P7 rat.

Cellular compartment and cell type		Stroke			Hypoxia-ischemia
		Model	Responses	References	Responses	References
Neurovascular unit	BBB	pMCAo+tCCAo	Early T2WI—IgG extravasation [2–72 h]	(19, 20, 72)	Early IgG extravasation (6 h) and intense extravasation at 24 h	(69)
		tfMCAo	Low Evans Blue extravasation and dextran restricted to blood vessels at 24 h—Tight junctions preserved	(67)
	Mast cells	pMCAo+tCCAo	Increase 2–12 h with histamine Degranulation [12–48 h]	(82)	Early increase 0 to 48 h with TNF-α Cromolyn reduced damage and glial activation	(83, 84)
	Microglia	pMCAo+tCCAo	Increase in the WM [24–72 h] Increase in the cortex [72 h−2 w] and Bcl2+ at 72 h Ameboid [96 h−14 d] and phagocytosis	(18, 72)	Increase [4–24 h] M1 phenotype (3–24 h) M2 phenotype (24 h)	(83, 80)
		tfMCAo	Limited phagocytosis Endogenous protection (depletion of microglia exacerbates injury) Increase [24–72 h] core and penumbra	(78, 14)
	Macrophages	pMCAo+tCCAo	24 h in the WM (migration along the corpus callosum)	(48, 72)	N.E
		tfMCAo	Increase [4–24 h]	(14)
	Granulocytes	pMCAo+tCCAo	From 24 h to 7 days—Peak at 72–96 h	(72)	N.E
		tfMCAo	N.E
Parenchyma	Astrocytes	pMCAo+tCCAo	Increase [24–48 h] Reactive [48 h−7 d] GFAP-TUNEL+ [6–72 h] and GFAP-Bax+ [14–1 m] Clasmatodendrosis [14 d−1 m]	(22, 71, 72)	Increase [4–24 h]	(83)
		tfMCAo	Reactive astrocytes [24–72 h]	(14)

T2WI, T2-weighted images; h, hour; d, day; m, month; w, week; N.E., Not extensively evaluated.