Reduced postnatal cerebral glucose metabolism measured by PET after asphyxia in near term fetal lambs.
The effects of fetal asphyxia on cerebral function and development, involve the transition from fetal to neonatal life. Changes in cerebral glucose metabolism may be an early postnatal indicator of fetal asphyxia. The objective is to develop an experimental lamb model involving the transition from fetal to neonatal life and to examine the effect of fetal asphyxia with cerebral hypoxic ischemia on early postnatal cerebral glucose metabolism. Fetal asphyxia was induced by total umbilical cord occlusion in eight near-term fetal lambs (134-138 days) with the ewe under isoflurane-opiate anesthesia. The mean occlusion time until cardiac arrest was 14.5 (4.2) min (SD). Lambs were immediately delivered and standardized resuscitation was instituted after 2 min asystole. At 4 hr postnatal age, [18-F]Fluoro-2-deoxy-glucose (18-FDG) was injected intravenously in eight asphyxiated lambs and in eight controls. Cerebral glucose metabolism was examined by positron emission tomography (PET). As a result the mean arterial blood pressure, acid-base values, blood glucose and serum lactate at 4 hr postnatal age did not differ significantly between lambs subjected to umbilical cord occlusion and controls. EEG was abnormal in all lambs subjected to cord occlusion and normal in the controls at 4 hr postnatal age. Global cerebral metabolic rate (CMRgl) as determined by PET was significantly lower in lambs subjected to cord occlusion mean/median (SD) 22.2/19.6 (8.4) micromol/min/100 g) than in controls mean/median (SD) 37.8/35.9 (6.1); P < 0.01). Global CMRgl is significantly reduced in newborn lambs 4 hr after fetal asphyxia induced by umbilical cord occlusion. A reduction in CMRgl is an early indicator of global hypoxic cerebral ischemia.
Thorngren-Jerneck
K
K
Department of Pediatrics, University Hospital, Lund University, SE-221 85 Lund, Sweden. kristina.thorngren-jerneck@pedi.lu.se
Ley
D
D
Hellström-Westas
L
L
Hernandez-Andrade
E
E
Lingman
G
G
Ohlsson
T
T
Oskarsson
G
G
Pesonen
E
E
Sandell
A
A
Strand
S E
SE
Werner
O
O
Marsal
K
K
D000138:Acidosis / Q000000981:diagnostic imaging / Q000209:etiology; D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism; D001238:Asphyxia Neonatorum / Q000000981:diagnostic imaging*; D001794:Blood Pressure / Q000502:physiology; D002540:Cerebral Cortex / Q000000981:diagnostic imaging*; D002560:Cerebrovascular Circulation / Q000502:physiology; D004195:Disease Models, Animal; D004569:Electroencephalography; D005260:Female; D005311:Fetal Hypoxia / Q000000981:diagnostic imaging*; D005333:Fetus / Q000378:metabolism* / Q000503:physiopathology; D005947:Glucose / Q000378:metabolism*; D006323:Heart Arrest / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D020925:Hypoxia-Ischemia, Brain / Q000000981:diagnostic imaging*; D007231:Infant, Newborn; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D009410:Nerve Degeneration / Q000000981:diagnostic imaging; D011247:Pregnancy; D012756:Sheep; D014055:Tomography, Emission-Computed; D014470:Umbilical Cord / Q000293:injuries
D019344:Lactic Acid; D005947:Glucose