scholarly journals Cerebral Oxygen Metabolism in Neonatal Hypoxic Ischemic Encephalopathy during and after Therapeutic Hypothermia

2013 ◽  
Vol 34 (1) ◽  
pp. 87-94 ◽  
Author(s):  
Mathieu Dehaes ◽  
Alpna Aggarwal ◽  
Pei-Yi Lin ◽  
C Rosa Fortuno ◽  
Angela Fenoglio ◽  
...  

Pathophysiologic mechanisms involved in neonatal hypoxic ischemic encephalopathy (HIE) are associated with complex changes of blood flow and metabolism. Therapeutic hypothermia (TH) is effective in reducing the extent of brain injury, but it remains uncertain how TH affects cerebral blood flow ( CBF) and metabolism. Ten neonates undergoing TH for HIE and seventeen healthy controls were recruited from the NICU and the well baby nursery, respectively. A combination of frequency domain near infrared spectroscopy (FDNIRS) and diffuse correlation spectroscopy (DCS) systems was used to non-invasively measure cerebral hemodynamic and metabolic variables at the bedside. Results showed that cerebral oxygen metabolism ( CMRO 2i) and CBF indices ( CBF i) in neonates with HIE during TH were significantly lower than post-TH and age-matched control values. Also, cerebral blood volume ( CBV) and hemoglobin oxygen saturation ( SO 2) were significantly higher in neonates with HIE during TH compared with age-matched control neonates. Post-TH CBV was significantly decreased compared with values during TH whereas SO 2 remained unchanged after the therapy. Thus, FDNIRS–DCS can provide information complimentary to SO 2 and can assess individual cerebral metabolic responses to TH. Combined FDNIRS–DCS parameters improve the understanding of the underlying physiology and have the potential to serve as bedside biomarkers of treatment response and optimization.

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Takashi Temma ◽  
Kazuhiro Koshino ◽  
Tetsuaki Moriguchi ◽  
Jun-ichiro Enmi ◽  
Hidehiro Iida

Understanding cerebral oxygen metabolism is of great importance in both clinical diagnosis and animal experiments because oxygen is a fundamental source of brain energy and supports brain functional activities. Since small animals such as rats are widely used to study various diseases including cerebral ischemia, cerebrovascular diseases, and neurodegenerative diseases, the development of a noninvasivein vivomeasurement method of cerebral oxygen metabolic parameters such as oxygen extraction fraction (OEF) and cerebral metabolic rate of oxygen (CMRO2) as well as cerebral blood flow (CBF) and cerebral blood volume (CBV) has been a priority. Although positron emission tomography (PET) with15O labeled gas tracers has been recognized as a powerful way to evaluate cerebral oxygen metabolism in humans, this method could not be applied to rats due to technical problems and there were no reports of PET measurement of cerebral oxygen metabolism in rats until an15O-O2injection method was developed a decade ago. Herein, we introduce an intravenous administration method using two types of injectable15O-O2and an15O-O2gas inhalation method through an airway placed in the trachea, which enables oxygen metabolism measurements in rats.


2013 ◽  
Vol 114 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Zachary M. Smith ◽  
Erin Krizay ◽  
Jia Guo ◽  
David D. Shin ◽  
Miriam Scadeng ◽  
...  

Acute mountain sickness (AMS) is a common condition occurring within hours of rapid exposure to high altitude. Despite its frequent occurrence, the pathophysiological mechanisms that underlie the condition remain poorly understood. We investigated the role of cerebral oxygen metabolism (CMRO2) in AMS. The purpose of this study was to test 1) if CMRO2 changes in response to hypoxia, and 2) if there is a difference in how individuals adapt to oxygen metabolic changes that may determine who develops AMS and who does not. Twenty-six normal human subjects were recruited into two groups based on Lake Louise AMS score (LLS): those with no AMS (LLS ≤ 2), and those with unambiguous AMS (LLS ≥ 5). [Subjects with intermediate scores (LLS 3–4) were not included.] CMRO2 was calculated from cerebral blood flow and arterial-venous difference in O2 content. Cerebral blood flow was measured using arterial spin labeling MRI; venous O2 saturation was calculated from the MRI of transverse relaxation in the superior sagittal sinus. Arterial O2 saturation was measured via pulse oximeter. Measurements were made during normoxia and after 2-day high-altitude exposure at 3,800 m. In all subjects, CMRO2 increased with sustained high-altitude hypoxia [1.54 (0.37) to 1.82 (0.49) μmol·g−1·min−1, n = 26, P = 0.045]. There was no significant difference in CMRO2 between AMS and no-AMS groups. End-tidal Pco2 was significantly reduced during hypoxia. Low arterial Pco2 is known to increase neural excitability, and we hypothesize that the low arterial Pco2 resulting from ventilatory acclimatization causes the observed increase in CMRO2.


2012 ◽  
Vol 323 (1-2) ◽  
pp. 173-177 ◽  
Author(s):  
Zhaoxia Wang ◽  
Jiangxi Xiao ◽  
Sheng Xie ◽  
Danhua Zhao ◽  
Xiwei Liu ◽  
...  

1990 ◽  
Vol 28 (1) ◽  
pp. 50-51 ◽  
Author(s):  
Billie Lou Short ◽  
L Kyle Walker ◽  
Christine A Gleason ◽  
M Douglas Jones ◽  
Richard J Traystman

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