Cerebral blood flow during experimental endotoxemia in volunteers

Pollard, Valerie; Prough, Donald S.; Conroy, B.; Uchida, Tatsuo; Daye, Andrea; Traber, Lillian D.; Traber, Daniel L.

doi:10.1097/00003246-199710000-00020

Cited by 41 publications

(27 citation statements)

References 38 publications

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“…In a previous study in healthy volunteers, Pollard et al (1997) observed no change in CBF after an intravenous endotoxin dose of 4 ng/kg. In that study, CBF was measured hourly after endotoxin, and the PaCO 2 was not reported.…”

Section: Figmentioning

confidence: 74%

Cerebral Blood Flow and Oxidative Metabolism during Human Endotoxemia

Møller

Strauss

Qvist

et al. 2002

J Cereb Blood Flow Metab

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Summary:The proinflammatory cytokine, tumor necrosis factor-alpha (TNF-␣), has been suggested to mediate septic encephalopathy through an effect on cerebral blood flow (CBF) and metabolism. The effect of an intravenous bolus of endotoxin on global CBF, metabolism, and net flux of cytokines and catecholamines was investigated in eight healthy young volunteers. Cerebral blood flow was measured by the Kety-Schmidt technique at baseline (during normocapnia and voluntary hyperventilation for calculation of subject-specific cerebrovascular CO 2 reactivity), and 90 minutes after an intravenous bolus of a reference Escherichia coli endotoxin. Arterial TNF-␣ peaked at 90 minutes, coinciding with a peak in subjective symptoms. At this time, CBF and PaCO 2 were significantly reduced compared to baseline; the CBF decrease was readily explained by hypocapnia. The cerebral metabolic rate of oxygen remained unchanged, and the net cerebral flux of TNF-␣, interleukin (IL)-1␤, and IL-6 did not differ significantly from zero. Thus, high circulating levels of TNF-␣ during human endotoxemia do not induce a direct reduction in cerebral oxidative metabolism.

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Section: Figmentioning

confidence: 74%

Cerebral Blood Flow and Oxidative Metabolism during Human Endotoxemia

Møller

Strauss

Qvist

et al. 2002

J Cereb Blood Flow Metab

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“…Previous studies focusing on the cerebral effects of a bolus of endotoxin have provided divergent results (Moller et al, 2002;Pollard et al, 1997). Firstly, in contrast to the present study, healthy subjects were investigated.…”

Section: Cerebral Circulation and Metabolismmentioning

confidence: 87%

Cerebral Vascular and Metabolic Response to Sustained Systemic Inflammation in Ovine Traumatic Brain Injury

Stubbe¹,

Greiner²,

Aken³

et al. 2004

Journal of Cerebral Blood Flow & Metabolism

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Summary: Traumatic brain injury (TBI) is frequently accompanied by a systemic inflammatory response secondary to multiple trauma, shock, or infections. This study investigated the impact of sustained systemic inflammation on cerebral hemodynamics and metabolism in ovine traumatic brain injury. Fifteen sheep were investigated for 14 hours. Head injury was induced with a nonpenetrating stunner in anesthetized, ventilated animals. One group (TBI/Endo, n ‫ס‬ 6) subsequently received a continuous endotoxin infusion for 12 hours, whereas a second group (TBI, n ‫ס‬ 6) received the carrier. Three instrumented animals served as sham controls. Head impact significantly increased intracranial pressure from 9 ± 4 mm Hg to 21 ± 15 mm Hg (TBI/Endo) and from 10 ± 3 mm Hg to 24 ± 19 mm Hg (TBI) (means ± SD). Internal carotid blood flow increased and cerebral vascular resistance decreased (P < 0.05) during the hyperdynamic inflammatory response between 10 and 14 hours in the TBI/Endo group, whereas these parameters were at baseline level in the TBI group. Intracranial pressure remained unchanged during this period, but increased during hypercapnia. The CMRO 2 , PaCO 2 , and arterial hematocrit values were identical among the groups between 10 and 14 hours. It is concluded that chronic endotoxemia in ovine traumatic brain injury was associated with cerebral vasodilation uncoupled from global brain metabolism. Different mechanisms appear to induce cerebral vasodilation in response to inflammation and hypercapnia.

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“…Nicotine increases both regional cerebral blood flow and local cerebral glucose utilization in regions that are rich in nicotinic receptors, but this does not include the striatum where it remains unchanged [23][24][25][26]. Although it is obvious that doses of endotoxin that are high enough to produce hypotension also will cause some reduction of cerebral blood flow [27], an endotoxic challenge in the range used in this study will cause an increased flow and hyperemia in the brain, although higher doses are needed than for systemic vasodilation [28,29]. In an anesthetized dog model, the combined effects of endotoxic challenge and moderate hypoxemia (oxygen saturation in arterial blood of 50%), was still an increased cerebral blood flow and increased cerebral metabolic rate of oxygen [30].…”

Section: Discussionmentioning

confidence: 98%

Detrimental Effects of Nicotine and Endotoxin in the Newborn Piglet Brain during Severe Hypoxemia

Frøen¹,

Amerio

Stray‐Pedersen³

et al. 2002

Neonatology

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Hypoxia-ischemia is a major cause of perinatal brain damage, but evidence shows that brain injury also is associated with intrauterine infections and maternal smoking. The mechanisms are not known, and we therefore explored the effects of experimental inflammation or nicotine on perinatal brain metabolism and injury during severe hypoxemia. Twenty-eight 1-week-old piglets were anesthetized and instrumented with microdialysis probes in the striatum and brainstem. We studied three pretreatment groups: (1) 20 µg/kg i.v. nicotine (n = 9); (2) 1 µg/kg i.v. endotoxin from Escherichia coli (n = 11), or (3) control (n = 8). The piglets were subsequently exposed to 30 min of hypoxemia (6% O₂). In order to minimize any ischemic component and increase survival, this was abrupted for 1 min if blood pressure fell to 30 mm Hg. During hypoxemia, both the pretreatment with endotoxin and nicotine induced higher levels of extracellular lactate and peak lactate/pyruvate ratio compared with controls (54.7 ± 9.6 (p < 0.01) and 65.2 ± 13.1 (p < 0.02) vs. 15.9 ± 7.4, respectively), reflecting a deterioration of the metabolic status in these groups. The two pretreated groups reached significantly higher peak levels of extracellular glycerol (30.9 ± 4.1 vs. 77.9 ± 12.7 and 89.4 ± 14.2 µmol/l, respectively, p = 0.01), indicating a higher level of cellular membrane disintegration or leakage. In addition, 3 endotoxin piglets and 4 nicotine piglets died during reoxygenation, while all controls survived (p = 0.13 and p < 0.04, respectively). Mortality was associated with a rise in extracellular glutamate at the end of hypoxemia/start reoxygenation (p = 0.02). These findings contribute in explaining how nicotine and inflammatory response to bacterial toxins could act as cofactors for hypoxic-ischemic neurologic injury in the immature brain.

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Cerebral blood flow during experimental endotoxemia in volunteers

Abstract: A dose of endotoxin sufficient to induce systemic vasodilation in healthy subjects does not influence cerebral blood flow or the cerebral metabolic rate for oxygen.

Cited by 41 publications

References 38 publications

Cerebral Blood Flow and Oxidative Metabolism during Human Endotoxemia

Cerebral Blood Flow and Oxidative Metabolism during Human Endotoxemia

Cerebral Vascular and Metabolic Response to Sustained Systemic Inflammation in Ovine Traumatic Brain Injury

Detrimental Effects of Nicotine and Endotoxin in the Newborn Piglet Brain during Severe Hypoxemia

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