Direct comparison of cerebrovascular effects of norepinephrine and dopamine in head-injured patients

Steiner, Luzius A.; Johnston, Andrew James; Czosnyka, Marek; Chatfield, Doris A.; Salvador, Raymond; Coles, Jonathan P.; Gupta, Arun Kumar; Pickard, John D.; Menon, David

doi:10.1097/01.ccm.0000120054.32845.a6

Cited by 127 publications

(57 citation statements)

References 25 publications

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“…9,10 Maintaining CPP within these levels is often managed by use of vasoactive agents to increase CPP and optimize CBF. However, vasoactive agents clinically used to elevate MAP to increase CPP after TBI, such as phenylephrine (Phe), dopamine (DA), and norepinephrine (NE), [11][12][13] have not sufficiently been compared regarding effect on CPP, CBF, autoregulation, and survival after TBI, and clinically, current vasoactive agent use is variable.…”

Section: Introductionmentioning

confidence: 99%

Retracted:Norepinephrine Protects Cerebral Autoregulation and Reduces Hippocampal Necrosis after Traumatic Brain Injury via Blockade of ERK MAPK and IL-6 in Juvenile Pigs

Armstead

Riley

Vavilala

2016

Journal of Neurotrauma

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Traumatic brain injury (TBI) contributes to morbidity in children, and boys are disproportionately represented. Cerebral autoregulation is impaired after TBI, contributing to poor outcome. Cerebral perfusion pressure (CPP) is often normalized by use of vasoactive agents to increase mean arterial pressure (MAP). In prior studies of 1-to 5-day-old newborn piglets, we observed that norepinephrine (NE) preferentially protected cerebral autoregulation and prevented hippocampal necrosis in females but not males after fluid percussion injury (FPI). The ERK isoform of mitogen activated protein kinase (MAPK) produces hemodynamic impairment after FPI, but less is known about the role of the cytokine interleukin-6 (IL-6). We investigated whether NE protects autoregulation and limits histopathology after FPI in older juvenile (4-week-old) pigs and the role of ERK and IL-6 in that outcome by sex. Results show that NE significantly protects autoregulation and prevents reduction in cerebral blood flow (CBF) in both male and female juvenile pigs after FPI; co-administration of the ERK antagonist U 0126 with NE fully protects both indices of outcome. Papaverine induced dilation was unchanged by FPI and NE. NE blunted ERK MAPK and IL-6 upregulation in both males and females after FPI. NE attenuated loss of neurons in CA1 and CA3 hippocampus of males and females after FPI. These data indicate that NE protects autoregulation and limits hippocampal neuronal cell necrosis via blockade of ERK and IL-6 after FPI in both male and female juvenile pigs. These data suggest that use of NE to improve outcome after TBI is both sex and age dependent.

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Section: Introductionmentioning

confidence: 99%

Retracted:Norepinephrine Protects Cerebral Autoregulation and Reduces Hippocampal Necrosis after Traumatic Brain Injury via Blockade of ERK MAPK and IL-6 in Juvenile Pigs

Armstead

Riley

Vavilala

2016

Journal of Neurotrauma

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“…However, Johnston et al [21] showed that although there was no difference in ICP and cerebral oxygenation between dopamine and norepinephrine, dopamine had a more variable effect on arterial venous oxygen difference than norepinephrine. The third study showed no difference in mean ICP between dopamine and norepinephrine, yet reported that norepinephrine had predictable and significant increases in the mean flow velocity within the middle cerebral artery, whereas results with dopamine were variable and inconsistent [22]. These studies suggest that norepinephrine may be the preferred vasopressor to augment blood pressure after TBI.…”

Section: Discussionmentioning

confidence: 97%

“…However, 2 out of the 3 studies comparing dopamine and norepinephrine found that cerebral blood flow was better with norepinephrine [17,18]. There are 3 small (n = 19, 11, 10) human adult studies (prospective crossover trials) comparing the use of dopamine versus norepinephrine to augment CPP in adult TBI patients [20,21,22]. In 1 study, ICP was higher with dopamine than norepinephrine for the same MAP [20].…”

Section: Discussionmentioning

confidence: 99%

Use and Effect of Vasopressors after Pediatric Traumatic Brain Injury

et al. 2010

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Background: Vasopressors are commonly used to increase mean arterial blood pressure (MAP) and cerebral perfusion pressure (CPP) after traumatic brain injury (TBI), but there are few data comparing vasopressor effectiveness after pediatric TBI. Objective: To determine which vasopressor is most effective at increasing MAP and CPP in children with moderate-to-severe TBI. Methods: After institutional review board approval, we performed a retrospective cohort study of children 0–17 years old admitted to a level 1 trauma center (Harborview Medical Center, Seattle, Wash., USA) between 2002 and 2007 with moderate-to-severe TBI who received a vasopressor to increase blood pressure. Baseline demographic and physiologic characteristics and hourly physiologic monitoring for 3 h after having started a vasopressor were abstracted. We evaluated differences in MAP and CPP at 3 h after initiation of therapy between phenylephrine, dopamine and norepinephrine among patients who did not require a second vasopressor during this time. Multivariate linear regression was used to adjust for age, gender, injury severity score and baseline MAP or CPP and to cluster by subject. Results: Eighty-two patients contributed data to the entire dataset. The most common initial medication was phenylephrine for 47 (57%). Patients receiving phenylephrine and norepinephrine tended to be older than those receiving dopamine and epinephrine. Thirteen (16%) of the patients received a second vasopressor during the first 3 h of treatment and were thus not included in the regression analyses; these patients received more fluid resuscitation and exhibited higher in-hospital mortality (77 vs. 32%; p = 0.004) compared to patients receiving a single vasopressor. The norepinephrine group exhibited a 5 mm Hg higher MAP (95% CI: –4 to 13; p = 0.31) and a 12 mm Hg higher CPP (95% CI: –2 to 26; p = 0.10) than the phenylephrine group, and a 5 mm Hg higher MAP (95% CI: –4 to 15; p = 0.27) and a 10 mm Hg higher CPP (95% CI: –5 to 25; p = 0.18) than the dopamine group. However, in post hoc analysis, after adjusting for time to start of vasopressor, hypertonic saline and pentobarbital, the effect on MAP was lost, but the CPP was 8 mm Hg higher (95% CI: –10 to 25; p = 0.39) than in the phenylephrine group, and 5 mm Hg higher (95% CI: –14 to 24; p = 0.59) than in the dopamine group. Conclusions: Vasopressor use varied by age. While there was no statistically significant difference in MAP or CPP between vasopressor groups, norepinephrine was associated with a clinically relevant higher CPP and lower intracranial pressure at 3 h after start of vasopressor therapy compared to the other vasopressors examined.

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“…Prospective comparative studies regarding vasopressor selection are lacking in this population. These authors recommend against the use of dopamine because of the arrhythmogenic potential that has been observed in clinical trials and unreliable effects of dopamine on cerebral blood flow [16,19]. …”

Section: Subarachnoid Hemorrhagementioning

confidence: 97%

Role of Vasopressor Administration in Patients with Acute Neurologic Injury

Muzevich

Voils

2009

Neurocrit Care

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Direct comparison of cerebrovascular effects of norepinephrine and dopamine in head-injured patients

Abstract: Norepinephrine may be more predictable and efficient to augment cerebral perfusion in patients with traumatic brain injury.

Cited by 127 publications

References 25 publications

Retracted:Norepinephrine Protects Cerebral Autoregulation and Reduces Hippocampal Necrosis after Traumatic Brain Injury via Blockade of ERK MAPK and IL-6 in Juvenile Pigs

Retracted:Norepinephrine Protects Cerebral Autoregulation and Reduces Hippocampal Necrosis after Traumatic Brain Injury via Blockade of ERK MAPK and IL-6 in Juvenile Pigs

Use and Effect of Vasopressors after Pediatric Traumatic Brain Injury

Role of Vasopressor Administration in Patients with Acute Neurologic Injury

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