Review Article

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

Table 2

Early studies report improvement in experimental proxies of CVS in various models.

Studies involving modifications of the inflammatory process with effects on CVS
Author (year)Parameter assessedModelFindings

Tokiyoshi et al. (1991) [146]Symptomatic vasospasmHuman TXA2 synthetase inhibition decreased symptomatic vasospasm
Lin et al. (2005) [67]ACA diameterMurineAnti-E selectin mAb prevents SAH induced angiographic vasospasm
Fei and Golwa (2007) [101] MCA velocityHumanTopical dexamethasone prevents angiographic vasospasm
Iseda et al. (2007) [147]BA diameter, IL-1BLeporineCaspase inhibitor (Z-VAD-FMK) decreased angiographic BA vasospasm and IL-1B levels
Lin et al. (2007) [66]ICAM-1, BA diameterLeporineEndothelin converting enzyme inhibitor (CGS 26303) decreases ICAM-1 levels and BA vasospasm
Chen et al. (2008) [69]JAK2LeporineJAK2 inhibitor (AG490) decreases JAK2 activation and angiographic BA vasospasm
Yoshimoto et al. (2009) [148]Angiography Human Cilostazol prevents angiographic vasospasm after SAH
Wu et al. (2010) [149]TLR4, TNF1In vitroPPAR gamma agonist decreases TLR4 expression and cytokine release
Chang et al. (2010) [150]ICAM-1, VCAM-1, E-Selectin, and BA diameterMurine6-MP decreases ICAM-1 and E-Selectin and increases angiographic BA vasospasm after SAH

TXA2: thromboxane A2, PAF: platelet activating factor, LFA-1: lymphocyte function associated antigen, NO: nitrous oxide, JNK: c-Jun N terminal kinase, mAb: monoclonal antibody, HMG-CoA: 3-hydroxy-3-methylglutaryl-coenzyme A, JAK2: Janus kinase 2, PDE: phosphodiesterase, 6-MP: 6-mercaptopurine, and PPAR gamma: peroxisome proliferator activated receptor gamma.