{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T16:27:30Z","timestamp":1774369650475,"version":"3.50.1"},"reference-count":52,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1989,10]]},"abstract":"<jats:p content-type=\"fine-print\">\u2713 This study tested the hypothesis that ischemia-reperfusion injury initiated by the superoxide anion radical is a major component of postdecompression hypoperfusion and cerebral edema, and could be attenuated by superoxide dismutase (SOD). A supratentorial extradural balloon was placed in 20 fasting, lightly anesthetized, mechanically ventilated dogs and inflated in 0.5-ml increments (0.07 ml\/sec) at 15-minute intervals. The endpoint of balloon expansion was the onset of an isoelectric electroencephalogram, near-arrest of hemispheric cerebral blood flow (CBF) (measured by H<jats:sub>2<\/jats:sub> clearance), and the appearance of a suprainfratentorial intracranial pressure gradient, which was held for 15 minutes. The <jats:italic>in vivo<\/jats:italic> development of brain edema was detected by measuring brain elastic response (BER) extradurally, and was correlated with postmortem measurement of brain water content (gravimetry); blood-brain barrier integrity was tested by Evans blue dye given after the insult. After decompression, the dogs were randomly assigned to one of four treatment groups: Group I received hyperventilation (PaCO<jats:sub>2<\/jats:sub> 28 \u00b1 1 mm Hg, mean \u00b1 standard deviation); Group II received furosemide (2.4 mg\/kg) and pentobarbital (10 mg\/kg) every 8 hours; Group III received 20% mannitol in a 1.4-gm\/kg bolus plus furosemide, 0.5 mg\/kg; and Group IV received SOD, 15,000 U\/kg every 15 minutes for 3 hours. At 4 hours of decompression Group IV had significantly greater recovery in local CBF and BER than Groups I, II, and III (p &lt; 0.05). The 24-hour survival rate was 20% for Group I, 60% for Group II, 80% for Group III, and 100% for Group IV. The survival rate appeared to correlate with a variable degree of postmortem intraparenchymal hemorrhages, blood-brain barrier disruption, and moderate to severe brain edema for Groups I, II, and III. In contrast, Group IV had the least brain edema (p &lt; 0.05) and Evans blue dye extravasation (p &lt; 0.05) and the fewest intraparenchymal hemorrhages. These data support the hypothesis that, under the experimental conditions described here, the superoxide anion plays a major role in the pathophysiology of postdecompression ischemic edema.<\/jats:p>","DOI":"10.3171\/jns.1989.71.4.0578","type":"journal-article","created":{"date-parts":[[2009,5,8]],"date-time":"2009-05-08T16:23:22Z","timestamp":1241799802000},"page":"578-587","source":"Crossref","is-referenced-by-count":28,"title":["Attenuation of decompressive hypoperfusion and cerebral edema by superoxide dismutase"],"prefix":"10.3171","volume":"71","author":[{"given":"Alfonso","family":"Schettini","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H. 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