Rosenberg A A, Murdaugh E
Department of Pediatrics, University of Colorado School of Medicine, Denver 80262.
Pediatr Res. 1990 May;27(5):454-9. doi: 10.1203/00006450-199005000-00008.
The effect of preasphyxia blood glucose concentration on postasphyxia (PA) cerebral hemodynamics was examined in 21 newborn lambs. Glucose was unregulated in one group (n = 7), and controlled throughout the study by glucose clamp in hyperglycemic (n = 7) and hypoglycemic (n = 7) groups. Cerebral blood flow, determined using radiolabelled microspheres, and arterial and sagittal sinus O2 contents were measured at control, 5 min, 1, 2, and 4 h after resuscitation from an asphyxial insult. Preasphyxia blood glucoses were 6.48 +/- 0.55 mM (mean +/- SEM), 12.08 +/- 0.80, and 2.66 +/- 0.14 in the three study groups. In all three groups, 5 min PA cerebral blood flow was significantly increased from control. In the late period after asphyxia, the unregulated group had decreased cerebral blood flow compared with control, 53.2 +/- 3.8 mL.100 g-1.min-1, mean +/- SEM, p less than 0.01; 49.6 +/- 2.0, p less than 0.005; 53.4 +/- 3.0, p less than 0.01, at 1, 2, and 4 h PA, respectively, versus 85.7 +/- 6.9 at control, whereas both the hyper- and hypoglycemic groups did not differ significantly from control measurements. Cerebral oxygen consumption (CMRO2) was significantly decreased in all three groups 5 min PA and remained decreased in the late period after asphyxia in both the unregulated and hypoglycemic groups. In the unregulated group, CMRO2 was 191 +/- 14 microM.100 g-1.min-1, mean +/- SEM, p less than 0.05; 200 +/- 4; and 181 +/- 10, p less than 0.05 at 1, 2, and 4 h, respectively, PA versus 251 +/- 12 at control.(ABSTRACT TRUNCATED AT 250 WORDS)
