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Fig. 1. (
a
) Ruptured intracerebral aneurysm results in rapid hemorrhage into the subarachnoid spaces. Increased intracra-
nial pressure, reduced cerebral blood fl ow, and perfusion pressure lead to cellular injury. Auto-oxidation of oxyhemoglobin
(OxyHb) in the CSF thought to produce superoxide anion and hydroxyl radical. These strong oxidizing agents result in
signifi cant lipid, protein and DNA damage. Breakdown products may also contribute to delayed cerebral vasospasm.
(
b
) Computed tomography with angiography demonstrating ruptured anterior communicating artery aneurysm. Three-
dimensional reconstruction of ruptured 1.1 cm
3
saccular ACA aneurysm. Head CT without contrast reveals hemorrhage
within the central interhemispheric fi ssure and frontal lobe parenchyma, resulting in surrounding vasogenic edema forma-
tion 48 h following subarachnoid hemorrhage.
Acute phase injury is caused by rapid distribution of blood into the
subarachnoid space, elevation of intracranial pressure (ICP) (
3
),
reduced cerebral perfusion pressure (CPP), and cerebral blood
fl ow (CBF) (
4-6
). These insults have been shown to cause direct
microvascular injury, plugging of vessels and release of vasoactive
substances by platelet aggregates (
7-9
), alterations in the nitric
oxide (NO)/nitric oxide synthase (NOS) pathways and lipid per-
oxidation (
10
) (Fig.
2
). Investigators have utilized various meth-
ods to assess the cellular and molecular cascades following the
hemorrhagic event. Signaling pathways, which ultimately deter-
mine degree and distribution parenchymal injury, are activated
within seconds of aneurysm rupture (
11
).
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