DIFFERENT CEREBRAL HEMODYNAMIC-RESPONSES FOLLOWING FLUID PERCUSSION BRAIN INJURY IN THE NEWBORN AND JUVENILE PIG

The present study was designed to characterize the influence of early developmental changes on the relationship among systemic arterial pres sure, cerebral hemodynamics, and cerebral oxygenation during the first 3 h following percussion brain injury. Anesthetized newborn (1-5 days old) and juvenile (3-4 weeks old) pigs equipped with a closed cranial window were connected to a percussion device consisting of a saline-f illed cylindrical reservoir with a metal pendulum. Brain injury of mod erate severity (1.9-2.3 atm) was produced by allowing the pendulum to strike a piston on the cylinder. Mean arterial blood pressure increase d after brain injury in juveniles (68 +/- 4 to 93 +/- 2 mm Hg within 3 min, n = 6), whereas it decreased after injury in newborns (70 +/- 3 to 51 +/- 3 mm Hg within 3 min, n = 6). Fluid percussion brain injury decreased pial artery diameter more in newborns (132 +/- 5 to 110 +/- 5 mu m within 10 min, n = 5) than in juveniles (141 +/- 3 to 133 +/- 3 mu m within 10 min, n = 5). Pial arterioles constricted to a greater extent than small pial arteries following brain injury in both age gro ups. Within 30 sec, brain injury produced a transient increase in cere bral hemoglobin O-2 saturation (27 +/- 4%, n = 5) that was reversed to a profound decrease in cerebral hemoglobin O-2 saturation (45 +/- 2%, n = 5) in the newborn as measured by near infrared spectroscopy. In c ontrast, brain injury produced modest increases in hemoglobin O-2 satu ration (10 +/- 1%, n = 5), followed by mild desaturation (4 +/- 1%, n = 5) in juveniles. Additionally, regional cerebral blood flow was redu ced within 10 min of injury in both newborn and juvenile pigs and rema ined depressed for 180 min in newborns. In contrast, cerebral blood fl ow returned to control values within 180 min in juveniles. These data show that the effects of comparable brain injury level were very diffe rent in newborn and juvenile pigs. Further, these data suggest that re ductions in cerebral blood flow following brain injury are more depend ent on changes in reactivity of arterioles. Finally, these data sugges t that the decrease in cerebral oxygenation, an index of metabolism, c oupled with reduced cerebral blood flow, could result in profound hypo perfusion after brain injury.