Yeah, another paper on hemorrhage.
http://scholar.google.com/scholar_url?hl=en&q=http://downloads.hindawi.com/journals/srt/2013/425281.pdf&sa=X&scisig=AAGBfm0CNg2J04M7tLmWYuYh11Fbfm-72w&oi=scholaralrt
1. Introduction
Subarachnoid hemorrhage (SAH) is a type of hemorrhagic
stroke, most commonly caused by a ruptured intracranial
aneurysm. At the time of aneurysm rupture, blood pours
into the subarachnoid space, and the intracranial pressure
(ICP) inside the rigid calvarium increases sharply, causing
a corresponding decrease in cerebral blood flow (CBF). The
patient’s clinical presentation on arrival to the hospital can
depend on the degree and duration of this initial global
cerebral ischemia.
Patients with aneurysmal SAHmay develop angiographic
vasospasm and delayed cerebral ischemia (DCI) with onset
3–12 days after the initial rupture [1]. DCI may or may
not be accompanied by large artery vasospasm as seen with
vascular imaging [2]. A multicenter randomized clinical trial
has not shown improvement in neurologic outcome despite
ameliorating the delayed large artery vasospasm [3].Whether
this is due to efficacy of rescue therapy in the placebo
groups or drug toxicity abrogating beneficial effects in the
clazosentan groups has not been resolved. Nevertheless, as
a result of these results, research in SAH has also investigated
early brain injury and acute microvascular changes
[4]. Nimodipine, an L-type calcium channel antagonist, is
the only pharmacologic agent that has been shown to consistently
improve neurologic outcomes in clinical trials of
patients with SAH [5].
Similarly, cardiac arrest (CA) results in global cerebral
ischemia that is transient in clinically relevant cases, since
if cardiac function is not restored, the situation is of pathological
interest only. Other causes of transient global cerebral
ischemia (tGCI) include asphyxia, shock, and complex
cardiac surgery [6]. The clinical presentation depends on the
duration of cardiac arrest and time to initiating cardiopulmonary
resuscitation. After global cerebral ischemia from
SAH or tGCI, a cascade of molecular events occurs, resulting
in variable degrees of brain injury and cerebrovascular
changes.
Global cerebral ischemia in postcardiac arrest has also
been studied extensively for many decades in various animal
models. Other than early induced mild hypothermia [7, 8],
clinical translation of neuroprotective strategies and therapeutics
has largely been unsuccessful.
The study of the microcirculation after tGCI and SAH
remains a difficult undertaking, but this strategy of study
may reveal potential therapeutic targets and new insights
into disease pathophysiology.The purpose of this paper is to
look at relevant animal and preclinical studies investigating
2 Stroke Research and Treatment
acute microvascular changes (within the first 48 hours)
occurring after either SAH or tGCI. Cerebral microvessels
may be defined as vessels less than or equal to 100 micrometers
in diameter [9]. Animal studies of focal ischemia or
studies focused on the large cerebral vessels (i.e., circle of
Willis arteries, basilar artery, etc.) are not included in this
paper. While we acknowledge that tGCI may occur in a
large heterogeneous group of disorders (i.e., traumatic brain
injury, intracerebral hemorrhage, etc.), we have chosen to
focus solely on tGCI secondary to cardiac arrest or mechanisms
mimicking cardiac arrest, such as extracranial arterial
occlusion. After providing an overview of various animal
models and general trends in cerebral hemodynamics after
SAH and tGCI, we provide an in-depth review of studies
investigating specific microvascular changes that occur in
these two conditions: (1) microvascular constriction; (2)
increased leukocyte-endothelial cell interactions; (3) blood
brain barrier (BBB) breakdown; and (4) platelet aggregation
and microthrombosis.
9 pages in total.
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