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 [
- Miller J.D.
- Garibi J.
- North J.B.
- et al.
Effects of increased arterial pressure on blood flow in the damaged brain.
J Neurol Neurosurg Psychiatry. 1975; 38: 657
2]. However, these responses may not be physiologic [
- McLeod A.A.
- Neil-Dwyer G.
- Meyer C.H.
- et al.
Cardiac sequelae of acute head injury.
Br Heart J. 1982; 47: 221
3]. Cardiac function is also regulated by baroreceptors, which are mediated by central paraganglionic neurons [
- McMahon C.G.
- Kenny R.
- Bennett K.
- et al.
Modification of acute cardiovascular homeostatic responses to hemorrhage following mild to moderate traumatic brain injury.
Crit Care Med. 2008; 36: 216
4]. Activation results in a vagal-mediated bradycardia and a reduction in cardiac output. Trauma and central neurological injury may suppress this reflex [
- Dampney R.A.
Functional organization of central pathways regulating the cardiovascular system.
Physiol Rev. 1994; 74: 324
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 [
- Nosaka S.
- Murata K.
- Kobyashi M.
- et al.
Inhibition of baroreflex vagal bradycardia by activation of the rostral ventrolateral medulla in rats.
Am J Physiol Heart Circ Physiol. 2000; 279: H1239
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 [
- Malhotra A.K.
- Schweitzer J.B.
- Fox J.L.
- et al.
Cerebral perfusion pressure elevation with oxygen-carrying pressor after traumatic brain injury and hypotension in swine.
J Trauma. 2004; 56: 1049
7]. This loss of the autoregulation has been associated with increased mortality [
- Lodi C.A.
- Minassian A.T.
- Beydon L.
- et al.
Modeling cerebral autoregulation and CO2 reactivity in patients with severe head injury.
Am J Physiol Heart Circ Physiol. 1998; 274: H1729
- Panerai R.B.
- Kerins V.
- Fan L.
- et al.
Association between dynamic cerebral autoregulation and mortality in severe head injury.
Br J Neurosurg. 2004; 18: 471
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- Effects of increased arterial pressure on blood flow in the damaged brain.J Neurol Neurosurg Psychiatry. 1975; 38: 657
- Cardiac sequelae of acute head injury.Br Heart J. 1982; 47: 221
- Modification of acute cardiovascular homeostatic responses to hemorrhage following mild to moderate traumatic brain injury.Crit Care Med. 2008; 36: 216
- Functional organization of central pathways regulating the cardiovascular system.Physiol Rev. 1994; 74: 324
- Inhibition of baroreflex vagal bradycardia by activation of the rostral ventrolateral medulla in rats.Am J Physiol Heart Circ Physiol. 2000; 279: H1239
- Cerebral perfusion pressure elevation with oxygen-carrying pressor after traumatic brain injury and hypotension in swine.J Trauma. 2004; 56: 1049
- Modeling cerebral autoregulation and CO2 reactivity in patients with severe head injury.Am J Physiol Heart Circ Physiol. 1998; 274: H1729
- Association between dynamic cerebral autoregulation and mortality in severe head injury.Br J Neurosurg. 2004; 18: 471
- The cytokine response to human traumatic brain injury: temporal profiles and evidence for cerebral parenchymal production.J Cereb Blood Flow Metab. 2011; 31 (Epub 2010 Aug 18): 658
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Nassenstein K, Orzada S, Haering L, et al. Cardiac MRI: evaluation of phonocardiogram-gated cine imaging for the assessment of global und regional left ventricular function in clinical routine. Eur Radiol 2011. epub ahead of print DOI: 10.1007/s00330-011-2279-z.
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Published online: November 21, 2011
Accepted: October 26, 2011
Received: October 25, 2011
© 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.