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In-Depth Information
Subarachnoid Hemorrhage
Increased ICP
Increased ICP
Liberation of Red Blood Cells
Oxidative Stresses
Hemoglobin
- Scavenge NO
Acute Vasospasm
Acute Vasospasm
Inflammatory
Inflammatory
Response
Blood products
Response
Delayed Vasospasm
CSF and Blood
CSF and Blood
Markers Released
Markers Released
Neurologic decline,
Coma, Death
Fig. 1. In this figure, we see the major physiological events that occur following
subarachnoid hemorrhage in the
left hand column
. The
arrows pointing to the left
hand column
represent the biological, molecular, and biochemical correlates associated
with those events.
understanding of those markers leads to more information
concerning the events in the brain with concomitant information
that will be clinically relevant concerning risks to the patients' brain.
Following hemorrhaging, there are a fairly well-characterized
series of chemical and local events that because of and to the blood
following the bleed. These form the centerpiece of the molecular
and chemical events to be discussed posthemorrhage. Clark and
Sharp reviewed some of the events (
1
) and these are summarized
in Fig.
1
. Briefl y posthemorrhage there is blood, mass effect, blood
clot, cell lysis, oxidation and oxidative stress, local signaling events,
infl ammatory responses, wound healing, and eventual resolution.
These are discussed as to their contribution to chemical and molec-
ular events postsubarachnoid hemorrhage and how they can con-
tribute to the assessments of subarachnoid hemorrhage patients.
2. Logos
2.1. Oxidative
Reactions
The logos or logic of events postsubarachnoid hemorrhage is that
the oxygen-rich arterial blood and activated lymphocytes,
macrophages, microglia, etc., are combining to contribute to oxi-
dative stress. With oxidative stress, there are oxygen-free radicals
and reactive oxygen species. Radicals and reactive oxygen species
are not the same. An oxygen-free radical is an ionized form of
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