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Objective. Preterm infants are often presumed to have a pressure passive cerebral circulation implying that a low mean arterial blood pressure (MABP) results in reduced cerebral perfusion. The aim of this study was to determine whether cerebral blood flow (CBF) was compromised in preterm infants whose MABP fell below 30 mm Hg (4 kPa). Methods. Thirty preterm infants undergoing intensive care were studied within the first 24 hours of life. CBF was measured using near infrared spectroscopy. The infants were analyzed in two groups on the basis of their MABP at the time of study: group 1 had a MABP below 30 mm Hg and group 2 more than 30 mm Hg. CBF in the two groups was compared. Results. There was no significant difference in the mean CBF between the two groups. In group 1 the median MABP was 27.2 mm Hg (range, 23.7-29.9 mm Hg) and CBF was 13.9 (standard deviation, ±6.9) mL . 100 g -1 . min -1 . In group 2 the median MABP was 35.3 mm Hg (range, 30.1-39.3 mm Hg) and CBF was 12.3 (standard deviation, ±6.4) mL 100 g -1 . min -1 . Mortality and incidence of cranial ultrasound scan abnormalities were also not significantly different. Conclusion. These results indicate that preterm infants undergoing intensive care are able to maintain adequate cerebral perfusion at a MABP in the range of 23.7 to 39.3 mm Hg. Pediatrics 1998;102:337-341; near infrared spectroscopy, cerebral blood flow, cerebral autoregulation, blood pressure, preterm infant.

AIM To measure changes in cerebral haemodynamics over the first three days of life in very preterm infants with normal brains. METHODS Eleven mechanically ventilated infants (median gestational age 26 weeks) without evidence of major abnormalities on cranial ultrasound examination were studied. Cerebral blood flow (CBF) and cerebral blood volume (CBV) were measured using near infrared spectroscopy at least twice over the first three days of life. RESULTS Cerebral blood flow increased significantly with time (p=0.02; stepwise linear regression) and this was independent of mean arterial blood pressure, PaCO2, and haematocrit. CONCLUSION This change is likely to represent a normal adaptive response of the cerebral circulation to postnatal life.

We have used an intensity modulated optical spectrometer, which measures the phase shift across tissue experienced by intensity modulated near-infrared light, to determine the absolute optical pathlength through tissue. The instrument is portable and takes only 5 s to record pathlength at four wavelengths (690 nm, 744 nm, 807 nm and 832 nm). The absolute pathlength divided by the known spacing between the light source and detector on the skin is the differential pathlength factor (DPF) which previous studies have shown is approximately constant for spacings greater than 2.5 cm. DPF results are presented for measurements on 100 adults and 35 newborn infants to determine the statistical variation on the DPF. All measurements were made at a frequency of 200 MHz with source-detector spacings of > 4 cm. Results at 807 nm show a DPF of 4.16(+/- 18.8%) for adult arm, 5.51(+/- 18%) for adult leg, 6.26(+/- 14.1%) for adult head and 4.99(+/- 9%) for the head of a newborn infant. A wavelength dependence was obtained for DPF on all tissues and a difference in DPF between male and female was observed for both the adult arm and leg. The results can be used to improve the quantitation of chromophore concentration changes in adults and newborn infants.

We report a neonate with cutis marmorata telangiectatica congenita and clinical features of Adams-Oliver syndrome in association with severe pulmonary vascular disease. We provide an overview of cutis marmorata telangiectatica congenita, distinguishing it from cutis marmorata, a common and benign physiologic cutaneous disorder seen in neonates. We highlight the need for thorough medical evaluation in cutis marmorata telangiectatica congenita to exclude associated congenital anomalies.

Aims—To investigate the relation between cerebral blood flow on the first day of postnatal life and the severity of any subsequent germinal matrix haemorrhage‐ intraventricular haemorrhage (GMH‐ IVH). Methods—Cerebral blood flow was measured in 24 babies during the first 24 hours of life using near infrared spectroscopy. Repeated cerebral ultrasound examination was performed to define the maximum extent of GMH‐IVH. Infants were classified as: normal scan, minor periventricular haemorrhage (haemorrhage that resolved), or severe GMH‐IVH (haemorrhage distending the ventricles, that progressed to either post haemorrhagic dilatation or porencephalic cyst formation). Results—Cerebral blood flow was significantly lower in the infants with GMH‐IVH (median 7.0 ml/100 g/min) than those without haemorrhage (median 12.2 ml/100 g/min), despite no diVerence in carbon dioxide tension and a higher mean arterial blood pressure. On subgroup analysis, those infants with severe GMH‐IVH had the lowest cerebral blood flow. Conclusion—A low cerebral blood flow on the first day of life is associated with the subsequent development of severe intraventricular haemorrhage. (Arch Dis Child Fetal Neonatal Ed 1999;81:F15‐F18)

This study tested the hypothesis that mild hypothermia after severe transient hypoxia-ischemia reduces the subsequent delayed rise in cerebral lactate peak-area ratios as determined by proton (1H) magnetic resonance spectroscopy (MRS) in the newborn piglet. Nine piglets aged < 24 h underwent temporary occlusion of the common carotid arteries and hypoxemia. Resuscitation was started when cerebral [phosphocreatine]/[inorganic phosphate] had fallen close to zero and [nucleotide triphosphate (NTP)]/[exchangeable phosphate pool (EPP)] was below about a third of baseline. On resuscitation rectal and tympanic temperatures were lowered to 35 degrees C for 12 h after which normothermia (38.5 degrees C) was resumed. 1H MRS data collected over 48 or 64 h after resuscitation were compared with concurrently established data from 12 piglets similarly subjected to transient cerebral hypoxia-ischemia, but maintained normothermic, and six sham-operated controls. The severity of the primary insult (judged from the time integral of depletion of [NTP]/[EPP]) was similar in the hypothermic and normothermic groups. The maximum lactate/N-acetylaspartate ratio observed between 24 and 48 h after resuscitation in the hypothermic group was 0.10 (0.05-0.97), median (interquartile range), which was significantly lower than that observed in the normothermic group, 1.28 (0.97-2.14), and not significantly different from that observed in the control group, 0.08 (0.06-0.11). Similar results were obtained for lactate/choline and lactate/total creatine. We conclude that mild hypothermia after a severe acute cerebral hypoxic-ischemic insult reduces the delayed elevation in lactate peak-area ratios, thus reflecting reduced lactate accumulation.

Severely birth-asphyxiated human infants develop delayed ("secondary") cerebral energy failure, which carries a poor prognosis, during the first few days of life. This study tested the hypothesis that i.v. magnesium sulfate (MgSO4) after severe transient cerebral hypoxia-ischemia decreases the severity of delayed energy failure in the newborn piglet. Twelve piglets underwent temporary occlusion of the common carotid arteries and hypoxemia. Resuscitation was started when cerebral [phosphocreatine (PCr)]/[inorganic phosphate (Pi)], as determined by phosphorus magnetic resonance spectroscopy, had fallen virtually to zero, and nucleotide triphosphate (NTP) had fallen below a third of baseline. The piglets were randomized to receive, blind, either: 1) three i.v. infusions of 12.5% MgSO4 heptahydrate solution: 400 mg.kg-1 MgSO4.7H2O starting 1 h after resuscitation, and 200 mg.kg-1 12 and 24 h later (n = 6); or 2) three infusions of placebo, 0.9% NaCl (n = 6). Phosphorus and proton spectroscopy were continued until 48 h after resuscitation, and values were compared between the two groups. Mean plasma magnesium levels, 1 h after each of the three doses of MgSO4, were 2.1, 2.0, and 1.9 mmol.L-1, respectively. The severity of the primary insult, determined by the time-integral of depletion of cerebral [NTP]/[exchangeable phosphate pool (EPP)], was similar in the MgSO4-treated and placebo groups. After resuscitation, there was no difference in the progression or severity of delayed energy failure between the two groups, as judged by cerebral [PCr]/[Pi], [NTP]/[EPP], or lactate/creatine and N-acetylaspartate/creatine peak-area ratios. We conclude that MgSO4 did not decrease the severity of delayed cerebral energy failure.

Saturation measurements have long been used to provide information about oxygenation levels within tissue in the form of a single percentage value. Whilst the measurement of peripheral arterial oxygen saturation (SaO2) provides useful information about the delivery of oxygen to the brain, a measure of the actual level of cerebral oxygen consumption and uptake would be a more useful guide for the direction of therapies. Oxygen consumption is the product of cerebral blood flow (CBF) and the difference between arterial and venous oxygen content. Measurements of cerebral venous saturation can therefore be used as an indicator of oxygen consumption and have been shown to be a useful clinical parameter in the management of patients with compromised cerebral haemodynamics (Garlick et al., 1987, Cruz et al., 1991).

Although near infrared spectroscopy (NIRS) is primarily used to probe changes in oxyhaemoglobin (HbO2) and deoxyhaemoglobin (dHb) concentrations, it has long been realised that there is a significant oxygen-concentration dependent near infrared signal from the mitochondrial enzyme cytochrome c oxidase. In this paper we discuss the origins of this near infrared (NIR) signal, the possible factors affecting its intensity and its likely physiological and clinical significance. This paper complements our recent review on this subject1.

The CuA redox centre of cytochrome oxidase has a distinct redox-sensitive absorbance band in the near infrared that enables it to be detected non-invasively (Jobsis 1977). We have been recently developing novel in vitro (Matcher et al. 1995) and in vivo (Cooper et al. 1996a) tests for the validity of algorithms claiming to be able to measure these redox changes, successfully deconvoluted from the greater spectroscopic perturbations induced by haemoglobin oxygenation and concentration changes. However, even if this problem is solved completely there still remains the question as to what the redox state of this metal centre is actually telling us about mitochondrial function in vivo. We are therefore performing parallel in vitro studies of the effect of energization, electron flow and oxygen tension on the redox state of CuA, similar to those originally outlined by Chance as aids to understanding NADH surface fluorescence measurements (Chance et al. 1973). This paper studies the effect of varying the rate of electron entry to cytochrome oxidase on the CuA redox state in vivo and in vivo and therefore relates to the value of the normal, physiological oxidation state of CuA.

Cerebral hyperaemia following hypoxic-ischaemic injury injury in the anaesthetised, newborn piglet

Background: Transient HI leads to a delayed decline in cerebral nucleotide triphosphate (NTP)/exchangeable phosphate pool (EPP) ratios measured by phosphorus magnetic resonance spectroscopy (MRS). We measured changes in CuA during the development of delayed energy failure in order to investigate the relationship between mitochondrial cytochrome redox state and cerebral phosphorus high energy metabolites.

The use of near-infrared spectroscopy to measure noninvasively changes in the redox state of cerebral cytochrome oxidase in vivo is controversial. We therefore tested these measurements using a multiwavelength detector in the neonatal pig brain. Exchange transfusion with perfluorocarbons revealed that the spectrum of cytochrome oxidase in the near-infrared was identical in the neonatal pig, the adult rat, and in the purified enzyme. Under normoxic conditions, the neonatal pig brain contained 15 μmol/L deoxyhemoglobin, 29 μmol/L oxyhemoglobin, and 1.2 μmol/L oxidized cytochrome oxidase. The mitochondrial inhibitor cyanide was used to determine whether redox changes in cytochrome oxidase could be detected in the presence of the larger cerebral hemoglobin concentration. Addition of cyanide induced full reduction of cytochrome oxidase in both blooded and bloodless animals. In the blooded animals, subsequent anoxia caused large changes in hemoglobin oxygenation and concentration but did not affect the cytochrome oxidase near-infrared signal. Simultaneous blood oxygenation level-dependent magnetic resonance imaging measurements showed a good correlation with near-infrared measurements of deoxyhemoglobin concentration. Possible interference in the near-infrared measurements from light scattering changes was discounted by simultaneous measurements of the optical pathlength using the cerebral water absorbance as a standard chromophore. We conclude that, under these conditions, near-infrared spectroscopy can accurately measure changes in the cerebral cytochrome oxidase redox state.