Table 3.

Cohorts in which microvascular abnormalities were examined after SAH

	Species	SAH method	Time after SAH (days)	Microvascular abnormality	Tissue assessment	Distribution	Refs.
Microthrombi	Mouse	PCI	2	Fibrinogen (+) arteriolesa	IHC	Cortex, hippocampus	[42]
	Mouse	PCI	2	Fibrinogen (+) parenchymal microvesselsa	IHC	Cortex, hippocampus	[41]
	Mouse	PCI	2	Fibrinogen (+) parenchymal microvessel	IHC	Cortex, hippocampus	[39]
	Mouse	EVP	1, 2, 3, 4	Antithrombin (+) parenchymal microvessels	IHC	Cortex	[47]
	Rat	PCI	7	Fibrinogen (+) parenchymal microvessels, microclot on H&E	H&E	Cortex, cerebellum	[66]
	Dog	CMI	14	Fibrinogen (+) parenchymal microvesselsa	IHC	Cortex	[122]
Constriction	Mouse	PCI	2	Parenchymal arteriole diameter 35% smaller than controls	EM	Cortex	[39]
	Mouse	EVP	1, 3	Pial arteriole diameter 10% smaller than controls at both time points	OCT	Cortex	[14]
	Mouse	CMI	6 h	Pial artery diameter 15–20% smaller than controls	2P	Cortex	[37]
				Parenchymal arteriole diameter 28–42% smaller than controls
	Mouse	CMI	2	Pial arteriole diameter 14% smaller than controls	2P	Cortex	[38]
	Dog	CMI	3, 7, 14	Parenchymal arteriole diameter 40% smaller than controls on days 3, 7	EM, EVG	Cortex	[116]

Cohorts are sorted by microvascular abnormality, followed by species and SAH method

^aNo comparison to a sham control group

CMI cisterna magna blood injection ×1–3, EM electron microscopy, EVG elastic van Gieson stain, EVP endovascular perforation of internal carotid artery terminus, H&E hematoxylin–eosin staining, IHC immunohistochemistry, OCT optical coherence tomography-based microangiography, PCI prechiasmatic blood injection, SAH subarachnoid hemorrhage, 2P two-photon microscopy