The present study was undertaken to characterize acute changes in cerebral hemodynamics subsequent to fluid-percussion brain injury in an infant animal model. We hypothesized that increased sympathetic outflow to the cephalic vasculature may cause decreases in CBF immediately following brain injury. Our results indicate that CBF and pial arteriolar diameter decrease immediately after injury, and that both decreases are blocked by adrenoceptor antagonists, consistent with the working hypothesis.
We acknowledge the technical assistance of Alexander Fedinec, Mildren Jackson, Jill S. Smith, Ellen B. Looney, and Annie M.-J. Shibata.
De Langen CDJMulder AH: On the role of calcium ions in the presynaptic alpha-receptor mediated inhibition of [3H]noradrenaline release from rat brain cortex synaptosomes. Brain Res 185:399–40819803H]noradrenaline release from rat brain cortex synaptosomes. Brain Res 185:
Lynch MABliss TVP: Noradrenaline modulates the release of [14C]glutamate from dentate but not from CA1/CA3 slices of rat hippocampus. Neuropharmacology 25:493–498198614C]glutamate from dentate but not from CA1/CA3 slices of rat hippocampus. Neuropharmacology 25:
Digitizing oscilloscope, Model 54201A, manufactured by Hewlett Packard, Palo Alto, California.
Radiolabeled microspheres obtained from DuPont Corp., Boston, Massachusetts.
Gamma counter MINAXIγ, Auto-Gamma 5000 series, manufactured by Packard Instrument Co., Downers Grove, Illinois.
This research was supported by Grants HL34059, HL42851, HL42875, and NS25122 from the National Institutes of Health, by the American Lebanese Syrian Associated Charities (ALSAC), and by Cancer Center CORE Grant CA-21765.