Blood pressure and intracranial pressure-volume dynamics in severe head injury: relationship with cerebral blood flow

Bouma, Gerrit J.; Muizelaar, J. Paul; Bandoh, Kuniaki; Marmarou, Anthony

doi:10.3171/jns.1992.77.1.0015

Cited by 315 publications

(113 citation statements)

References 27 publications

(5 reference statements)

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“…The HR may increase first, inducing a short increase of CBF (17), and in turn the increased CBF will bring more oxygenated hemoglobin, reduce the concentration of deoxyhemoglobin, and generate a positive BOLD signal. However, such a transient change in cerebral perfusion pressure or arterial blood pressure is autoregulated by either vasoconstriction or vasodilatation, resulting in altered vascular resistance so that CBF remains more or less constant (18). The weak, scattered, and transient BOLD signal changes may reflect such an autoregulation process.…”

Section: Discussionmentioning

confidence: 99%

Characterization of effects of mean arterial blood pressure induced by cocaine and cocaine methiodide on BOLD signals in rat brain

Luo

Zhu

et al. 2003

Magnetic Resonance in Med

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A total of 45 male Sprague-Dawley rats were employed to determine whether cocaine or cocaine methiodide (CM) administration can induce a significant increase in mean arterial blood pressure (MABP) in rats, and whether such an increase in MABP can produce a global increase in blood oxygenation level-dependent (BOLD) contrast in the rat brain detectable by functional magnetic resonance imaging (fMRI). Cocaine methiodide is a quaternary derivative of cocaine that shares the same cardiovascular effects of cocaine, but does not penetrate the blood-brain barrier ( Since the development of functional MRI (fMRI) in the early 1990s, this noninvasive neuroimaging modality has rapidly gained a prominent position in systems-level neuroscience research to map cognitive brain functions. Recent studies have applied fMRI methodologies to localize acute pharmacological effects and detect changes in regional brain activity of abused substances in humans (1-3) and animals (4 -6). However, there is concern as to whether fMRI methods used to map cognitive function can be simply and directly extended to neuropharmacological studies.There are several issues to be addressed. First, it is not clear how peripheral and cardiovascular changes induced by drug administration affect blood oxygenation level-dependent (BOLD) contrast in the brain. Since the most commonly used fMRI method relies on BOLD contrast, which is a result of oversupply of local cerebral blood oxygen during increased neuronal activity, it is conceivable that acute drug-induced respiratory changes, as well as mean arterial blood pressure (MABP) and heart rate (HR) increases, could cause global cerebral blood flow changes and result in BOLD signal changes. For example, we demonstrated previously (6) that heroin administration affects respiratory inhibition and causes a global decrease in the BOLD signal, although such a global decrease in BOLD contrast can be eliminated using the proper artificial respiratory rate with normal pressures of blood gases. It is not clear how MABP and HR changes affect detection of the BOLD signal in the brain.Second, the pharmacological administration of drugs such as cocaine can induce not only neuronal activity but also cerebral vascular constriction. In a pioneering pharmacological fMRI study, Breiter et al. (1) detected changes in the nucleus accumbens after acute cocaine administration, implicating changes in the brain networks associated with induced euphoria and craving. Data from Kaufman et al. (7), using MR angiography (MRA), suggest that cocaine administration can cause cerebral vasoconstriction in the human brain. These studies indicate that cocaine administration induces not only neuronal activity, but also a cerebrovascular response and a decrease in blood flow. It is necessary to characterize such confounding factors when interpreting BOLD signal changes in pharmacological fMRI research.Third, when applying pharmacological fMRI methods to the study of neuronal activity, the question of how druginduced peripheral and cerebral vasc...

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Section: Discussionmentioning

confidence: 99%

Characterization of effects of mean arterial blood pressure induced by cocaine and cocaine methiodide on BOLD signals in rat brain

Luo

Zhu

et al. 2003

Magnetic Resonance in Med

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“…4,21 Disturbed cerebral autoregulation has been shown to occur in patients after head injury, and in experimental models it has been observed even when the values of CPP and CBF are normal.…”

Section: Pathophysiology Of Cerebral Autoregulation In Tbimentioning

confidence: 99%

“…Autoregulatory vasoconstriction predominantly takes place in the largest arterioles (> 200 µm in diameter), although the bulk of the CBV is probably contained in smaller vessels, because they are so much more numerous, and in the venous system. 4 Additionally, endothelium-related factors have been suggested to contribute to autoregulatory responses, and some studies have indicated a possible role for NO as a vasodilator during reduced CPP.…”

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confidence: 99%

“…When autoregulation is intact, a decrease in CPP results in vasodilation (and increased CBV), leading to increased ICP due to impaired brain compliance. 4 With defective cerebral autoregulation, any decrease in CPP, regardless of its baseline value, will produce a decrease in CBF. Cerebral blood flow will decrease linearly with CPP and thus may reach ischemic levels, worsening secondary injury.…”

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confidence: 99%

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Cerebral pressure autoregulation in traumatic brain injury

Rangel-Castilla

Gasco

Nauta

et al. 2008

FOC

179

104

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An understanding of normal cerebral autoregulation and its response to pathological derangements is helpful in the diagnosis, monitoring, management, and prognosis of severe traumatic brain injury (TBI). Pressure autoregulation is the most common approach in testing the effects of mean arterial blood pressure on cerebral blood flow. A gold standard for measuring cerebral pressure autoregulation is not available, and the literature shows considerable disparity in methods. This fact is not surprising given that cerebral autoregulation is more a concept than a physically measurable entity. Alterations in cerebral autoregulation can vary from patient to patient and over time and are critical during the first 4–5 days after injury. An assessment of cerebral autoregulation as part of bedside neuromonitoring in the neurointensive care unit can allow the individualized treatment of secondary injury in a patient with severe TBI. The assessment of cerebral autoregulation is best achieved with dynamic autoregulation methods. Hyperventilation, hyperoxia, nitric oxide and its derivates, and erythropoietin are some of the therapies that can be helpful in managing cerebral autoregulation. In this review the authors summarize the most important points related to cerebral pressure autoregulation in TBI as applied in clinical practice, based on the literature as well as their own experience.

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“…However, quantification of CBF alone cannot define the relationship between oxygen supply and consumption because the adequacy of oxygenation is also determined by variables such as autoregulation, CO 2 reactivity, and coupling of CBF and cerebral metabolism that are disturbed in a significant number of head-injured patients. [2,3,9,14,26,34,36] Furthermore, confounding variables such as vasospasm, anemia, hypoxia, and seizures may reduce the oxygen carrying capacity. A measure of the balance between cerebral oxygen delivery and consumption, such as AVDO 2 , may therefore be useful and, when combined with multimodality monitoring, may provide a reasonable means to identify patients in which secondary ischemic damage can be ameliorated by therapeutic intervention directed at its pathophysiological mechanism.…”

Section: Applications For Jugular Oxygen Monitoringmentioning

confidence: 99%

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Blood pressure and intracranial pressure-volume dynamics in severe head injury: relationship with cerebral blood flow

Cited by 315 publications

References 27 publications

Characterization of effects of mean arterial blood pressure induced by cocaine and cocaine methiodide on BOLD signals in rat brain

Characterization of effects of mean arterial blood pressure induced by cocaine and cocaine methiodide on BOLD signals in rat brain

Cerebral pressure autoregulation in traumatic brain injury

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