Mitra · Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 2019 · prospective observational cohort study · n=23

Pressure passivity of cerebral mitochondrial metabolism is associated with poor outcome following perinatal hypoxic ischemic brain injury.

Cited 36 times in the scientific literature.

Level 3 - non-randomized controlled study

Prospective observational cohort study with 1-year neurodevelopmental follow-up

PubMed 28949271 · doi:10.1177/0271678X17733639 · record verified 2026-08-27

What was done

Researchers used broadband near-infrared spectroscopy (NIRS) and wavelet semblance analysis to assess cerebral metabolic autoregulation in 23 term infants undergoing therapeutic hypothermia for hypoxic ischemic encephalopathy (HIE). At a mean age of 48 hours, 60-minute epochs of mean arterial blood pressure (MABP) were compared against changes in oxidized cytochrome-c-oxidase (oxCCO), haemoglobin difference (HbD), and total haemoglobin (HbT). Results were compared against thalamic lactate/N-acetylaspartate (Lac/NAA) on proton magnetic resonance spectroscopy (MRS), brain MRI injury scores, and neurodevelopmental outcomes at one year of age.

What was found

OxCCO-MABP semblance (indicating pressure passivity of mitochondrial oxidative metabolism) correlated significantly with thalamic Lac/NAA ratio (r = 0.48, p = 0.02). OxCCO-MABP semblance was also significantly higher in infants with severe brain injury compared to those with mild-to-moderate injury as assessed by brain MRI score (p = 0.04), thalamic Lac/NAA (p = 0.04), and 1-year neurodevelopmental outcomes (p = 0.04).

Why it matters

Optical bedside monitoring of mitochondrial metabolism reactivity may identify neonates with impaired autoregulation and severe metabolic dysfunction during therapeutic hypothermia, providing early prognostic information after perinatal brain injury.

Limits

The sample size was small (n = 23), limiting statistical precision and subgroup analysis. Measurements were restricted to a single 60-minute epoch during therapeutic hypothermia, which may not capture dynamic physiological changes over time. Results and numerical values for HbD and HbT reactivity were not detailed in the abstract.

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