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Edward J. Kosnik, William E. Hunt and Carole A. Miller

✓ The history, physical findings, and treatment of dural arteriovenous malformations are reviewed. The importance of completely identifying and obliterating the fistula, even at the expense of obliterating major venous sinuses, is emphasized. Failure of surgical treatment usually is the result of mistaking the more obvious dilated feeding vessels for the lesion itself.

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David Yashon, William Stone, Alfred Magness, William E. Hunt and William Hamelberg

✓ The effect of halothane-induced profound systemic arterial hypotension on brain ischemia was evaluated by comparison with hypotension caused by oligemia and trimethaphan as well as nonhypotensive controls. Mean cerebral tissue lactate concentrations after halothane-induced hypotension at 5, 30, and 60 minutes were 4.34, 5.92, and 7.48 mM/kg. There was no significant difference between halothane and control animals during the experimental period. At 30 and 60 minutes, both oligemic and trimethaphan groups were higher than the control and halothane series. Definite protection from cerebral ischemia is provided by halothane during induced hypotension. Exact mechanisms of protection conveyed by halothane are unclear, but are probably not related to relative increased blood flow since cerebral vasodilation is maximal in these low blood-pressure ranges irrespective of etiology.

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William F. Collins, James L. O'Leary, William E. Hunt and Henry G. Schwartz

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Robert A. Feldman, David Yashon, George E. Locke and William E. Hunt

✓ Eleven anesthetized dogs underwent bilateral craniectomies. Four control dogs had serial resections of cerebral tissue in the normotensive state. After one control sample was removed from the remaining seven dogs, they were bled to a mean arterial pressure of 30 to 35 mm Hg and had cerebral tissue samples resected at 0, 30, and 60 min after the onset of hypotension. The tissue samples from the four normotensive dogs averaged 4.83 mM lactate/kg tissue with a range of 4.67 to 7.22 mM/kg. At 0 time post-shock the samples averaged 7.18 mM/kg, at 30 min post-shock 14.31 mM/kg, and at 60 min 18.76 mM/kg. It can be concluded that hemorrhagic shock causes a progressive elevation in cerebral tissue lactate, which correlates with the duration of shock. At low mean arterial pressures the brain is susceptible to the effects of poor tissue perfusion, which results in both inadequate oxygenation and lactate washout in spite of well-established mechanisms for preferential shunting of blood to the brain.

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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.

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George E. Locke, David Yashon, Robert A. Feldman and William E. Hunt

✓ Lactate accumulation in spinal cord tissue following trauma was determined to ascertain the role and magnitude of ischemia. High thoracic and low thoracic laminectomies were performed on each of nine rhesus monkeys. The lower exposed cord was traumatized with a calibrated blow of 300 gm cm. The upper exposed cord served as a nontraumatized control. At time intervals of 1.5 min to 48 hrs after trauma, both cord segments were removed and assayed for lactic acid. Lactate in nontraumatized segments averaged 3.64 mM/kg tissue, with a range of 2.20 to 4.95. Lactate in traumatized segments removed in from 1.5 min to 12 hrs from six monkeys averaged 5.50 mM/kg tissue, with a range of 4.32 to 6.46. Lactate in traumatized segments from three monkeys 18 to 40 hrs after trauma averaged 4.07 mM/kg, with a range of 3.20 to 5.18. This finding supports the concept that ischemia plays a role early in the traumatic process in spinal cord injury.

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Robert A. Feldman, David Yashon, George E. Locke and William E. Hunt

✓ In rhesus monkeys subjected to circulatory arrest, studies were made of the relationship of lactate production in the spinal cord to the duration of circulatory arrest and magnitude of lactate accumulation, and the results were compared to the magnitude of rise in cerebral tissue lactate. Both high and low thoracic laminectomies were performed on each of eight rhesus monkeys. Spinal cord tissue was excised for lactate assay at the upper laminectomy as a control, and a second tissue specimen was excised at the lower laminectomy site at time increments of 30 sec to 30 min after circulatory arrest. Tissue was excised from each site without circulatory arrest in one monkey and showed negligible increase in lactate production, indicating that excision of tissue itself does not result in increased lactate. Nonanoxic samples from seven monkeys averaged 4.60 millimoles (mM)/lactate/kg tissue, with a range of 2.22 to 6.49. Postcirculatory arrest samples from these monkeys averaged 11.10 mM lactate/kg tissue, with a range of 3.62 (at 30 sec) to 14.33 (at 10 min). Anoxic spinal tissue lactate was elevated above controls in each instance, and tissue lactate peaked between 5 to 10 min after circulatory arrest and remained stable with mild fluctuations beyond that time. Thus, the spinal cord responds to circulatory arrest much as cerebral tissue, but with some delay in the accumulation of lactic acid.

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William E. Hunt, W. Kemp Clark, Arthur B. Eisenbrey Jr., Louis Finney, William E. Hunt, Bryon C. Pevehouse, Walter W. Whisler and Richard L. Rovit

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