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to NO synthase dysfunction, direct vasoconstriction due to
spasmogenic proteins, and dysregulation of electrolyte channels,
such as K + and Mg 2+ in smooth muscle cells ( 3 ). These questions
have reinforced the importance of animal models in studying the
pathophysiology of vasospasm ( 4-8 ). The majority of these models
are based on post-mortem examination of arteries ( 4-8 ). The abil-
ity to examine vasospasm in vivo is limited. Current methods
include transcranial Doppler (TCD), angiography, computed
tomography (CT), magnetic resonance imaging (MRI), and posi-
tron emission tomography (PET).
2. Transcranial
Doppler
TCD measures the velocity of blood fl owing through the intracra-
nial blood vessels ( 9 ). Two probes are used in combination with
each other: one identifi es specifi c blood vessels, and the other
measures the velocity of the blood fl ow in the targeted vessels ( 9 ).
The latter probe emits a pulse (either ultrasound or laser) that
refl ects off the blood within the desired vessel and returns to the
probe ( 9 ). The velocity difference between the transmitted and
received pulses allows the Doppler probe to record a phase shift ( 9 ).
This phase shift correlates with the speed of the blood fl ow, which
is subsequently related to the caliber of the blood vessel (i.e., the
smaller the diameter of the vessel, the higher the velocity of the
blood fl ow) ( 9 ).
Advantages of TCD are that it is relatively inexpensive and
noninvasive ( 9 ). Disadvantages of this modality include its strong
operator dependence, limitation by high impedance materials (e.g.,
bone), and susceptibility to false negative and false positive
studies ( 9 ). Additional factors affecting blood fl ow velocity, such
as age, hematocrit, arterial carbon dioxide tension, and moment-
to-moment variability, may also limit its interpretation ( 9 ). Perhaps
most importantly, blood fl ow velocity does not always correlate
with the severity of vasospasm ( 9 ).
Animal studies using TCD to assess vasospasm are few and
limited ( 10 ). Cetas et al. ( 10 ) studied the role of the rostral ventro-
medial medulla in modulating cerebral perfusion following iatro-
genic SAH using a laser Doppler system in rats. In this study,
autologous blood was obtained and injected inter-hemispherically
into the prechiasmatic cistern ( 10 ). Blood fl ow velocity was evalu-
ated using a laser Doppler probe placed directly over the area of
thinned skull used for blood injection ( 10 ). They found that cere-
bral blood fl ow was persistently decreased for 40 min following
blood injection, while animals undergoing saline injection only
had decreased cerebral blood fl ow for a few minutes ( 10 ). Similar
methods have been used in other animal models, including mice ( 11 )
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