Inflammation, Cerebral Vasospasm, and Evolving Theories of Delayed Cerebral Ischemia

Table 3

Recent studies have shown improvements in clinical and experimental vasospasm with the use of other various pharmacological additives.

Recent assessments of potential treatments for vasospasm after SAH
Author (year)	Intervention	Parameter altered/assessed	Model	Findings
Meyers and Connolly (2011) [119]	Endothelial receptor antagonist	Delayed ischemic neurological decline	Human	Endothelial receptor antagonists (Clazosentan) have no effect on vasospasm related morbidity and mortality
Fathi et al. (2011) [89]	Sodium nitrate	Arterial diameter	Primates	IV sodium nitrite reverses CVS after SAH
Muehlschlegel et al. (2011) [151]	Dantrolene	TCD	Human	IV dantrolene decreases CBF after SAH
Echigo et al. (2012) [20]	Trehalose	NF-Kb, ET-1, COX-2, and NO𝑥	Leporine	Trehalose decreases lipid peroxidation, arachidonic acid release, vasospasm, and inflammatory markers after SAH
Hong et al. (2012) [115]	Hydrogen rich saline	SOD, GPx, and malondialdehyde	Murine	Molecular hydrogen reduces peroxidation and vasospasm after SAH
Pradilla et al. (2012) [23]	L-Citrulline	BA diameter, neurobehaviour, and NOS expression	Murine	Systemic L-citrulline prevents angiographic BA vasospasm and improves neurobehaviour and NOS expression after SAH
Zhang et al. (2012) [152]	mTOR inhibition	BA diameter, appetite, and activity scores	Canine	mTOR inhibitor (rapamycin) reduced CVS after SAH

SOD: superoxide dismutase, CBF: cerebral blood flow, GPx: glutathione peroxidase, NOS: nitric oxide synthase, BA: basilar artery, mTOR: mammalian target of rapamycin, and TCD: transcranial Doppler.