Noninvasive Detection of Changes in Cerebral Blood Flow by Near-Infrared Spectroscopy in a Piglet Model of Hydrocephalus

Soul, Janet S.; Taylor, George A.; Wypij, David; duPlessis, Adré J.; Volpe, Joseph J.

doi:10.1203/00006450-200010000-00005

Cited by 97 publications

(73 citation statements)

References 12 publications

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“…DHb is a well-validated measure of changes in intracerebral oxygenation (10). If arterial oxygen saturation is stable, DHb correlates closely with perfusion changes due to severe hypotension or changes in intracranial pressure (46,50). However, as shown in the present study, during severe, prolonged hypoxia, DHb fell well before cerebral perfusion was impaired, as shown by carotid or cortical blood flow or cerebral blood volume.…”

Section: Discussionsupporting

confidence: 49%

Regulation of cytochrome oxidase redox state during umbilical cord occlusion in preterm fetal sheep

Roelfsema¹,

Dean²,

Wassink³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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The preterm fetus is capable of surviving prolonged periods of severe hypoxia without neural injury for much longer than at term. To evaluate the hypothesis that regulated suppression of brain metabolism contributes to this remarkable tolerance, we assessed changes in the redox state of cytochrome oxidase (CytOx) relative to cerebral heat production, and cytotoxic edema measured using cerebral impedance, during 25 min of complete umbilical cord occlusion or sham occlusion in fetal sheep at 0.7 gestation. Occlusion was followed by rapid, profound reduction in relative cerebral oxygenation and EEG intensity and an immediate increase in oxidized CytOx, indicating a reduction in electron flow down the mitochondrial electron transfer chain. Confirming rapid suppression of cerebral metabolism there was a loss of the temperature difference between parietal cortex and body at a time when carotid blood flow was maintained at control values. As occlusion continued, severe hypotension/hypoperfusion developed, with a further increase in CytOx levels to a plateau between 8 and 13 min and a progressive rise in cerebral impedance. In conclusion, these data strongly suggest active regulation of cerebral metabolism during the initial response to severe hypoxia, which may help to protect the immature brain from injury. asphyxia; preterm; umbilical cord occlusion FETAL AND NEONATAL ANIMALS are well known to be able to survive much longer periods of hypoxia than adults (9, 22). More recently, it has become clear that preterm animals can withstand even longer periods of profound hypoxia and hypotension/hypoperfusion without neural injury than at term (17,28,35). In part, this remarkable tolerance to hypoxia may be related to greater anaerobic capacity in the immature brain (48), but an important additional factor is likely to be actively regulated suppression of cerebral activity. This mechanism, which is mediated by release of endogenous inhibitory neuromodulators such as ␥-aminobutyric acid (GABA) and adenosine during hypoxia, recently has been shown to be active in near-term (0.8 to 0.9 gestation) fetal sheep (6,23,33,49). For example, hypoxemia or adenosine infusion in near-term fetal sheep increased oxidation of cerebral cytochrome oxidase (CytOx) on near-infrared measurements, indicating a rapid reduction in electron flow down the mitochondrial electron transfer chain and, thus, a fall in metabolic activity (40, 41). Conversely, blockade of adenosine A 1 receptor activity during umbilical cord occlusion in near-term fetal sheep accelerated the onset and increased the magnitude of cerebral anoxic cytotoxic edema, with subsequently increased neuronal loss (23).This regulated suppression of metabolic rate during hypoxia or ischemia, before energy stores are depleted, has been termed adaptive hypometabolism (38). It may be of considerable importance not only before birth but also during birth itself and in other settings involving adaptation to low oxygen levels (34). The near-term fetus of the high-altitude, hypoxia-adapted llama...

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Section: Discussionsupporting

confidence: 49%

Regulation of cytochrome oxidase redox state during umbilical cord occlusion in preterm fetal sheep

Roelfsema¹,

Dean²,

Wassink³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…First, we used the NIRS HbD signal as a surrogate for CBF. This was based on the strong correlation between HbD and CBF in previous animal validation studies (9,23). It may be argued that in some instances, a change in HbD could reflect a change in oxygen extraction fraction.…”

Section: Discussionmentioning

confidence: 99%

“…We previously validated changes in HbD to be highly correlated with changes in CBF (9). We used transfer function analysis to determine the coherence between the MAP and HbD signals (10,11) in the frequency range of 0 -0.04 Hz.…”

Section: Subjectsmentioning

confidence: 99%

Fluctuating Pressure-Passivity Is Common in the Cerebral Circulation of Sick Premature Infants

et al. 2007

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Cerebral blood flow pressure-passivity results when pressure autoregulation is impaired, or overwhelmed, and is thought to underlie cerebrovascular injury in the premature infant. Earlier bedside observations suggested that transient periods of cerebral pressure-passivity occurred in premature infants. However, these transient events cannot be detected reliably by intermittent static measurements of pressure autoregulation. We therefore used continuous bedside recordings of mean arterial pressure (MAP; from an indwelling arterial catheter) and cerebral perfusion [using the nearinfrared spectroscopy (NIRS) Hb difference (HbD) signal) to detect cerebral pressure-passivity in the first 5 d after birth in infants with birth weight Ͻ1500 g. Because the Hb difference (HbD) signal [HbD ϭ oxyhemoglobin (HbO2) Ϫ Hb] correlates with cerebral blood flow (CBF), we used coherence between MAP and HbD to define pressure-passivity. We measured the prevalence of pressurepassivity using a pressure-passive index (PPI), defined as the percentage of 10-min epochs with significant low-frequency coherence between the MAP and HbD signals. Pressure-passivity occurred in 87 of 90 premature infants, with a mean PPI of 20.3%. Cerebral pressure-passivity was significantly associated with low gestational age and birth weight, systemic hypotension, and maternal hemodynamic factors, but not with markers of maternal infection. Future studies using consistent serial brain imaging are needed to define the relationship between PPI and cerebrovascular injury in the sick premature infant. C erebral pressure autoregulation maintains CBF relatively constant despite changes over a range of systemic blood pressures known as the autoregulatory plateau (1). Conversely, when changes in blood pressure result in concordant changes in CBF, the cerebral circulation is deemed "pressure passive." Current understanding is that cerebral pressurepassivity develops when changes in blood pressure exceed the capacity of the intact cerebral autoregulatory system or when the system is impaired by illness, injury, or vasoactive medications. Cerebral pressure-passivity is considered a risk factor for cerebrovascular injury in the sick premature infant (2-4). The current study extends our earlier work (3) using bedside NIRS to measure continuously cerebrovascular responses to spontaneous fluctuations in blood pressure. In our previous studies, we observed that cerebral pressure-passivity may wax and wane over relatively short periods in premature infants. To study the fluctuating nature of cerebral pressure-passivity and quantify its prevalence over time, we developed a continuous recording and analysis system because previously described techniques using intermittent static measurements (5-7) would be unable to measure the prevalence of fluctuating cerebral pressure-passivity over the highest risk for brain injury in premature infants. The principal aim of this technique is to make quantitative measurements of the prevalence of cerebral pressure-passivity rather...

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“…OI is the difference between oxygenated and deoxygenated Hb divided by a factor of 2. Changes in OI have been validated to represent changes in CBF in several animal studies (15)(16)(17).…”

Section: Methodsmentioning

confidence: 99%

Applicability of Near-Infrared Spectroscopy to Measure Cerebral Autoregulation Noninvasively in Neonates: A Validation Study in Piglets

Hahn

Heiring²,

Pryds

et al. 2011

Pediatr Res

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Impaired cerebral autoregulation (CA) is common and is associated with brain damage in sick neonates. Frequency analysis using spontaneous changes in arterial blood pressure (ABP) and cerebral near-infrared spectroscopy (NIRS) has been used to measure CA in several clinical studies. Coherence of the NIRS and ABP signals (i.e. correlation in the frequency domain) detects impairment of CA, whereas gain (i.e. magnitude of ABP variability passing from systemic to cerebral circulation) estimates the degree of this impairment. So far, however, this method has not been validated. In 12 newborn piglets, we compared NIRS-derived measures of CA with a conventional measure of CA: cerebral blood flow was measured by laser Doppler flowmetry, and changes in ABP were induced by inflating a thoracic aorta balloon. CA capacity was calculated as %⌬CVR/%⌬ABP (i.e. percentage of full autoregulatory capacity), where CVR (i.e. cerebral vascular resistance) was estimated as ABP/Doppler flux. Correlation between coherence and CA capacity (r ϭ Ϫ0.34, n ϭ 24, p Ͼ 0.05) and between gain and CA capacity (r ϭ Ϫ0.11, n ϭ 24, p Ͼ 0.05) was limited. As expected, however, gain was significantly associated with CA capacity in measurements with significant coherence (r ϭ Ϫ0.55, n ϭ 15, p ϭ 0.03). In conclusion, our data validate frequency analysis for estimation of CA in clinical research. Low precision, however, hampers its clinical application. (Pediatr Res 70: 166-170, 2011) C erebral autoregulation (CA) is a physiological mechanism that cushions the cerebral circulation from transient changes in arterial blood pressure (ABP). With intact CA, cerebral blood vessels dilate proportional to decreases in ABP and constrict with increases in ABP. In that way, cerebral blood flow (CBF) remains approximately constant over a wide range of ABP (1). CA may be disrupted not only in sick preterm infants but also in those that are clinically well (2). However, there is evidence that CBF is independent from ABP over a wide pressure range in preterm infants, suggesting that CA may actually be effective in the immature brain (3). In preterm infants, disrupted CA has been associated with development of intraventricular hemorrhage (IVH) and periventricular leukomalacia (4,5). Impairment of CA narrows the range of ABP where CBF is matched to metabolic needs causing a state with vulnerability to even modest changes in ABP. Therefore, optimal management of ABP would include a possibility to titrate ABP into that range, where CA is working most effectively. However, to date, no monitoring device that measures CA continuously exists. Near-infrared spectroscopy (NIRS) detects changes in cerebral oxygenation noninvasively and continuously. Assuming that these changes represent changes in CBF, frequency analysis yielding coherence and gain between spontaneous changes in ABP and cerebral NIRS could fill that role. Coherence (i.e. correlation in the frequency domain) is supposed to detect impairment of CA, whereas gain estimates the magnitude of this impairment ...

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Noninvasive Detection of Changes in Cerebral Blood Flow by Near-Infrared Spectroscopy in a Piglet Model of Hydrocephalus

Cited by 97 publications

References 12 publications

Regulation of cytochrome oxidase redox state during umbilical cord occlusion in preterm fetal sheep

Regulation of cytochrome oxidase redox state during umbilical cord occlusion in preterm fetal sheep

Fluctuating Pressure-Passivity Is Common in the Cerebral Circulation of Sick Premature Infants

Applicability of Near-Infrared Spectroscopy to Measure Cerebral Autoregulation Noninvasively in Neonates: A Validation Study in Piglets

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