Search Results

You are looking at 1 - 4 of 4 items for

  • Author or Editor: William E. Hunt x
  • All content x
  • By Author: Bingham, W. George x
Clear All Modify Search
Restricted access

Joseph H. Goodman, W. George Bingham Jr., and William E. Hunt

✓ Endothelial changes leading to edema formation are examined in the primate spinal cord (Macaca mulatta) following a lesion created by a 20-gm weight falling 15 cm onto the exposed dura. Intravascular perfusion of a paraformaldehyde-glutaraldehyde solution followed by carbon black provides adequate fixation of vascular structures and glial elements. Myelin is poorly preserved. Ultrastructural alterations of the blood-brain barrier consist of loss of integrity of the endothelial tight junctions. Edema caused by vascular disruption and parenchymatous extravasation of intravascular contents is observed along with glial swelling. Interglial gap junctions persist in areas of marked cellular separation and do not impede the migration of edema fluid.

Restricted access

David Yashon, W. George Bingham Jr., Edward M. Faddoul, and William E. Hunt

✓ Identification of central nervous system edema is based on increased water content in relation to nonvolatile residue per unit weight. Nonvolatile residue in spinal cord tissue following impact trauma was determined to ascertain the magnitude and persistence of edema. High and low thoracic laminectomies were carried out on each of 17 rhesus monkeys. The lower exposed cord was traumatized with a calibrated blow of 300 gm cm. All upper exposed cords and the lower exposed cord in one monkey served as nontraumatized controls. At time intervals of 5 minutes to 20 days after trauma, cord segments were removed and assayed for water content. Increased tissue water was evident within 5 minutes and persisted for 15 days. By the 20th day it had essentially subsided. Increased tissue water content in the traumatized segment reached a maximum of 7.4% over control values at 5 days and then gradually diminished. These findings support the concept that edema following spinal trauma is unrelated to secondary effects of ischemia after 18 hours. The protracted course of increased water content (15 to 20 days) was unexpected and may indicate that edema-reducing measures should be continued for 2 to 3 weeks following spinal cord trauma with severe neurological dysfunction.

Restricted access

David Yashon, George E. Locke, W. George Bingham Jr., Wigbert C. Wiederholt, and William E. Hunt

✓ Electrocortigraphic activity and common carotid blood flow were studied in 12 dogs during and following profound oligemic hypotension. Five animals survived but seven died within 75 min of hypotension. Although an 80% to 90% reduction in both mean arterial pressure and common carotid blood flow was observed, only a 20% diminution of intracranial pressure occurred and there was little change in electrocorticographic function. The preservation of cerebral function in the presence of profound systemic hypotension was demonstrated. When death occurred during shock, no prior change in central nervous system function was noted. With reinfusion, no change in parameters was noted, but common carotid blood flow was depressed to 35% to 50% of control levels for up to 2½ hrs of observation.

Restricted access

W. George Bingham, Harold Goldman, Stewart J. Friedman, Sharon Murphy, David Yashon, and William E. Hunt

✓ The authors used indicator fractionation techniques to determine blood flow in normal and bluntly traumatized spinal cords of Macaca rhesus monkeys. Normal flow rates were determined for several levels of spinal cord as well as differential values for white and gray matter from representative areas. Flow rates in traumatized tissue, obtained at several different time intervals up to 4 hours after injury, demonstrated marked differences in regional perfusion of the white matter and gray matter after trauma. Gray matter perfusion was nearly obliterated while white matter blood flow persisted and in fact was higher than uninjured controls. The findings do not support the concept of ischemia as a factor in white matter failure. If toxic pathobiochemical alterations are induced by trauma, it may be possible to reverse these changes by exploiting the preserved white matter blood flow for chemotherapeutic intervention.