The cardiovascular physiologic effects of traumatic brain injury remain only partially
understood. The autoregulatory manifestations of closed head injury have long been
considered to be a catecholamine-mediated phenomenon [
1
]. Tachycardia, hypertension, coronary vasoconstriction resulting in cardiac ischemia,
and arrhythmia have been attributed to sympathetic over activity [
2
]. However, these responses may not be physiologic [
3
]. Cardiac function is also regulated by baroreceptors, which are mediated by central
paraganglionic neurons [
4
]. Activation results in a vagal-mediated bradycardia and a reduction in cardiac output.
Trauma and central neurological injury may suppress this reflex [
5
]. The end result is in increased morbidity and mortality from neurologic injury, as
it not only affects cerebral perfusion pressure but also cardiac afterload [
6
]. In addition, the complex relationship between PaCO2 arterial blood pressure results in changes in intracranial pressure that also affect
intracranial dynamics and cerebral blood flow after neurological trauma [
7
]. This loss of the autoregulation has been associated with increased mortality [
8
].To read this article in full you will need to make a payment
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Article info
Publication history
Published online: November 21, 2011
Accepted:
October 26,
2011
Received:
October 25,
2011
Identification
Copyright
© 2012 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
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- Cardiac Reactive Oxygen Species After Traumatic Brain InjuryJournal of Surgical ResearchVol. 173Issue 2
- PreviewCardiovascular complications after traumatic brain injury (TBI) contribute to morbidity and mortality and may provide a target for therapy. We examined blood pressure and left ventricle contractility after TBI, and tested the hypothesis that β-adrenergic blockade would decrease oxidative stress after TBI.
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