Effects of propofol on cerebral blood flow and the metabolic rate of oxygen in humans

Oshima, Takashi; Karasawa, Fujio; Satoh, Tetsuo

doi:10.1034/j.1399-6576.2002.460713.x

Cited by 104 publications

(79 citation statements)

References 31 publications

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“…It is known that altered neurometabolic dynamics can occur in each of the conditions associated with burst suppression: in general anesthesia, through a reduction in neural activity and subsequent reductions in CMRO (25,36); in hypoxic/ischemic injury, through aberrant reductions in metabolic regulation due to diffuse injury or through direct oxidative stress (6,22); in hypothermia, through direct reductions in metabolic rate (3,35); and in developmental encephalopathy, through neural and metabolic dysfunction (23). Implicating brain metabolism in the neural mechanisms of burst suppression establishes a unifying physiologic connection between the main etiologies of the phenomenon.…”

Section: Discussionmentioning

confidence: 99%

“…The parameter J ATP is the production rate of ATP that is known to be directly coupled to the cerebral metabolic rate (32). As a surrogate for the metabolic rate, we directly manipulate J ATP over a range of 30−50% of baseline, consistent with studies of anesthetic and hypothermic effects on cerebral metabolism (35,36). Complete details of the model and simulation parameters are found in SI Methods.…”

Section: Methodsmentioning

confidence: 99%

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A neurophysiological–metabolic model for burst suppression

Ching

Purdon

Vijayan

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

259

326

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Burst suppression is an electroencepholagram (EEG) pattern in which high-voltage activity alternates with isoelectric quiescence. It is characteristic of an inactivated brain and is commonly observed at deep levels of general anesthesia, hypothermia, and in pathological conditions such as coma and early infantile encephalopathy. We propose a unifying mechanism for burst suppression that accounts for all of these conditions. By constructing a biophysical computational model, we show how the prevailing features of burst suppression may arise through the interaction between neuronal dynamics and brain metabolism. In each condition, the model suggests that a decrease in cerebral metabolic rate, coupled with the stabilizing properties of ATP-gated potassium channels, leads to the characteristic epochs of suppression. Consequently, the model makes a number of specific predictions of experimental and clinical relevance.B urst suppression-an electroencephalogram (EEG) pattern in which high voltage activity (burst) and flatline (suppression) periods alternate systematically but quasiperiodically (almost periodic but with variations in inter-and intra-burst duration) (1)-is a state of profound brain inactivation. It is frequently observed in deep general anesthesia (2). It is also observed in a range of pathological conditions including hypothermia (3-5), hypoxic-ischemic trauma/coma (6), and the so-called Ohtahara syndrome (7,8), a type of early infantile encephalopathy. These etiologies indicate that the burst suppression pattern represents a low-order dynamic mechanism that persists in the absence of higher-level brain activity. Indeed, the fact that many different conditions produce similar brain activity suggests that there may be a common pathway to the state of brain inactivation and may indicate fundamental properties of the brain's arousal circuits (2).The basic features of the burst suppression phenomenon have been established through a variety of EEG studies that are reviewed in ref. 9. The two most notable of these features are the spatial homogeneity of bursts and the quasi-periodic nature of the suppression. Later research has been directed at describing the phenomenon in vivo and in the specific context of general anesthesia. In particular, the early work of Steriade et al. (10) helped establish the neural correlates of burst suppression, including the differential participation of cortical and subcortical cell types. More recent studies (11,12) have suggested that burst suppression is associated with enhanced excitability in cortical networks. These studies implicate extracellular calcium as a correlate for the switches between burst and suppression.Despite the findings of these studies, a unifying mechanism for burst suppression-one that explains its prevailing features and also accounts for its range of etiologies-has not been proposed. Indeed, the existing characterizations of burst suppression in pathological situations are highly limited. Computational models offer a means of synthesizing the availabl...

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

A neurophysiological–metabolic model for burst suppression

Ching

Purdon

Vijayan

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

259

326

View full text Add to dashboard Cite

show abstract

“…The change in the a-vDO 2 also indicates a resetting of the relationship between CMRO 2 and CBF. Several studies have found an unchanged a-vDO 2 in healthy subjects during propofol sedation, 25,26 even at doses leading to an isoelectric electroencephalogram. 27 Taken together, the results suggest that cerebral metabolic coupling is impaired in patients with bacterial meningitis.…”

Section: Discussionmentioning

confidence: 99%

Cerebral Blood Flow and Metabolism During Infusion of Norepinephrine and Propofol in Patients With Bacterial Meningitis

Møller

Qvist

Tofteng

et al. 2004

Stroke

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Background and Purpose-In patients with severe bacterial meningitis, norepinephrine is often infused to increase mean arterial pressure (MAP). This increases cerebral blood flow (CBF), but it is unknown if this increase is caused by impaired cerebral autoregulation or by a cerebral effect of norepinephrine through increased cerebral metabolism. The latter possibility implies a CBF-metabolism coupling. This has not been studied during meningitis. We studied the effect of norepinephrine and propofol on CBF and oxidative metabolism in patients with severe bacterial meningitis. Methods-In seven patients with pneumococcal meningitis and 7 healthy subjects, norepinephrine was infused intravenously; patients also underwent intravenous propofol infusion. Global CBF was measured by the Kety-Schmidt technique; cerebral oxidative metabolism and net flux of norepinephrine and epinephrine were calculated from measured arterial-to-jugular venous concentration differences (a-vD). [54 to 77] mL/100 g per minute) but remained unchanged in controls. The cerebral metabolic rate of oxygen (CMRO 2 ) decreased in patients and remained unchanged in controls. No cerebral net flux of norepinephrine or epinephrine was found at any time in the 2 groups. During propofol infusion, CMRO 2 , and the a-vDO 2 decreased whereas CBF was unchanged. Conclusions-In patients with severe bacterial meningitis, norepinephrine increases both MAP and CBF but not CMRO 2 , indicating impaired autoregulation. Propofol reduces CBF relatively less than cerebral metabolism, suggesting a resetting of the CBF-CMRO 2 relationship. Results-During

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“…Patients with severe BAE can have increased intracranial pressure due to hypercapnia, and unconscious patients with increased intracranial pressure can have worse outcomes if ETI is performed without appropriate premedication [27]. Propofol is an attractive choice for premedication in this scenario because it can decrease intracranial pressure [28][29][30].…”

Section: Attenuation Of the Risks Of Eti-related Adverse Events In Bamentioning

confidence: 99%

Emergency endotracheal intubation-related adverse events in bronchial asthma exacerbation: can anesthesiologists attenuate the risk?

et al. 2015

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Number of tables: 6 2 AbstractPurpose Airway management in severe bronchial asthma exacerbation (BAE) carries very high risk and should be performed by experienced providers. However, no objective data are available on the association between the laryngoscopist's specialty and endotracheal intubation (ETI)-related adverse events in patients with severe bronchial asthma. In this paper, we compare emergency ETI-related adverse events in patients with severe BAE between anesthesiologists and other specialists.Methods This historical cohort study was conducted at a Japanese teaching hospital. We analyzed all BAE patients who underwent ETI in our emergency department from January 2002 to January 2014.Primary exposure was the specialty of the first laryngoscopist (anesthesiologist vs. other specialist).The primary outcome measure was the occurrence of an ETI-related adverse event, including severe bronchospasm after laryngoscopy, hypoxemia, regurgitation, unrecognized esophageal intubation, and ventricular tachycardia. Conclusion Anesthesiologist as first exposure was independently associated with attenuated risk of 3 ETI-related adverse events in patients with severe BAE. The skill and knowledge of anesthesiologists should be applied to high-risk airway management whenever possible. Results

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Effects of propofol on cerebral blood flow and the metabolic rate of oxygen in humans

Abstract: Propofol proportionally decreased CBF and CMRO2 without affecting a-vDO2 in humans, suggesting that normal cerebral circulation and metabolism are maintained.

Cited by 104 publications

References 31 publications

A neurophysiological–metabolic model for burst suppression

A neurophysiological–metabolic model for burst suppression

Cerebral Blood Flow and Metabolism During Infusion of Norepinephrine and Propofol in Patients With Bacterial Meningitis

Emergency endotracheal intubation-related adverse events in bronchial asthma exacerbation: can anesthesiologists attenuate the risk?

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