Inflammation, Vasospasm, and Brain Injury after Subarachnoid Hemorrhage

Table 1

Key inflammatory molecules implicated in the pathology of SAH.

Molecule	Function	Roles in animal studies	Roles in human studies	Comments
Selectins	Leukocyte adhesion	Inhibition of selectins decreases vasospasm [62, 63]	Higher levels in CSF correlate to vasospasm in some studies [3], found in walls of ruptured aneurysms [36]	Variable expression in patients with SAH [3, 8, 9], used to prognosticate outcome in critically ill patients without SAH [28]
Integrins	Leukocyte adhesion	Blocking reduces vasospasm [64–66]	Higher levels seen in patients with vasospasm [3]
TNFα	Proinflammatory cytokine produced by leukocytes	Induces neuronal apoptosis after SAH [52]; blockade reduces vasospasm [67]	Found in CSF in patients after SAH and correlates with vasospasm after SAH [68]	Variable expression in patients with SAH [2, 10–12]
MCP-1	Macrophage chemoattractant	Promotes repair of aneurysms [69]	Found in CSF after SAH and associated with poor outcomes but not vasospasm [9, 21]	Also associated with vascular injury [31]
ICAM-1	Leukocyte adhesion	Increased in animal SAH studies [47, 70]; blockade reduces vasospasm [71]	Increased in patients with SAH [3]	Used to prognosticate outcome in critically ill patients without SAH [28]
Interleukins	Mediate leukocyte interactions	Blockade reduces vasospasm [72]	Peak early in SAH [9, 11]	Peak at variable times in human studies [29, 30]
Endothelin-1	Potent vasoconstrictor	Inhibition reduces vasospasm [73, 74]	Produced by monocytes from SAH patients [13, 14], with no proved benefit in clinical trials [75]	Highly variable expression after SAH and may not correlate with vasospasm [13, 16, 76]